research proposal about cancer

Cancer research writing: how to plan and write a research proposal

Do’s and Don’ts in writing a scientific literature review for health care research

What are the reporting guidelines to be followed while writing a biomedical literature review for a manuscript?

• There are several approaches to treat cancer cells like immune therapy, gene therapy which resists the patients from cancer cells.
• Writing a cancer research paper is not a simple task; it’s more difficult while collecting research paper.Pubrica gives full support in writing research article in various disciplines like cancer, drug resistance, cancer cells, etc., Pubrica can also support in experimental researches too.

Introduction:

Cancer is a universal leading cause of death world wide; there are several types of cancers; mainly, they are brain cancer, breast cancer, lungs cancer, kidney cancer etc. If research thesis should be published in a specific journal , then the documents should contain specific elements like abstracts, the body of the text, methods, results, discussion and conclusion. The steps which include in the hypothesis are

• The main target should be researches, and the searching content should highly related to the topic.
• The quality and integrity of the research paper should be high.
• The reference list should befrom books, chapters, articles which are related to the topics.

Challenges in cancer research writing:

Essential investigation in cancer research is frequently seen as high-risk potential since the clinical applications give a unique detail about the scientific journal . From many cases, information is gathered for examining cancer cells, not as it made stride our understanding of the infection but it is necessary for the improvement of clinical progress which is more useful to the patients, as well as to theimmunotherapy and cancer immunizations outlines.

In many cases,the abilityof almost all the results of fundamental analysis about the cancer researchers are about the moderately small subsequence from so many sources, so that government financing for cancer research analysis about is critical. Collaborating over disciplines is progressively essential to get better vital instrument in cancer. In this manner, a few examiners may get to create apparatus and procedures for sharing and communicating their investigation through a scientific paper .

There are five steps to write an active cancer research proposal

• Preparation
• Development
• Specific points
• Background and importance
• Research plan and strategies
• Preparation:

This is the first step in writing a research paper. Identification of research journals . How long it would take to complete the process, what level of financing it would require, and finding of potential for particular compounds. 

• Development:

Given application undergo through these sequences 1. Unique 2. Presentation 3. Particular aims, 4. Significant 5. Investigation or research plans 6. Budget 7. Biographical sketch

• Specific point:

The particular point/ specific point is the question, speculations, or generally speculations that the research is looking to address or test. The author undergoes to represent the long-term objective or short-term objective, reasonable or extremely reasonable as well as particular point should aim the scientific research paper .

            Cancer research may address extensive and complex questions that are not continuously fully expressed. The author can take critical bits of knowledge that may rise amid the course of the study that will direct theproject in future headings.

This area briefly explains about the publication, critically evaluates existing information, and particularly distinguishes the reports which the project intends to fill. Briefly states the significance and healthy importance of the research paper described within the application by relating the particular points to the overall long-term objective. Here the author has the opportunity to show information of the field, the capacity to analyse the existing research about critically, and to appear how the proposed work will expand a investigate zone.

Sketch the research about plan and method to be utilized to achieve the specific aims of the development. Incorporate how the information will be collected, analysed and interpreted. Sketch any unused strategy and its advantages over existing methodology . Talk about the potential trouble and barrier of the proposed procedures and elective approaches to attain the points. As a part of this research area which gives a conditional arrangement or timetable for the extension point out.

Conclusion:

In cancer research and therapies, there are so many advancements which help to fasten the technology and record-breaking. There are so many limitations like drug properties, industrial scale-up and stability of drugs to a clinical trial. We are going with you through the whole circulating stages we help restorative specialists, backup, healing centres, pharma and apparatus producers in their journey for a solid collaboration. We have specialists over subjects such as life science, therapeutic and innovation

References:

• International Committee of Medical Journal Editors. Recommendations for the conduct, reporting, editing, and publication of scholarly work in medical journals. 2014. (accessed November 2016).
• Gopen G & Swan J. The science of scientific writing.  Am Sci . 1990; 78:550–558. (accessed November 2016)
•  Fisher JP, Jansen JA, Johnson PC  et al . Guidelines for writing a research article for publication. Mary Ann Liebert Inc. (accessed November 2016)
• World Association of Medical Editors. Professionalism Code of Conduct. 2016
• Bossuyt PM, Reitsma JB, Bruns DE  et al . Towards complete and accurate reporting of studies of diagnostic accuracy: The STARD Initiative.  Ann Int Med  2003; 138:40–44.

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• Open access
• Published: 26 November 2018

The 150 most important questions in cancer research and clinical oncology series: questions 94–101

Edited by Cancer Communications

Cancer Communications

Cancer Communications volume  38 , Article number:  69 ( 2018 ) Cite this article

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Since the beginning of 2017, Cancer Communications (former title: Chinese Journal of Cancer ) has published a series of important questions regarding cancer research and clinical oncology, to provide an enhanced stimulus for cancer research, and to accelerate collaborations between institutions and investigators. In this edition, the following 8 valuable questions are presented. Question 94. The origin of tumors: time for a new paradigm? Question 95. How can we accelerate the identification of biomarkers for the early detection of pancreatic ductal adenocarcinoma? Question 96. Can we improve the treatment outcomes of metastatic pancreatic ductal adenocarcinoma through precision medicine guided by a combination of the genetic and proteomic information of the tumor? Question 97. What are the parameters that determine a competent immune system that gives a complete response to cancers after immune induction? Question 98. Is high local concentration of metformin essential for its anti-cancer activity? Question 99. How can we monitor the emergence of cancer cells anywhere in the body through plasma testing? Question 100. Can phytochemicals be more specific and efficient at targeting P-glycoproteins to overcome multi-drug resistance in cancer cells? Question 101. Is cell migration a selectable trait in the natural evolution of carcinoma?

Until now, the battle against cancer is still ongoing, but there are also ongoing discoveries being made. Milestones in cancer research and treatments are being achieved every year; at a quicker pace, as compared to decades ago. Likewise, some cancers that were considered incurable are now partly curable, lives that could not be saved are now being saved, and for those with yet little options, they are now having best-supporting care. With an objective to promote worldwide cancer research and even accelerate inter-countries collaborations, since the beginning of 2017, Cancer Communications (former title: Chinese Journal of Cancer ) has launched a program of publishing 150 most important questions in cancer research and clinical oncology [ 1 ]. We are providing a platform for researchers to freely voice-out their novel ideas, and propositions to enhance the communications on how and where our focus should be placed [ 2 , 3 , 4 , 5 , 6 , 7 , 8 , 9 , 10 , 11 , 12 , 13 ]. In this edition, 8 valuable and inspiring questions, Question 94–101, from highly distinguished professionals from different parts of the world are presented. If you have any novel proposition(s) and Question(s), please feel free to contact Ms. Ji Ruan via email: [email protected].

Question 94: The origin of tumors: time for a new paradigm?

Background and implications.

“There is no worse blind man than the one who doesn’t want to see. There is no worse deaf man than the one who doesn’t want to hear. And there is no worse madman than the one who doesn’t want to understand.” —Ancient Proverb

In the past half-century, cancer biologists have focused on a dogma in which cancer was viewed as a proliferative disease due to mechanisms that activate genes (oncogenes) to promote cell proliferation or inactivate genes (tumor suppressor genes) to suppress tumor growth. In retrospect, these concepts were established based on functional selections, by using tissue culture (largely mouse NIH 3T3 cells) for the selection of transformed foci at the time when we knew virtually nothing about the human genome [ 14 ]. However, it is very difficult to use these genes individually or in combinations to transform primary human cells. Further, the simplified view of uncontrolled proliferation cannot explain the tumor as being a malignant organ or a teratoma, as observed by pathologists over centuries. Recently, the cancer genomic atlas project has revealed a wide variety of genetic alterations ranging from no mutation to multiple chromosomal deletions or fragmentations, which make the identification of cancer driver mutations very challenging in a background of such a massive genomic rearrangement. Paradoxically, this increase the evidences demonstrating that the oncogenic mutations are commonly found in many normal tissues, further challenging the dogma that genetic alteration is the primary driver of this disease.

Logically, the birth of a tumor should undergo an embryonic-like development at the beginning, similar to that of a human. However, the nature of such somatic-derived early embryo has been elusive. Recently, we provided evidence to show that polyploid giant cancer cells (PGCCs), which have been previously considered non-dividing, are actually capable of self-renewal, generating viable daughter cells via amitotic budding, splitting and burst, and capable of acquisition of embryonic-like stemness [ 15 , 16 , 17 ]. The mode of PGCC division is remarkably similar to that of blastomere, a first step in human embryogenesis following fertilization. The blastomere nucleus continuously divides 4–5 times without cytoplasmic division to generate 16–32 cells and then to form compaction/morulae before developing into a blastocyst [ 18 ]. Based on these data and similarity to the earliest stage of human embryogenesis, I propose a new theory that tumor initiation can be achieved via a dualistic origin, similar to the first step of human embryogenesis via the formation of blastomere-like cells, i.e. the activation of blastomere or blastomere-like cells which leads to the dedifferentiation of germ cells or somatic cells, respectively, which is then followed by the differentiation to generate their respective stem cells, and the differentiation arrest at a specific developmental hierarchy leading to tumor initiation [ 19 ]. The somatic-derived blastomere-like cancer stem cell follows its own mode of cell growth and division and is named as the giant cell cycle. This cycle includes four distinct but overlapping phases: the initiation, self-renewal, termination, and stability phases. The giant cell cycle can be tracked in vitro and in vivo due to their salient giant cell morphology (Fig.  1 ).

One mononucleated polyploid giant cancer cell (PGCC) in the background of regular size diploid cancer cells. The PGCC can be seen to be at least 100 times larger than that of regular cancer cells

This new theory challenges the traditional paradigm that cancer is a proliferative disease, and proposes that the initiation of cancer requires blastomere-like division that is similar to that of humans before achieving stable proliferation at specific developmental hierarchy in at least half of all human cancers. This question calls for all investigators in the cancer research community to investigate the role of PGCCs in the initiation, progression, resistance, and metastasis of cancer and to look for novel agents to block the different stages of the giant cell cycle.

The histopathology (phenotype) of cancers has been there all the time. It is just the theory of cancer origin proposed by scientists that changes from time to time. After all, trillions of dollars have been invested in fighting this disease by basing on its genetic origin in the past half-century, yet, little insight has been gained [ 14 ]. Here are two quotes from Einstein: “Insanity: doing the same thing over and over again expecting different results”, and “We cannot solve our problems with the same thinking we used when created them”.

In short, it is time to change our mindset and to start pursuing PGCCs, which we can observe under the microscope. But with very little understanding about these cells, it is time for a shift in paradigm.

Jinsong Liu.

Affiliation

Department of Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030-4095, USA.

Email address

[email protected]

Question 95: How can we accelerate the identification of biomarkers for the early detection of pancreatic ductal adenocarcinoma?

Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal cancers in the world with a dismal 5-year overall survival rate of less than 5%; which has not been significantly improved since the past decades. Although surgical resection is the only option for curative treatment of PDAC, only 15%–20% of patients with PDAC have the chance to undergo curative resection, leaving the rest with only palliative options in hope for increasing their quality of life; since they were already at unresectable and non-curative stages at their first diagnosis.

The lack of specific symptoms in the early-stage of PDAC is responsible for rendering an early diagnosis difficult. Therefore, more sensitive and specific screening methodologies for its early detection is urgently needed to improve its diagnosis, starting early treatments, and ameliorating prognoses. The diagnosis so far relies on imaging modalities such as abdominal ultrasound, computed tomography (CT), magnetic resonance imaging (MRI), endoscopic ultrasound (EUS), endoscopic retrograde cholangiopancreatography (ERCP), and positron emission tomography (PET). One may propose to screen for pancreatic cancer in high-risk populations, which is highly recommended, however screening intervention for all the people is not a wise choice; when considering the relatively low prevalence of PDAC, and the difficulty for diagnosing it in its early stage [ 20 ].

Therefore, alternative diagnostic tools for early detection of PDAC are highly expected. Among the biomarkers currently used in clinical practice, carbohydrate antigen 19–9 (CA19–9) is among the most useful one for supporting the diagnosis of PDAC, but it is neither sufficiently sensitive nor specific for its early detection. Yachida et al. reported in 2010 that the initiating mutation in the pancreas occurs approximately two decades before the PDAC to start growing in distant organs [ 21 ], which indicates a broad time of the window of opportunity for the early detection of PDAC. With the advancement in next-generation sequencing technology, the number of reported studies regarding novel potential molecular biomarkers in bodily fluids including the blood, feces, urine, saliva, and pancreatic juice for early detection of PDAC has been increasing. Such biomarkers may be susceptible to detect mutations at the genetic or epigenetic level, identifying important non-coding RNA (especially microRNA and long non-coding RNA), providing insights regarding the metabolic profiles, estimating the tumor level in liquid biopsies (circulating free DNA, circulating tumor cells and exosomes), and so on.

Another approach to identifying biomarkers for the early detection of pancreatic cancer is using animal models. In spontaneous animal models of pancreatic cancer, such as Kras-mutated mouse models, it is expected that by high throughput analyses of the genetic/epigenetic/proteomic alterations, some novel biomarkers might be able to be identified. For instance, Sharma et al. reported in 2017 that the detection of phosphatidylserine-positive exosomes enabled the diagnosis of early-stage malignancies in LSL-Kras G12D , Cdkn2a lox/lox : p48 Cre and LSL-Kras G12d/+ , LSL-Trp R172H/+ , and P48 Cre mice [ 22 ].

These analyses in clinical samples or animal models hold the clues for the early detection of PDAC, however, further studies are required to validate their diagnostic performance. What’s most important, will be the lining-up of these identified prospective biomarkers, to validate their sensitivities and specificities. This will determine their potential for widespread clinical applicability, and hopefully, accelerate the early diagnosis of PDAC.

Mikiya Takao 1,2 , Hirotaka Matsuo 2 , Junji Yamamoto 1 , and Nariyoshi Shinomiya 2 .

1 Department of Surgery, National Defense Medical College, 3-2 Namiki, Tokorozawa, Saitama 359-8513, Japan; 2 Department of Integrative Physiology and Bio-Nano Medicine, National Defense Medical College, 3-2 Namiki, Tokorozawa, Saitama 359-8513, Japan.

E-mail address

[email protected]; [email protected]; [email protected]; [email protected]

Question 96: Can we improve the treatment outcomes of metastatic pancreatic ductal adenocarcinoma through precision medicine guided by a combination of the genetic and proteomic information of the tumor?

Pancreatic ductal adenocarcinoma (PDAC) is one of the most malignant cancers, and nearly half of the patients had metastatic PDAC when they are initially diagnosed. When they are accompanied by metastatic tumors, unlike most solid cancer, PDAC cannot be cured with primary surgical resection alone [ 23 , 24 ]. Also, since PDAC has poor responses to conventional therapies, improvements in adjunctive treatment approach including chemo- and immuno-therapy are earnestly required. From this standpoint, recent results regarding the differences in the molecular evolution of pancreatic cancer subtypes provide a new insight into its therapeutic development [ 25 ], which may lead to the improvement of the prognosis of not only metastatic PDAC but also of locally advanced or recurrent PDAC.

In fact, new chemotherapeutic regimens such as the combination of gemcitabine with nab-paclitaxel and FOLFIRINOX have been reported to show improved prognosis despite a lack of examples of past successes in the treatment of patients with metastatic PDAC who had undergone R0 resection [ 26 ]. While many mutations including KRAS , CDKN2A , TP53, and SMAD4 are associated with pancreatic carcinogenesis, no effective molecular targeted drug has been introduced in the clinical setting so far. A recent report of a phase I/II study on refametinib, a MEK inhibitor, indicated that KRAS mutation status might affect the overall response rate, disease control rate, progression-free survival, and overall survival of PDAC in combination with gemcitabine [ 27 ].

While immunotherapy is expected to bring a great improvement in cancer treatment, until now, immune checkpoint inhibitors have achieved limited clinical benefit for patients with PDAC. This might be because PDAC creates a uniquely immunosuppressive tumor microenvironment, where tumor-associated immunosuppressive cells and accompanying desmoplastic stroma prevent the tumor cells from T cell infiltration. Recently reported studies have indicated that immunotherapy might be effective when combined with focal adhesion kinase (FAK) inhibitor [ 28 ] or IL-6 inhibitor [ 29 ], but more studies are required to validate their use in clinical practice.

As such, we believe that if the dynamic monitoring of drug sensitivity/resistance in the individual patients is coupled with precision treatment based on individualized genetics/epigenetics/proteomics alterations in the patients’ tumor, this could improve the treatment outcomes of PDAC.

Mikiya Takao 1,2 , Hirotaka Matsuo 2 , Junji Yamamoto 1 , and Nariyoshi Shinomiya 2.

Question 97: What are the parameters that determine a competent immune system that gives a complete response to cancers after immune induction?

Recently, cancer immunotherapy has shown great clinical benefit in multiple types of cancers [ 30 , 31 , 32 ]. It has provided new approaches for cancer treatment. However, it has been observed that only a fraction of patients respond to immunotherapy.

Much effort has been made to identify markers for immunotherapeutic response. Tumor mutation burden (TMB), mismatch repair (MMR) deficiency, PD-L1 expression, and tumor infiltration lymphocyte (TIL) have been found to be associated with an increased response rate in checkpoint blockade therapies. Unfortunately, a precise prediction is still challenging in this field. Moreover, when to stop the treatment of immunotherapy is an urgent question that remains to be elucidated.

In other words, there is no available approach to determine if a patient has generated a good immune response against the cancer after immunotherapy treatments. All of these indicate the complexity and challenges that reside for implementing novel man-induced cancer-effective immune response therapeutics. A variety of immune cells play collaborative roles at different stages to recognize antigens and eventually to generate an effective anti-cancer immune response. Given the high complexity of the immune system, a rational evaluation approach is needed to cover the whole process. Moreover, we need to perfect vaccine immunization and/or in vitro activation of T cells to augment the function of the immune system; particularly the formation of immune memory.

Edison Liu 1 , Penghui Zhou 2 , Jiang Li 2 .

1 The Jackson Laboratory, Bar Harbor, ME 04609, USA; 2 Sun Yat-sen University Cancer Center, Guangzhou, Guangdong 510060, P. R. China.

[email protected]; [email protected]; [email protected]

Question 98: Is high local concentration of metformin essential for its anti-cancer activity?

Metformin was approved as a first line of anti-diabetic drug since decades. Interestingly, the fact that clinical epidemiological studies have shown that metformin can reduce the risk of a variety of cancers stimulates considerable recognition to explore its anticancer activity.

Although the in vitro and in vivo experimental results have demonstrated that metformin can have some potential anti-tumor effects, more than 100 clinical trials did not achieve such desirable results [ 33 ]. We and others believe that the main problem resides in the prescribing doses used. For cancer treatment, a much higher dose may be needed for observing any anti-tumor activities, as compared to the doses prescribed for diabetics [ 34 , 35 , 36 ].

Further, if the traditional local/oral administration approach is favored, the prescribed metformin may not be at the required dose-concentration once it reaches the blood to have the effective anti-cancer activities. We, therefore, propose that intravesical instillation of metformin into the bladder lumen could be a promising way to treat for bladder cancer, at least. We have already obtained encouraging results both in vitro and in vivo experiments, including in an orthotopical bladder cancer model [ 36 , 37 ]. Now, we are waiting to observe its prospective clinical outcome.

Mei Peng 1 , Xiaoping Yang 2 .

1 Department of Pharmacy, Xiangya Hospital, Central South University. Changsha, Hunan 410083, P. R. China; 2 Key Laboratory of Study and Discovery of Small Targeted Molecules of Hunan Province, Department of Pharmacy, School of Medicine, Hunan Normal University, Changsha, Hunan 410013, P. R. China.

[email protected]; [email protected]

Question 99: How can we monitor the emergence of cancer cells anywhere in the body through plasma testing?

The early detection of cancer is still a relentless worldwide challenge. The sensitivity and specificity of traditional blood tumor markers and imaging technologies are still to be greatly improved. Hence, novel approaches for the early detection of cancer are urgently needed.

The emergence of liquid biopsy technologies opens a new driveway for solving such issues. According to the definition of the National Cancer Institute of the United States, a liquid biopsy is a test done on a sample of blood to look for tumorigenic cancer cells or pieces of tumor cells’ DNA that are circulating in the blood [ 38 ]. This definition implies two main types of the current liquid biopsy: one that detects circulating tumor cells and the other that detects non-cellular material in the blood, including tumor DNA, RNA, and exosomes.

Circulating tumor cells (CTCs) are referred to as tumor cells that have been shed from the primary tumor location and have found their way to the peripheral blood. CTCs were first described in 1869 by an Australian pathologist, Thomas Ashworth, in a patient with metastatic cancer [ 39 ]. The importance of CTCs in modern cancer research began in the mid-1990s with the demonstration that CTCs exist early in the course of the disease.

It is estimated that there are about 1–10 CTCs per mL in whole blood of patients with metastatic cancer, even fewer in patients with early-stage cancer [ 40 ]. For comparison, 1 mL of blood contains a few million white blood cells and a billion erythrocytes. The identification of CTCs, being in such low frequency, requires some special tumoral markers (e.g., EpCAM and cytokeratins) to capture and isolate them. Unfortunately, the common markers for recognizing the majority of CTCs are not effective enough for clinical application [ 41 ]. Although accumulated evidences have shown that the presence of CTCs is a strong negative prognostic factor in the patients with metastatic breast, lung and colorectal cancers, detecting CTCs might not be an ideal branch to hold on for the hope of early cancer detection [ 42 , 43 , 44 , 45 ].

Circulating tumor DNA (ctDNA) is tumor-derived fragmented DNA in the circulatory system, which is mainly derived from the tumor cell death through necrosis and/or apoptosis [ 46 ]. Given its origin, ctDNA inherently carries cancer-specific genetic and epigenetic aberrations, which can be used as a surrogate source of tumor DNA for cancer diagnosis and prognostic prediction. Ideally, as a noninvasive tumor early screening tool, a liquid biopsy test should be able to detect many types of cancers and provide the information of tumor origin for further specific clinical management. In fact, the somatic mutations of ctDNA in different types of tumor are highly variable, even in the different individuals with the same type of tumor [ 47 ]. Additionally, most tumors do not possess driver mutations, with some notable exceptions, which make the somatic mutations of ctDNA not suitable for early detection of the tumor.

Increased methylation of the promoter regions of tumor suppressor genes is an early event in many types of tumor, suggesting that altered ctDNA methylation patterns could be one of the first detectable neoplastic changes associated with tumorigenesis [ 48 ]. ctDNA methylation profiling provides several advantages over somatic mutation analysis for cancer detection including higher clinical sensitivity and dynamic range, multiple detectable methylation target regions, and multiple altered CpG sites within each targeted genomic region. Further, each methylation marker is present in both cancer tissue and ctDNA, whereas only a fraction of mutations present in cancer tissue could be detected in ctDNA.

In 2017, there were two inspiring studies that revealed the values of using ctDNA methylation analysis for cancer early diagnosis [ 49 , 50 ]. After partitioning the human genome into blocks of tightly coupled CpG methylation sites, namely methylation haplotype blocks (MHBs), Guo and colleagues performed tissue-specific methylation analyses at the MHBs level to accurately determine the tissue origin of the cancer using ctDNA from their enrolled patients [ 49 ]. In another study, Xu and colleagues identified a hepatocellular carcinoma (HCC) enriched methylation marker panel by comparing the HCC tissue and blood leukocytes from normal individuals and showed that methylation profiles of HCC tumor DNA and matched plasma ctDNA were highly correlated. In this study, after quantitative measurement of the methylation level of candidate markers in ctDNA from a large cohort of 1098 HCC patients and 835 normal controls, ten methylation markers were selected to construct a diagnostic prediction model. The proposed model demonstrated a high diagnostic specificity and sensitivity, and was highly correlated with tumor burden, treatment response, and tumor stage [ 50 ].

With the rapid development of highly sensitive detection methods, especially the technologies of massively parallel sequencing or next-generation sequencing (NGS)-based assays and digital PCR (dPCR), we strongly believe that the identification of a broader “pan-cancer” methylation panel applied for ctDNA analyses, probably in combination with detections of somatic mutation and tumor-derived exosomes, would allow more effective screening for common cancers in the near future.

Edison Liu 1 , Hui-Yan Luo 2 .

[email protected]; [email protected]

Question 100: Can phytochemicals be more specific and efficient at targeting P-glycoproteins to overcome multi-drug resistance in cancer cells?

Though several anticancer agents are approved to treat different types of cancers, their full potentials have been limited due to the occurrence of drug resistance. Resistance to anticancer drugs develops by a variety of mechanisms, one of which is increased drug efflux by transporters. The ATP-binding cassette (ABC) family drug efflux transporter P-glycoprotein (P-gp or multi-drug resistance protein 1 [MDRP1]) has been extensively studied and is known to play a major role in the development of multi-drug resistance (MDR) to chemotherapy [ 51 ]. In brief, overexpressed P-gp efflux out a wide variety of anticancer agents (e.g.: vinca alkaloids, doxorubicin, paclitaxel, etc.), leading to a lower concentration of these drugs inside cancer cells, thereby resulting in MDR. Over the past three decades, researchers have developed several synthetic P-gp inhibitors to block the efflux of anticancer drugs and have tested them in clinical trials, in combination with chemotherapeutic drugs. But none were found to be suitable enough in overcoming MDR and to be released for marketing, mainly due to the side effects associated with cross-reactivity towards other ABC transporters (BCRP and MRP-1) and the inhibition of CYP450 drug metabolizing enzymes [ 52 , 53 ].

On the other hand, a number of phytochemicals have been reported to have P-gp inhibitory activity. Moreover, detailed structure–activity studies on these phytochemicals have delineated the functional groups essential for P-gp inhibition [ 53 , 54 ]. Currently, one of the phytochemicals, tetrandrine (CBT-1 ® ; NSC-77037), is being used in a Phase I clinical trial ( http://www.ClinicalTrials.gov ; NCT03002805) in combination with doxorubicin for the treatment of metastatic sarcoma. Before developing phytochemicals or their derivatives as P-gp inhibitors, they need to be investigated thoroughly for their cross-reactivity towards other ABC transporters and CYP450 inhibition, in order to avoid toxicities similar to the older generation P-gp inhibitors that have failed in clinical trials.

Therefore, the selectivity for P-gp over other drug transporters and drug metabolizing enzymes should be considered as important criterias for the development of phytochemicals and their derivatives for overcoming MDR.

Mohane Selvaraj Coumar and Safiulla Basha Syed.

Centre for Bioinformatics, School of Life Sciences, Pondicherry University, Kalapet, Puducherry 605014, India.

[email protected]; [email protected]

Question 101: Is cell migration a selectable trait in the natural evolution of carcinoma?

The propensity of solid tumor malignancy to metastasize remains the main cause of cancer-related death, an extraordinary unmet clinical need, and an unanswered question in basic cancer research. While dissemination has been traditionally viewed as a late process in the progression of malignant tumors, amount of evidence indicates that it can occur early in the natural history of cancer, frequently when the primary lesion is still barely detectable.

A prerequisite for cancer dissemination is the acquisition of migratory/invasive properties. However, whether, and if so, how the migratory phenotype is selected for during the natural evolution of cancer and what advantage, if any, it may provide to the growing malignant cells remains an open issue. The answers to these questions are relevant not only for our understating of cancer biology but also for the strategies we adopt in an attempt of curbing this disease. Frequently, indeed, particularly in pharmaceutical settings, targeting migration has been considered much like trying “to shut the stable door after the horse has bolted” and no serious efforts in pursuing this aim has been done.

We argue, instead, that migration might be an intrinsic cancer trait that much like proliferation or increased survival confers to the growing tumor masses with striking selective advantages. The most compelling evidence in support for this contention stems from studies using mathematical modeling of cancer evolution. Surprisingly, these works highlighted the notion that cell migration is an intrinsic, selectable property of malignant cells, so intimately intertwined with more obvious evolutionarily-driven cancer traits to directly impact not only on the potential of malignant cells to disseminate but also on their growth dynamics, and ultimately provide a selective evolutionary advantage. Whether in real life this holds true remains to be assessed, nevertheless, work of this kind defines a framework where the acquisition of migration can be understood in a term of not just as a way to spread, but also to trigger the emergence of malignant clones with favorable genetic or epigenetic traits.

Alternatively, migratory phenotypes might emerge as a response to unfavorable conditions, including the mechanically challenging environment which tumors, and particularly epithelial-derived carcinoma, invariably experience. Becoming motile, however, may not per se being fixed as phenotypic advantageous traits unless it is accompanied or is causing the emergence of specific traits, including drug resistance, self-renewal, and survival. This might be the case, for example, during the process of epithelial-to-mesenchymal transition (EMT), which is emerging as an overarching mechanism for dissemination. EMT, indeed, may transiently equip individual cancer cells not only with migratory/invasive capacity but also with increased resistance to drug treatment, stemness potential at the expanse of fast proliferation.

Thus, within this framework targeting pro-migratory genes, proteins and processes may become a therapeutically valid alternative or a complementary strategy not only to control carcinoma dissemination but also its progression and development.

Giorgio Scita.

IFOM, The FIRC Institute of Molecular Oncology, Via Adamello 16, 20139 Milan, Italy; Department of Oncology and Hemato-Oncology (DIPO), School of Medicine, University of Milan, Via Festa del Perdono 7, 20122, Italy.

[email protected]

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• How to Write a Research Proposal | Examples & Templates

How to Write a Research Proposal | Examples & Templates

Published on October 12, 2022 by Shona McCombes and Tegan George. Revised on November 21, 2023.

A research proposal describes what you will investigate, why it’s important, and how you will conduct your research.

The format of a research proposal varies between fields, but most proposals will contain at least these elements:

Introduction

Literature review.

• Research design

Reference list

While the sections may vary, the overall objective is always the same. A research proposal serves as a blueprint and guide for your research plan, helping you get organized and feel confident in the path forward you choose to take.

Table of contents

Research proposal purpose, research proposal examples, research design and methods, contribution to knowledge, research schedule, other interesting articles, frequently asked questions about research proposals.

Academics often have to write research proposals to get funding for their projects. As a student, you might have to write a research proposal as part of a grad school application , or prior to starting your thesis or dissertation .

In addition to helping you figure out what your research can look like, a proposal can also serve to demonstrate why your project is worth pursuing to a funder, educational institution, or supervisor.

Research proposal length

The length of a research proposal can vary quite a bit. A bachelor’s or master’s thesis proposal can be just a few pages, while proposals for PhD dissertations or research funding are usually much longer and more detailed. Your supervisor can help you determine the best length for your work.

One trick to get started is to think of your proposal’s structure as a shorter version of your thesis or dissertation , only without the results , conclusion and discussion sections.

Download our research proposal template

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Writing a research proposal can be quite challenging, but a good starting point could be to look at some examples. We’ve included a few for you below.

• Example research proposal #1: “A Conceptual Framework for Scheduling Constraint Management”
• Example research proposal #2: “Medical Students as Mediators of Change in Tobacco Use”

Like your dissertation or thesis, the proposal will usually have a title page that includes:

• The proposed title of your project
• Your supervisor’s name
• Your institution and department

The first part of your proposal is the initial pitch for your project. Make sure it succinctly explains what you want to do and why.

Your introduction should:

• Introduce your topic
• Give necessary background and context
• Outline your  problem statement  and research questions

To guide your introduction , include information about:

• Who could have an interest in the topic (e.g., scientists, policymakers)
• How much is already known about the topic
• What is missing from this current knowledge
• What new insights your research will contribute
• Why you believe this research is worth doing

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As you get started, it’s important to demonstrate that you’re familiar with the most important research on your topic. A strong literature review  shows your reader that your project has a solid foundation in existing knowledge or theory. It also shows that you’re not simply repeating what other people have already done or said, but rather using existing research as a jumping-off point for your own.

In this section, share exactly how your project will contribute to ongoing conversations in the field by:

• Comparing and contrasting the main theories, methods, and debates
• Examining the strengths and weaknesses of different approaches
• Explaining how will you build on, challenge, or synthesize prior scholarship

Following the literature review, restate your main  objectives . This brings the focus back to your own project. Next, your research design or methodology section will describe your overall approach, and the practical steps you will take to answer your research questions.

To finish your proposal on a strong note, explore the potential implications of your research for your field. Emphasize again what you aim to contribute and why it matters.

For example, your results might have implications for:

• Improving best practices
• Informing policymaking decisions
• Strengthening a theory or model
• Challenging popular or scientific beliefs
• Creating a basis for future research

Last but not least, your research proposal must include correct citations for every source you have used, compiled in a reference list . To create citations quickly and easily, you can use our free APA citation generator .

Some institutions or funders require a detailed timeline of the project, asking you to forecast what you will do at each stage and how long it may take. While not always required, be sure to check the requirements of your project.

Here’s an example schedule to help you get started. You can also download a template at the button below.

Download our research schedule template

If you are applying for research funding, chances are you will have to include a detailed budget. This shows your estimates of how much each part of your project will cost.

Make sure to check what type of costs the funding body will agree to cover. For each item, include:

• Cost : exactly how much money do you need?
• Justification : why is this cost necessary to complete the research?
• Source : how did you calculate the amount?

To determine your budget, think about:

• Travel costs : do you need to go somewhere to collect your data? How will you get there, and how much time will you need? What will you do there (e.g., interviews, archival research)?
• Materials : do you need access to any tools or technologies?
• Help : do you need to hire any research assistants for the project? What will they do, and how much will you pay them?

If you want to know more about the research process , methodology , research bias , or statistics , make sure to check out some of our other articles with explanations and examples.

Methodology

• Sampling methods
• Simple random sampling
• Stratified sampling
• Cluster sampling
• Likert scales
• Reproducibility

 Statistics

• Null hypothesis
• Statistical power
• Probability distribution
• Effect size
• Poisson distribution

Research bias

• Optimism bias
• Cognitive bias
• Implicit bias
• Hawthorne effect
• Anchoring bias
• Explicit bias

Once you’ve decided on your research objectives , you need to explain them in your paper, at the end of your problem statement .

Keep your research objectives clear and concise, and use appropriate verbs to accurately convey the work that you will carry out for each one.

I will compare …

A research aim is a broad statement indicating the general purpose of your research project. It should appear in your introduction at the end of your problem statement , before your research objectives.

Research objectives are more specific than your research aim. They indicate the specific ways you’ll address the overarching aim.

A PhD, which is short for philosophiae doctor (doctor of philosophy in Latin), is the highest university degree that can be obtained. In a PhD, students spend 3–5 years writing a dissertation , which aims to make a significant, original contribution to current knowledge.

A PhD is intended to prepare students for a career as a researcher, whether that be in academia, the public sector, or the private sector.

A master’s is a 1- or 2-year graduate degree that can prepare you for a variety of careers.

All master’s involve graduate-level coursework. Some are research-intensive and intend to prepare students for further study in a PhD; these usually require their students to write a master’s thesis . Others focus on professional training for a specific career.

Critical thinking refers to the ability to evaluate information and to be aware of biases or assumptions, including your own.

Like information literacy , it involves evaluating arguments, identifying and solving problems in an objective and systematic way, and clearly communicating your ideas.

The best way to remember the difference between a research plan and a research proposal is that they have fundamentally different audiences. A research plan helps you, the researcher, organize your thoughts. On the other hand, a dissertation proposal or research proposal aims to convince others (e.g., a supervisor, a funding body, or a dissertation committee) that your research topic is relevant and worthy of being conducted.

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Proposal for cervical cancer screening in the era of HPV vaccination

Yung-taek ouh.

Department of Obstetrics and Gynecology, Guro Hospital, Korea University College of Medicine, Seoul, Korea.

Jae Kwan Lee

Eradication of cervical cancer involves the expansion of human papillomavirus (HPV) vaccine coverage and the development of efficient screening guidelines that take vaccination into account. In Korea, the HPV National Immunization Program was launched in 2016 and is expected to shift the prevalence of HPV genotypes in the country, among other effects. The experiences of another countries that implement national immunization programs should be applied to Korea. If HPV vaccines spread nationwide with broader coverage, after a few decades, cervical intraepithelial lesions or invasive cancer should become a rare disease, leading to a predictable decrease in the positive predictive value of cervical screening cytology. HPV testing is the primary screening tool for cervical cancer and has replaced traditional cytology-based guidelines. The current screening strategy in Korea does not differentiate women who have received complete vaccination from those who are unvaccinated. However, in the post-vaccination era, newly revised policies will be needed. We also discuss on how to increase the vaccination rate in adolescence.

Introduction

Cervical cancer is the fourth most common female cancer worldwide, with an estimated 265,700 deaths per year, and remains the most common female cancer in 42 countries (primarily developing countries) [ 1 ]. In addition, cervical cancer has relatively early onset, occurring primarily during reproductive ages, and is one of the 3 most common cancers among women under age 45 in most countries [ 2 ]. There has been a lot of effort to prevent cervical cancer through primary screening and human papillomavirus (HPV) vaccination; as a result, the disease has been gradually reduced in several developed countries [ 3 , 4 ]. In Korea, for example, the incidence rate of cervical cancer has gradually decreased to a rate of 9.0 per 10 5 in 2014, compared to 16.3 per 10 5 in 1999 [ 5 ].

HPV has been clearly demonstrated as a cause of invasive cervical cancer [ 6 ]. It is the most common sexually transmitted virus, and the progression of it is unusual in that the greatest prevalence is within 5 years from the initiation of first coitus, then decreases with age [ 7 ]. Most women infected with high-risk HPV self-clear and acquire immunity against certain types. However, in about 15% of HPV infections, the virus persists and induces precancerous lesions or invasive cervical cancer [ 8 ]. HPV 16 and 18 have been the most causative types among high-risk HPV viruses, and up to now those 2 genotypes have accounted for 70% of all cervical cancer [ 9 ]. HPV 6 and 11, which are also covered by the quadrivalent vaccine, are responsible for most anogenital warts [ 10 ].

In a randomized controlled trial, HPV testing in combination with liquid-based cytology or alone was more effective than cytology for cervical cancer screening, although HPV screening might result in over-diagnosis in patients with regressive moderate dysplasia [ 11 ]. The primary HPV DNA test has a higher sensitivity and reproducibility than cervical cytology for detecting cervical intraepithelial lesions [ 12 ]. In the HPV vaccination era, the prevalence of cervical lesions as precancerous lesions or invasive cancer should decrease, and as a result, the HPV test will largely replace cytology for screening [ 13 ].

The introduction of a national HPV immunization program in Korea is expected to make various changes in Korea, including the eradication of specific HPV types and a shift in the distribution of HPV genotypes. As the vaccination rate increases, the prevalence of precancerous cervical lesions and cervical cancer will decrease, which will require revision of screening strategies in the post-vaccination era. Two major strategies for cancer prevention and eradication should be considered in future guidelines. First, the efficiency of screening should be improved through HPV DNA tests or new screening tools. Second, efforts should be made to improve the vaccination rate and coverage ( Fig. 1 ).

Two different strategies against human papillomavirus (HPV) in the era of HPV vaccination.

Effects of HPV vaccination

1. mechanism: antibodies against major l1 capsid proteins.

The HPV vaccine plays both preventive and treatment roles for precancerous lesions or cervical cancer. HPV 16/18 E7 antigen-pulsed dendritic cell vaccination can be used as a treatment option for invasive cervical cancer [ 14 ]. In addition, recurrent laryngeal papillomatosis is treated successfully by HPV vaccination [ 15 , 16 ]. Previous studies have shown that the HPV vaccine produces HPV-specific antibodies against L1 capsid proteins into the cervical epithelium [ 17 ]. Furthermore, HPV vaccination induces T-cell responses and antigen-presenting cells for local cell-mediated immunity, enhancing adaptive immunity [ 18 ]. The major capsid antigen L1 synthesizes virus-like particles, which lead to the production of neutralizing antibodies and a humoral response [ 19 ].

In the United States, the National Center for Health Statistics reported the impact of vaccination on the prevalence of HPV in the population by comparing HPV DNA prevalence in the pre-vaccination era (2003–2006) and vaccination era (2009–2012). They showed a 64% decrease in the prevalence of quadrivalent HPV vaccine types [ 6 , 11 , 16 , 18 ] in women aged 14 to 19 years, and a 34% decrease in women aged 20 to 24 years [ 20 ].

2. HPV vaccine against high-grade cervical intraepithelial neoplasia

Clinical trials to evaluate the HPV vaccine against high-grade cervical intraepithelial lesions, including HPV-023, Patricia, Costa Rica, Future I, II, and {"type":"clinical-trial","attrs":{"text":"NCT00543543","term_id":"NCT00543543"}} NCT00543543 , reached a consensus result of nearly 100% efficacy ( Table 1 ) [ 21 , 22 , 23 , 24 , 25 , 26 ].

RCT, randomized controlled trial; CIN, cervical intraepithelial neoplasia.

a) Efficacy against CIN 2 or more severe lesions.

The HPV vaccine impact monitoring project (HPV-IMPACT) in the United States was a sentinel system for monitoring the impact of HPV vaccination targeting cervical intraepithelial neoplasia (CIN) 2/3 in 18 to 39-year-old women from 2008 to 2012. The authors reported a decrease in screening rates, with the largest decreases among 18 and 20-year-olds, as well as a significant decrease in the incidence of CIN 2+. Nevertheless, an impact of vaccination on declining CIN 2+ was still demonstrated because the decrease in CIN 2+ was larger than the decrease in screening [ 27 ].

A phase 3 double-blind trial, Females United to Unilaterally Reduce Endo/Ectocervical Disease, was conducted to estimate the efficacy of the quadrivalent vaccine against high-grade cervical lesions. Vaccine efficacy for the prevention of CIN 2/3, adenocarcinoma in situ, or cervical cancer was 98.2% (95.89% confidence interval [CI], 86–100) [ 24 ].

3. Seroconversion rate after vaccination

HPV vaccination induces seroconversion in nearly all women who were vaccinated, and titer levels are higher than in women with seroconversion as a consequence of natural infection [ 28 , 29 ]. Although natural infection also induces cell-mediated immunity and protects against the identical HPV type, the seroconversion rate is much lower than HPV vaccination; 60% for HPV 16, 54% for HPV 18, and 69% for HPV 6. Natural infection results in lower titer levels and a delay of about 1 year for seroconversion compared to HPV vaccination [ 30 ]. Although HPV antibodies are sustained for at least 4.5 to 5 years, the sustainability of seropositivity after HPV vaccination has yet to be established since no long-term follow-up data are available [ 31 , 32 ].

4. Impact on HPV distribution

In the era of HPV vaccination, a shift in the prevalence of HPV genotypes is expected. In a German population-based cohort study, a significant decrease in HPV 16, 18, and 31 was found among women aged ≤22 years, compared with women aged 23 to 29 years [ 33 ]. Notably, HPV 31 was reduced via cross-protection. On the other hand, other types not included in the vaccine such as HPV 51, 53, and 56 occurred at a higher percentage in vaccinated women.

In Scotland, a national HPV immunization program was implemented for girls aged 12 and 13 years in 2008, with 90% of all subjects receiving the 3-dose uptake of the bivalent vaccine annually. They demonstrated a significant reduction in the prevalence of HPV 16 and 18, as well as HPV 31, 33, and 45 from a cross-protective effect. HPV 51 and 56 rose as most prevalent HPV genotypes among the HPV types not covered by the vaccine [ 34 ]. The Scottish HPV prevalence in Vaccinated women (SHEVa) study was designed to analyze the impact of vaccination on the performance of HPV testing [ 35 ]. Using clinically validated HPV assays which target both DNA and RNA, there was a 23% to 32% reduction of HPV prevalence in vaccinated women compared to unvaccinated women following the coverage rate was over 90% in the target population. The prevalence of high-risk types other than HPV 16 and 18 was not different between the vaccinated and unvaccinated groups. However, the prevalence of HPV 16 and 18 significantly decreased by 75%.

1. HPV prevalence and type distribution in Korea

In a meta-analysis of HPV type distribution between 1995 and 2007 in Korea, the overall HPV prevalence was 23.9% (95% CI, 23.8–24.1%) in women with normal cytology compared to 95.8% (95% CI, 95.4–96.2%) in women with cervical cancer. HPV 16 was the most common type regardless of cervical disease status. In cervical cancer, HPV 16 accounted for 65.1% of cases, followed by HPV 18 (11.9%), HPV 58 (8.6%), HPV 33 (3.7%), and HPV 52 (3.4%). In high-grade precancerous lesions (CIN 2, 3, and CIS), HPV 58 was the second most common type (14.1%), while HPV 16 accounted for 40.6% [ 36 ]. Likewise, Lee et al. [ 37 ] investigated liquid-based cytology, HPV DNA analysis, and cervical biopsies of 2,358 women, finding that HPV 16 was the most common in any cervical lesions, normal, CIN and squamous cell carcinoma (SCC) lesions. HPV 16 and 58 were the most common in CIN 2/3 patients and HPV 16, 18, 58, and 33 were common in patients with SCC.

Recent studies demonstrated that HPV type distribution has been changing and is different from previous studies, in that HPV 16 is no longer the most common genotype in Korea. A retrospective study in 7,014 women who received a health check-up indicated that the overall positivity for high-risk HPV was 8.4%; HPV 58 (23.8%) was most common, followed by HPV 16 (21.8%) and HPV 52 (16.6%). The type most strongly related to increasing severity of cervical cytology was HPV 56 [ 38 ]. In a single-center study of healthy women who received a health check-up in 2013, HPV 53 (6.5%) was the most common HPV genotype, followed by HPV 52 (6.1%) [ 39 ]. As expected, HPV 16 was the most common type in high-grade CIN lesions. In an analysis of 874 invasive cervical cancer cases over 47 years (1958–2004), HPV 16 accounted for 63.1% of cases, followed by HPV 18 (8.5%), HPV 33 (4.5%), HPV 58 (3.9%), and HPV 31 (3.0%) [ 40 ]. Continued monitoring of the shift in prevalence and distribution of HPV genotypes should continue as vaccination increases.

2. Korean guidelines for cervical cancer screening

The well-established national cancer screening program in Korea has led to 71% and 66% reduced risk of invasive cancer and carcinoma in situ compared to unscreened patients, respectively [ 41 ]. The distribution of age at cervical cancer diagnosis has been shifting, and revised guidelines regarding the timing for cervical cancer screening have been newly implemented in various organizations [ 42 , 43 , 44 ]. Moreover, cervical cancer is definitively influenced by HPV infection, and HPV tests have emerged as important screening tools for precancerous lesions and cervical cancer. Therefore, the practice guidelines for the early detection of cervical cancer by Korean Society of Gynecologic Oncology recommended the HPV DNA test in combination with a cervical cytology test is recommended for women aged ≥30 years old. The screening interval can be extended to 2 years if both tests are negative [ 45 ]. Because the mortality of cervical cancer in Korea and other countries increases with age, the recommendation was made to end cervical cancer screening after the age of 74 [ 46 ]. Within the guidelines, no special considerations were specified for HPV-vaccinated women.

3. HPV vaccination rate in Korea in the present and future

The Korean National Immunization Program (NIP) for HPV was first implemented in June 2016 for girls 11–12 years of age with a 2-dose schedule. Of the 464,932 total subjects aged 11–12 years, 232,303 (50.0%) girls initiated vaccination in the first year of the NIP, especially during the vacation period of July (8.3%), August (9.1%), and December (16.6%) ( Fig. 2 ). Initiation of vaccination rates of girls born in 2004 were 86.3% in Gokseong, a county in South Jeolla, with a highly cooperative public health center and school-based vaccination program [ 47 ]. Regional disparities in HPV vaccination rate were reported as a maximum of 11% points up to June 2017 [ 48 ]. The greatest success was found when public health centers contacted the parents of girls, and they subsequently encouraged children to participate in the vaccination program. Educational newsletters handed out at school also helped enhance the vaccination rate in certain counties. In spite of these efforts, according to the latest analysis in June 2017, nationwide initiation rates were only 35.7% among girls born in 2004 and 2005 [ 49 ].

The monthly number of human papillomavirus vaccination rates in 2016. The data contained only from June to December because the Korean National Immunization Program for HPV was first implemented in June 2016 for girls 11–12 years of age with a 2-dose schedule. The vaccination rates were relatively higher during vacation period (July, August, and December).

4. Future strategies

Although various randomized controlled trials around the world have described the efficacy and impacts of HPV vaccination, the complete effect on future strategies for the prevention of cervical cancer remains undefined. Because the oncogenesis of HPV infection is slow progression from CIN to cervical cancer, it will take decades to thoroughly analyze the effects of vaccination on the prevalence of HPV and incidence of cervical cancer. In terms of immunology, the long-term effects of seropositivity and clinical protection following HPV vaccination should be studied with more vaccinated women, although antibody responses to HPV vaccination have been observed in previous studies [ 26 ].

1) The need for cervical cancer screening

As shown in a German population-based study, there has been a shift in the distribution of HPV types that are not included in the vaccine in the post-HPV vaccination era [ 33 ]. Vaccination for HPV 16/18 had a cross-protective effect against 4 non-vaccine HPV types (HPV 31, 33, 45, and 51) in the randomized, double-blind trial [ 50 ]. Induced cross-reactive T-cells and specific antibodies to other HPV genotypes not included in the quadrivalent HPV vaccine, such as HPV 31, 33, and 45, have been demonstrated in previous studies, and the prevalence of HPV 31, 33, and 45 is also declining [ 51 ]. Debates continue on whether the bivalent HPV vaccine is cross-protective against HPV 6 and HPV 11 [ 52 , 53 , 54 ]. For these reasons, screening for HPV DNA is still important for the time being, because none of the currently available vaccines has been proven to provide complete protection against all high-risk HPV genotypes.

As described above, there was a 75% reduction of HPV 16 and 18 in Scotland following a national vaccination program with a coverage rate of over 90% [ 35 ]. Nevertheless, other high-risk HPV types were prevalent in vaccinated women with low grade cervical lesions. The phenomenon of increasing non-HPV 16/18 genotypes highlights the importance of utilizing different HPV detection strategies in women who have been vaccinated and those who are unvaccinated. However, in a recent randomized trial evaluating type replacement after HPV vaccination, HPV type replacement did not occur in vaccinated population within 4 years, and the authors predicted that it was unlikely to occur in vaccinated populations [ 55 ].

2) Reassessment of HPV screening initiation age and intervals (distinguishing between vaccinated and unvaccinated women)

Since HPV 16 and 18 positivity is expected to decline rapidly over the decades following implementation of a national immunization program, specific screening protocols and intervals should be implemented for vaccinated groups. There have been some studies about the correlation between HPV vaccination and changes in cervical cancer screening rates, although none have focused on Korea. In spite of concerns that women who have been vaccinated would be less likely to seek out cervical cancer screening, women who received the HPV vaccine more often received cervical cancer screening than those who had not been vaccinated [ 56 , 57 ]. Research on awareness of cervical cancer screening for women who have been vaccinated is needed in Korea, as well as a serious discussion about strategies to induce unvaccinated women to seek screening.

In the era of vaccination, we should provide different strategies for cervical cancer screening. HPV 16 and 18 are expected to nearly disappear; as a consequence, the positivity of screening tests would be lower than 30% [ 58 ]. Furthermore, the prevalence of lesions more advanced than severe dysplasia would also be reduced more than half, making screening less predictive and decreasing the benefit-harm ratio [ 59 ]. Cervical cancer caused by HPV types other than HPV 16 and 18 appears at a median of 5 years later than that caused by HPV 16 and 18. In particular, short term persistence of HPV 16 infection more strongly predicts a subsequent moderate dysplasia or more advanced pathology compared to other HPV genotypes [ 60 ]. Although there are not enough data to suggest revised recommendations other than older initial screening age and extended screening intervals, one option would be routine screening with HPV testing at 30, 45, and 60 years of age for women who were fully vaccinated before first sexual contact [ 61 ]. It would be more efficient to provide separate screening guidelines for vaccinated and unvaccinated women. In Italy, primary HPV screening is recommended starting at 30 years and at 5-year intervals for vaccinated women who were vaccinated in 2007/2008 and became 25 years old in 2017 [ 62 ]. An optimal cervical cancer screening model for women who have been vaccinated with all 3 doses was proposed in 2017 from a US model based-analysis of benefits and costs. They suggested that screening could be modified to start later with decreased frequency, with either cervical cytology or HPV testing alone every 5 years starting at age 25 or 30, and only primary HPV testing recommended every 10 years starting at age 30 or 35 for women vaccinated with the nonavalent vaccine [ 63 ].

3) Shift in screening from cytology or cytology/HPV to HPV alone

In April 2014, an HPV DNA test was approved as a primary screening tool by the Food and Drug Administration. Nevertheless, further investigation is needed to evaluate the efficacy of using only an HPV DNA test and the adverse effects of increased false-positivity. The issues of the primary HPV screening test are to distinguish high-risk HPV positive with ≥CIN 2 from patients with transient positivity. There will be an increase in false positivity due to high-risk HPV infection without ≥CIN 2. As the number of patient with transient high-risk HPV infection increases, unnecessary follow-up and cost burdens will be a problem to be solved [ 64 ]. The positive predictive value of cervical cytology for cervical cancer screening is expected to decrease along with the incidence of precancerous or cancerous lesions in the cervix after implementation of the NIP of HPV. Normal cervical cytology will correspondingly increase, leading to an increase in false negative results and a decrease in the sensitivity of cytology, further reducing the value of cytology as screening tool [ 65 , 66 ]. However, endocervical adenocarcinoma with gastric type in which the HPV was rarely detected could be a potential pitfall of HPV vaccination and HPV DNA testing although the incidence was low [ 67 ].

A retrospective population-based cohort study documented the effect of HPV vaccination on abnormal cervical cytology in women born between 1988 and 1993, using data from the Scottish Cervical Screening Program [ 68 ]. The authors observed a significant reduction in positive predictive value and abnormal predictive values for detecting CIN 2+ in vaccinated women, as well as a significant reduction in abnormal cytology.

4) New screening tools

New screening tools are an alternative in the context of a lower prevalence of HPV-positive tests and related abnormal cytology of the cervix. Although various new tools have been proposed with more specific markers, additional verification and certification are needed before commercialization. First, HPV E6 protein detection is more specific than the HPV DNA test for high-grade cervical lesions, and so far at a lower cost. This test targets HPV 16, 18, and 45 and has the greatest positive values for detecting severe dysplasia or more severe lesions compared to high-risk HPV DNA testing [ 69 , 70 ]. Second, p16 INK4a immunohistochemistry is useful for identifying moderate dysplasia or more severe lesions in high-risk HPV-positive women [ 71 ]. In a study of the endpoint of moderate dysplasia or more severe lesions in HPV-positive women, the sensitivity of p16 INK4a immunohistochemistry was 88% (81 of 92; 95% CI, 80–94) and specificity was 61% (633 of 1,045; 95% CI, 57–64) without an increase in the implementation of colposcopy [ 72 ]. Finally, p16/Ki-67 dual-stained cytology is more sensitive than Pap cytology for detecting high-grade CIN. Even with normal cytology, p16/Ki-67 dual-stained cytology detected more than two-thirds of severe dysplasia lesions in women with high-risk HPV and helped select colposcopy referral patients [ 73 , 74 , 75 ].

5) How to increase vaccination coverage levels (i.e., school-based vaccination)

Because 2 doses of the HPV vaccine provided more compliance than 3 doses, 2 doses tended to increase the rate of vaccination completion. In a combined analysis of data from the Costa Rica Vaccine and PATRICIA trials, the efficacy of 2 dose-vaccination was evaluated. Both 3 doses and fewer than 3 doses of bivalent vaccine showed comparable efficacy 4 years following vaccination of women between 15 and 25 years old. Cross-protective activity against HPV 31, 33, and 45 was obtained only for cases in which the interval of the 2 doses was 6 months [ 76 ]. In a cluster-randomized trial, the vaccination coverage rate was increased by education delivered to mothers of adolescent daughters [ 77 ]. In addition, the vaccination and completion rate was improved by consistent recommendations from health care providers [ 78 ]. Social efforts such as educating providers and clinic-specific feedback to encourage patients will increase vaccination rates.

To eradicate cervical cancer in an era when HPV infection and related diseases rarely occur, screening methods must account for vaccine programs. Primary HPV DNA tests will be substituted for conventional Pap smears in screening tests, allowing Pap smears to be applied only to HPV-positive women. Education of patients and providers, an effective vaccination program to increase vaccine coverage rate, and school-based encouragement can help eliminate HPV-related disease and invasive cervical cancer.

In Korea, a national immunization program has been implemented since 2016, and strategies to further increase the vaccination rate should involve the government, schools, and parents. Because HPV vaccines do not cover all types of high-risk HPV, screening for precancerous lesions and cervical cancer will not be eliminated. In the decades following a national HPV vaccine program with a high coverage rate, existing screening strategies based on primary cytology such as Pap smear should be reviewed, because the low prevalence of abnormal cytology of the cervix will make screening less cost-effective and inefficient. Primary HPV testing will play an important role as a screening test and cytology should be reserved for women with an HPV positive test. In addition, reassessment of HPV screening initiation age and intervals that distinguish vaccinated women from unvaccinated women should be discussed in the near future.

Conflict of interest: No potential conflict of interest relevant to this article was reported.

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Research Proposal: Cancer Patients’ Survival: Comparing Integrated Alternative Therapies and Chemotherapy / Radiotherapy Treatment

by Sandra Goodman PhD (more info)

listed in cancer , originally published in issue 217 - October 2014

Background, Introduction and Abstract

I recently re-discovered on my hard drive the Consensus Statement document published in 1994 of which I was the lead author - Nutrition and Life-Style Guidelines for People with Cancer . I am most impressed at how prescient it was 20 years ago regarding providing more options for cancer patients, and also disappointed in how little cancer treatment has progressed in directions providing patients with more options that merely chemotherapy and radiation therapy as adjunctive treatments. http://informahealthcare.com/doi/ref/10.3109/13590849409034555 www.positivehealth.com/article/cancer/nutrition-and-life-style-guidelines-for-people-with-cancer

Some 20+years on from the publication of that Consensus document, there has been a myriad of Research, Clinical papers and books published regarding many aspects of cancer treatment. These have demonstrated molecular sequelae resulting from toxic conventional cancer treatments, i.e. chemotherapy and radiotherapy, which may be causative factors in the development of multi-drug resistance, cancer stem cells and other gene mutations and which may influence temporary cancer regression and then future recurrence and metastases. Furthermore it has been suggested by a strand of practitioners who utilize integrated alternative protocols that the body has difficulty recovering from the toxicity of chemotherapy and radiotherapy and may not be responsive to more biological cancer treatments.  Additionally, perhaps >50% of cancer patients utilize some form of alternative treatments, and such data are not included in standard cancer registries. I have therefore been persuaded of the need to attempt to establish and compare cancer patient survival without toxic chemotherapy / radiotherapy treatments but with a robust integrated / alternative protocol and attach a brief proposal as a starting point for this research. Given the legal constraints in the UK and USA prohibiting alternative treatments for cancer patients, it is difficult to see how this much-needed research project can progress, as it would require a professional team with technical, medical and ethical experience,  access to cancer patients and the construction of a multi-disciplinary, multi-field database. Initially results would merely compare survival of matched cancer patients who have or have not undergone chemotherapy and radiotherapy with those who have undergone an integrated multi-component alternative protocol. This is a fairly long-term project which would need to be followed up for 5-10 years. Research Proposal for Discussion: Cancer Patients’ Outcomes: Comparing Integrated Alternative Therapies and Chemotherapy / Radiotherapy Treatment

Standard cancer treatments - surgery, chemotherapy and radiotherapy - are the only ones currently sanctioned by law for use by physicians and oncologists.[1,2] Hence, epidemiological research and statistics regarding cancer incidence, clinical efficacy, survival / mortality which have been amassed, consolidated and publicly disseminated usually pertain to only these treatments.[3,4] And, despite the development of numerous innovative clinical alternative and complementary cancer treatments internationally over the past 120 years, many of these have been suppressed.[5]

The toxic, sometimes fatal side effects and lack of efficacy regarding long-term survival outcomes for many chemotherapy and radiotherapy treatments are published and well-known in the medical and research literature. Clinically, between 10%-25% of cancer patients may die as a result of undergoing these highly toxic treatments.[6-10] which may be factors in multi-drug resistance, cancer stem cell formation, mutated p53 and other cancer gene mutations which may explain short term remission, subsequent recurrence, metastases and secondary cancers years later following conventional cancer treatment.[11] A well-known questionnaire of McGill University oncologists in the early 1990s reported by Ralph Moss established that >80% would refuse chemotherapy with cisplatin for themselves or families.[12]

Integrated Oncology Protocols - Alternative and Complementary approaches to cancer treatments have burgeoned, encompassing many regimes - diet, exercise, nutritional supplementation, infusions / injections, orthomolecular, herbal, homeopathic, Ayurvedic, Chinese and energy medicine, mind-body - visualization, mindfulness meditation - to name but a few.[13-23] A limited body of research has started to document their clinical efficacy effects in cancer patients; however in many instances these treatments have been carried out in addition to conventional cancer treatments.

A strand of researchers and clinicians have suggested that cancer patients may never fully recover from the toxic effects exerted from chemotherapy and radiotherapy treatments and that biological treatment approaches may not be effective once they have undergone these treatments.[24-26] And, given the significant proportion of cancer patients who also use complementary / alternative cancer therapies,[27-28] it becomes even more important to establish the efficacy of alternative and complementary treatments in cancer patients, who have and have not been subjected to chemotherapy and radiotherapy.

Data comparing cancer survival in patients undergoing chemotherapy and radiotherapy with those who forgo these treatments has been difficult to uncover, due to legal constraints and overwhelming dominance of the conventional treatment establishment. It is proposed to research and compile data with a view to assessing and comparing outcomes for cancer patients being treated with Integrated Oncology - alternative and complementary treatments - who have and have not undergone chemotherapy and radiotherapy treatments. Data comparing patient survival with and without adjunctive therapy could be extracted from cancer registry databases. Data regarding survival with Integrated Alternative Therapies would require multi-factorial clinical database creation either from clinicians or patients once this treatment is no longer deemed illegal.

© Sandra Goodman PhD 2014

1. UK 1939 Cancer Act

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2. The Stranglehold that the UK 1939 Cancer Act Exerts in Great Britain. The Cambridge Institute of Complementary Health. http://cichealth.org.uk/#/1939-cancer-act/4567446788

Goodman S. Integration of Alternative Cancer Treatments. Positive Health PH Online Issue 208. Aug 2013. www.positivehealth.com/article/editorial/editorial-issue-208

3. Dr Tim O’Shea. To the Cancer Patient: Natural Cures vs. Traditional. TheDoctorWithin.com. www.thedoctorwithin.com/cancer/to-the-cancer-patient/ .  2014.

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Published online Dec 12, 2006. doi:  10.1038/sj.bjc.6603498

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M E R O'Brien , 1,* A Borthwick , 1 A Rigg , 1 A Leary , 1 L Assersohn , 1 K Last , 1 S Tan , 1 S Milan , 1 D Tait , 1 and I E Smith 1 Mortality within 30 days of chemotherapy: a clinical governance benchmarking issue for oncology patients

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9. Steven Ransom. Fraught With Risks and Side-Effects. June 09, 2013. www.cancertutor.com/category/chemotherapy/  

10. PharmaTimes Online

Chemotherapy causes death in more than 25% of cancer patients

UK News / World News | November 13, 2008

Katrina Megget

Read more at: www.pharmatimes.com/Article/08-11-13/Chemotherapy_causes_death_in_more_than_25_of_cancer_patients.aspx#ixzz33DzAOLIW

11. Dr Peter Kay. Cancer Diagnostic Tests and Treatments: Advantages and Limitations to Existing Conventional Treatments; Introduction to Alternative Approaches

Positive Health PH Online Issue 213 - April 2014.

www.positivehealth.com/article/cancer/cancer-diagnostic-tests-and-treatments-advantages-and-limitations-to-existing-conventional-treatment

12. Ralph Moss. Questioning Chemotherapy. Equinox Press. ISBN 978-1881025252. 1996.

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Ralph Moss. The Cancer Industry. Equinox Press. ISBN 978-1881025092. 1996.

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13. Dwight McKee MD. Integrative Cancer Medicine: An Oncologist Takes a Practical Look at Facts, Fiction and the Future. Cancer Strategies Journal: 1(1): 2-8. www.cancerstrategiesjournal.com/McKeeMDReprint.pdf . Winter 2013.

14. Moshe Frenkel, MD. Integrative Oncology Exceptional Patients -  Thoughts and Reflections. Cancer Strategies Journal

Volume 1, Issue 2. Spring 2013. www.cancerstrategiesjournal.com/FrenkelMDReprint.pdf

15. Ronald Peters MD. The Connection Between Spontaneous Remission of Cancer and MindBody Medicine. Cancer Strategies Journal. 1-8. Summer 2013.

http://healmindbody.com/wp-content/uploads/2013/12/Peters-article-Cancer-Strategies.pdf  

16. Mitchell Gaynor, MD, et. al. Complete Remission of Widely Metastatic Melanoma: A Case Report. Cancer Strategies Journal. 2(2): 1-4. Spring 2014. http://gaynoroncology.com/wp-content/uploads/2014/04/GaynorReprintCSJSpring2014.pdf

17. DM Seely, LC Weeks PhD, and S. Young, MA. A systematic review of integrative oncology programs. Curr Oncol. 19(6): e436–e461. doi:  10.3747/co.19.1182. PMCID: PMC3503675. Dec 2012. www.ncbi.nlm.nih.gov/pmc/articles/PMC3503675/  

18. Shneerson C, Taskila T, Gale N, Greenfield S and Chen Y. The effect of complementary and alternative medicine on the quality of life of cancer survivors: A systematic review and meta-analyses. Complementary Therapies in Medicine 21(4): 417-429.  August 2013.

www.complementarytherapiesinmedicine.com/article/S0965-2299%2813%2900088-5/abstract

www.complementarytherapiesinmedicine.com/article/S0965-2299(13)00088-5/references

19. Dr Maurice Orange. Mistletoe Therapy and Hyperthermia for Cancer: Turning Up the Heat. Positive Health PH Online Issue 209 - October 2013.

www.positivehealth.com/article/cancer/mistletoe-therapy-and-hyperthermia-for-cancer-turning-up-the-heat

20. Katharina Gaertner, Michael Müllner, Helmut Friehs, Ernst Schuster, Christine Marosi, Ilse Muchitsch, Michael Frass and Alan David Kaye. Additive Homeopathy in cancer patients: Retrospective survival data from a homeopathic outpatient unit at the Medical University of Vienna. Complementary Therapies in Medicine 22: 320-332. 2014. www.complementarytherapiesinmedicine.com/article/S0965-2299%2813%2900212-4/references

www.complementarytherapiesinmedicine.com/article/S0965-2299%2813%2900212-4/abstract

21. Dr Tasos Vartholomeos. Cancer Control through Pathology-Based Homeopathic Medicine.

Positive Health PH Online Issue 214 - May 2014.

www.positivehealth.com/article/cancer/cancer-control-through-pathology-based-homeopathic-medicine

22. Yingchun Zeng, Taizhen Luo, Huaan Xie, Meiling Huang, Andy SK Cheng. Health Benefits of Qigong or Tai Chi for Cancer Patients: a Systematic Review and Meta-Analyses. Complementary Therapies in Medicine 22: 173-186. 2014. www.complementarytherapiesinmedicine.com/article/S0965-2299%2813%2900195-7/fulltext

www.complementarytherapiesinmedicine.com/article/S0965-2299%2813%2900195-7/abstract

www.complementarytherapiesinmedicine.com/article/S0965-2299%2813%2900195-7/references

23. Goodman S, MacLaren J and Barker W. Nutrition and Life-style Guidelines for People with Cancer. Journal of Nutritional and Environmental Medicine. Vol 4 No. 2: Pages 199-214. 1994. http://informahealthcare.com/doi/ref/10.3109/13590849409034555

24. Chemotherapy Heals Cancer and the Earth is Flat

by Lothar Hirneise

Published by Nexus. 2005. Hardcover.  £34.90. ISBN-10: 3981050207; ISBN-13: 978-3981050202

www.positivehealth.com/review/chemotherapy-heals-cancer-and-the-earth-is-flat

25. Shattering the Cancer Myth - Positive and Practical Tools to Heal Your Life

by Katrina Ellis

Published by Publicious Self-Publishing. Softback. £18.80. 2013 4th edition. ISBN 0987466941.

www.positivehealth.com/review/shattering-the-cancer-myth-a-positive-guide-to-beating-cancer-4th-edition

26. Medicine Hands, Massage Therapy for People with Cancer

by Gayle MacDonald

Published by Findhorn Press. April 2014. £29.99 / $25.27. ISBN: 978-1-84409-639-8.

www.amazon.co.uk/Medicine-Hands-Massage-Therapy-People/dp/1844096394/ref=sr_1_1?s=books&ie=UTF8&qid=1398362414&sr=1-1&keywords=Medicine+Hands+3rd+edition

27. Molassiotis A et al. Use of complementary and alternative medicine in cancer patients: a European survey. Ann Oncol 16:655-63. 2005.

www.ncbi.nlm.nih.gov/pubmed/15699021

www.medscape.com/viewarticle/586874_6

  www.medscape.com/viewarticle/586874_6

www.medscape.com/viewarticle/586874_7

28. The prevalence of complementary/Alternative medicine in cancer

A systematic review

Edzard Ernst M.D., Ph.D., Barrie R. Cassileth, Ph.D.*

Article first published online: 9 NOV 2000

DOI: 10.1002/(SICI)1097-0142(19980815)83:4<777::AID-CNCR22>3.0.CO;2-O

http://onlinelibrary.wiley.com/doi/10.1002/%28SICI%291097-0142%2819980815%2983:4%3C777::AID-CNCR22%3E3.0.CO;2-O/full

Dr.Peter H Kay said..

Dr. Goodman, Thank you for initiating this very important project, the Goodman Project. As you mention and refer to, there is a huge volume of information relating to the pros and cons of anti-cancer treatments such as chemotherapy and radiotherapy. There are, however, many alternative treatments available that are not associated with the same dangers of chemotherapy and radiotherapy. For those who suffer from cancer and would like to avoid the dangers of the forms of treatment that you have mentioned,there is a lack of information that can be used by cancer sufferers to help them to decide which form of alternative treatment may be of benefit to them. Congratulations Dr. Goodman, the Goodman Project has set the ball rolling to begin to respond to this lack of information. Much data collection is required. As a beginning, I would urge all sufferers of cancer who have accepted treatments other than chemotherapy and radiotherapy to contact Dr. Goodman and report their experiences.

Dr Ranjitsinh Solanki said..

Dr Goodman,Thanks from bottom of my hearts for important project.so many patient are survive and benefited with alternative/integrative approach. lack of proper platform and advocacy. Most of cytogenic drug which are in practice to day in conventional therapy rooted in botanical kingdom.In India due to vast traditional knowledge with biodiversity India could play major role. We have huge data of 'Evidence based cases' treated with Herbal therapy with encouraging outcome. Cancer is a cause of so many biological fector,it needs multilevel multi molecular approach to address this diseases.Technological advances can reveal Novel compound and activities in plant remedies could play great role.

Richard Eaton LL.B said..

Thank you, Dr Goodman, for initiating this vitally important and innovative project which has the potential of bringing much needed help, advice and treatment to so many cancer patients across the world. The Goodman Project also accords with the World Health Organisation Strategy 2014-2023 which, amongst other things, aims to: '...support Member States in...prioritising health services and systems, including traditional and complementary medicine products, practises and practitioners.' http://www.who.int/medicines/publications/traditional/trm_strategy14_23/en/ http://apps.who.int/iris/bitstream/10665/92455/1/9789241506090_eng.pdf?ua=1 As indicated, the main difficulty to be overcome is how to compile and analyse the research data having regard to the time, expense and technical expertise and resources required. Could those professionals with 'technical, medical and ethical experience' please now come forward with constructive suggestions as to how the Goodman Project can be implemented, administered and funded. For cancer patients everywhere (existing and prospective) the success of this enormously welcome project cannot be too soon.

Dr Alyssa Burns-Hill said..

Thanks, Sandra for this work. Speaking as someone who decided against drugs and radiotherapy for breast cancer in 2001 I fully support you. It came down to a simple realisation for me. What does conventional medicine offer me? It's toxic, it's passive (I'm a patient) and it's focused on disease. What does the alternative approach offer me? It's non-toxic, I'm actively involved in the process and making choices that are right for me and it's focused on health and wellbeing. What did I want to be - WELL! It's not easy for people receiving a diagnosis of cancer and I am always very mindful of this, but unfortunately it's often just a mechanical pathway for conventional medicine and, for me, I was also worried about my treatment strategies in the UK being led by economic policies rather than what was actually the best for me! So much to think about. Wishing everyone everywhere - good health, from a positive perspective :-)

Sandra Goodman PhD said..

07-04-2015 Despite my pessimism regarding the feasibility of funding and carrying out the above research comparing cancer survival of patients receiving alternative vs conventional, i.e. chemotherapy treatment in the UK, I am delighted with several clinical developments taking place mainly in North America.

A recent announcement (27 March 2015) online and on Twitter https://twitter.com/Bastyr stated that a $3M Research Grant has been Awarded to Canada-US Researchers Investigating the Impact of Naturopathic Medicine on Late Stage Cancer Survival. This is the largest-ever North American observational study to assess integrative oncology for advanced cancer patients. www.positivehealth.com/article/letters-to-the-editor/letters-to-the-editor-issue-222

American and Canadian healthcare professionals, including those from Bastyr University, will work together to study the effectiveness of advanced integrative oncology (AIO) treatment for patients with late stage cancer. AIO treatment includes elements of conventional and naturopathic medicine. The funding was jointly announced today by the Bastyr University Research Institute and Ottawa Integrative Cancer Centre (OICC), an arm of the Canadian College of Naturopathic Medicine (CCNM). The $3 million grant, provided by a private Canadian foundation that wishes to remain anonymous, will fund the Canadian/US Integrative Oncology Study (CUSIOS).

This is the largest-ever North American observational study to assess integrative oncology for people with late stage cancer. The goals of CUSIOS are to observe and measure the overall survival of a cohort of late stage cancer (III and IV) patients who receive AIO treatments and, to describe integrative therapies provided by naturopathic doctors across the cohort. A total of 400 people with advanced breast, colorectal, pancreatic and ovarian cancer will be studied in seven clinics across North America over three years. Each selected site provides comprehensive whole-person care in naturopathic oncology, applying advanced science-based treatment for people with late stage cancer. Integrative oncology aims to combine the best of conventional and whole-person naturopathic care seamlessly and safely to: improve survival, enhance quality of life, reduce side effects from conventional treatment and help prevent recurrence.

AIO therapies used by naturopathic doctors for late stage cancer are directed at multiple mechanisms to slow tumour progression, prevent metastatic spread and improve survival. The therapies are variable but may include intravenous vitamin C, intravenous artemisinin intravenous dichloroacetate, mistletoe, hyperthermia, nutritional protocols and the use of immunomodulatory, anti-cancer, and anti-inflammatory natural health products. www.bastyr.edu/news/general-news-home-page/2015/03/3m-research-grant-awarded-canada-us-researchers-investigating

I have also discussed some of of these protocols in a review of the book You Can Beat Lung Cancer Using Alternative / Integrative Interventions by Carl O Helvie RN DrPH, as well as in the Editorial from Issue 219: www.positivehealth.com/review/you-can-beat-lung-cancer-using-alternative-integrative-interventions www.positivehealth.com/article/editorial/editorial-issue-219

“Dr Contreras describes in valuable clinical detail the IRT-C protocol employed at the Oasis of Hope Hospital in Tijuana, Mexico, including a fully referenced description of Oxidative Stress in lung cancer and how the IRT-C protocol employs several “novel adjuvant measures intended to boost production of hydrogen peroxide in the tumor.”

These include a ‘perfluorocarbon’ oxygen-carrier molecule known as ‘Perftec’, originally developed in Russia - ‘Perftoran’ which when infused intravenously, greatly enhances the oxygen-carrying capacity of blood, as well as on the day prior to ascorbate infusion, treatment with ozone autohemotherapy, which renders red blood cells more flexible, able to more readily surrender oxygen to tissues.

“Dr Contreras compared the survival rates at Oasis of Hope with conventional treatment for years 1 through 5 also documented graphically: “Comparing IRT-C with conventional therapy, 1-year survivals were 82% vs 20%; 2-year survivals 50% vs 6%; 3-year survivals 27% vs 3%; 4-year survivals 23% vs 2% and 5-year survivals 9% vs 1.6%. At the conclusion of their clinical study, results with IRT-C were nearly 6 times better than the results using conventional therapy.”

“Dr James Forsythe MD HMD describes his integrative treatment protocols at Cancer Screening and Treatment Center of Nevada and Century Wellness Clinic which include sugar-free diets, alkalinizing diets, bio-oxidative therapies, specific vitamin supplement therapies, herbal therapies, amino acid supplements, together with low-dose fractionated chemotherapy or insulin potentiating therapies and chemosensitivity testing.

Dr Forsythe has also conducted studies, the results of which have shown over a 30% continued overall survivorship, compared with 2.1% survival rate in conventional oncology.”

Carl Helvie noted that “July, 2014 marked 40-years since my diagnosis making me the longest living lung cancer survivor known.” www.positivehealth.com/review/you-can-beat-lung-cancer-using-alternative-integrative-interventions www.positivehealth.com/article/editorial/editorial-issue-219

In the UK the demise of the long-awaited Saatchi Innovation Bill was accomplished as the bill was 'killed' by the refusal of the Liberal Democrats to provide time to debate the Bill prior to the dissolution of Parliament. www.telegraph.co.uk/news/health/saatchi-bill/11437789/Fury-as-Lib-Dems-kill-off-Saatchi-Bill.html?utm_source=Saatchi+Bill&utm_campaign=1780efe4e5-28th_Feb2_28_2015&utm_medium=email&utm_term=0_87c59b6bfe-1780efe4e5-338080097

The funding of superior quality research regarding the efficacy of alternative integrative oncology treatment for late-stage cancer patients, as well as clinical treatments by physicians internationally are milestones in documenting the efficacy or otherwise of less toxic / injurious treatments.

Christine Johnston said..

Great project Sandra and I hope you get funding and lots of support. This information is direly needed - it has been delayed for too long. Dr Peter Kay is right to ask for all cancer sufferers who have used complementary and/or alternative treatments to contact you with their experiences.

Christine Johnston, Therapist This is an important project and I hope you get the funding and support needed. I agree with Dr Peter Kay that all cancer patients who have used complementary and/or alternative treatments to contact Dr Goodman with their experiences.

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About  Sandra Goodman PhD

Sandra Goodman PhD, Co-founder and Editor of Positive Health , trained as a Molecular Biology scientist in Agricultural Biotechnology in Canada and the US, focusing upon health issues since the 1980s in the UK. Author of 4 books, including Nutrition and Cancer: State-of-the-Art , Vitamin C – The Master Nutrient , Germanium: The Health and Life Enhancer and numerous articles, Dr Goodman was the lead author of the Consensus Document Nutritional and LifeStyle Guidelines for People with Cancer and compiled the Cancer and Nutrition Database for the Bristol Cancer Help Centre in 1993. Dr Goodman is passionate about making available to all people, particularly those with cancer, clinical expertise in Nutrition and Complementary Therapies. Dr Goodman was recently featured as Doctor of the Fortnight in ThinkWellness360 .

Dr Goodman and long-term partner Mike Howell seek individuals with vision, resources, and organization to continue and expand the Positive Health PH Online legacy beyond the first 30 years, with facilities for training, to fund alternative cancer research, and promote holistic organizations internationally. Read about Dr Goodman and purchase  Nutrition and Cancer: State-of-the-Art .   She may be contacted privately for Research, Lectures and Editorial services via:  [email protected]      www.drsgoodman.com   [email protected]    and www.positivehealth.com

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Racial Disparities in Cancer Outcomes, Screening, and Treatment

Michelle Tong, Latoya Hill , and Samantha Artiga Published: Feb 03, 2022

Except for during surges in COVID-19 cases, cancer is the second leading cause of death in the U.S in both men and women nationally , with the majority of cancer related-deaths being due to breast, prostate, lung, and colon cancers. Racial disparities in cancer incidence and outcomes are well-documented , with research showing that they are driven by a combination of structural, economic, and socioenvironmental inequities that are rooted in racism and discrimination, as well as genetic and hereditary factors that may be influenced by the environment. Despite significant advancements and improvements in cancer outcomes and treatment over time, disparities persist.

This brief provides an overview of recent data on cancer incidence and mortality, risk factors, screening, treatment, and outcomes by race and ethnicity. It is based on KFF analysis of United States Cancer Statistics cancer incidence and mortality data (latest available data as of 2018), 2020 Behavioral Risk Factor Surveillance System cancer screening data, and published research. Although this brief focuses on racial disparities in cancer, disparities also occur across other dimensions , including socioeconomic status, exposure to risk factors, geographic location, and receipt of preventive measures.

Overall cancer incidence rates decreased for all racial and ethnic groups between 2013 and 2018, with the largest decreases among American Indian and Alaska Native (AIAN) and Black people. This decrease eliminated a disparity in overall cancer incidence for Black people, although they still have the highest incidence rate for some cancer types. Black people have higher new cancer rates for prostate, and colon and rectum cancer compared to other groups and one of the highest rates of new breast cancers. Moreover, across all cancers and for each cancer type, there are differences within racial and ethnic groups, such as by gender, country of origin, and geographic location.

Cancer mortality rates have also declined across all racial and ethnic groups, with the largest decrease among Black people, but Black people continued to have the highest cancer mortality rate in 2018. As is the case for cancer incidence rates, racial and ethnic patterns of cancer mortality vary by cancer type. Black people have the highest mortality rate for most leading cancer types, including female breast, prostate, and colon and rectum cancer. The higher mortality rate among Black people partly reflects a later stage of disease at diagnosis among Black patients, although Black patients additionally have lower stage-specific survival for most cancer types.

Research shows that the overall rate of cancer screening is lower among Black, Hispanic, Asian, and AIAN populations compared to their White counterparts. However, screening patterns vary across screening types, and people of color are more likely than White people to receive certain types of cancer screening. Data suggest that the COVID-19 pandemic contributed to decreases or delays in cancer screening, which may have exacerbated disparities in cancer screening.

Despite mixed findings regarding cancer screening disparities, r esearch suggests people of color receive later stage diagnoses for some types of cancer compared to their White counterparts. For certain cancers, disparities in stage of diagnosis despite comparable screening rates may be related to screening guidelines not accounting for earlier onset and increased age-specific cancer incidence for different groups, as well as disparities in quality of screening techniques and delays in diagnostic evaluation . Racial disparities in cancer care and treatment have also been identified, particularly for diagnostic and treatment delays, which contribute to worse survival outcomes.

Research suggests that cancer disparities are driven by a combination of inequities within and beyond the health system that are rooted in racism and discrimination. People of color are more likely than their White counterparts to be uninsured and to face other barriers to accessing health care that may limit access to cancer screening, care, and treatment. Beyond health coverage and access to care, discrimination and bias within the health care system and disparities in exposure to risk factors, due largely to underlying social and economic inequities, also drive cancer disparities. While socioeconomic and health care access factors are primary drivers of cancer disparities, research also suggests that hereditary risk and genetic determinants for specific cancer subtypes may explain a portion of disparities. Underrepresentation of people of color in the development of current screening guidelines and in oncology cancer trials may also contribute to disparities.

Overall, the data suggest that continued efforts within and beyond the health care system will be important to reduce ongoing racial disparities in cancer. Within the health care system, these may include efforts to reduce gaps in health insurance, increase access to care, and eliminate discrimination and bias in care and treatment. Beyond the health care system, it will also be important to address broader social and economic factors, including exposure to environmental risks and disparities in behavioral risks. Furthermore, there are ongoing discussions about reevaluating the implications of current cancer screening guidelines for disparities and whether to adjust guidelines or cancer screening approaches to account for higher prevalence and risk and earlier age of onset for certain cancers among different communities. Moving forward, increasing diversity among oncology clinical trials and within the health care workforce also will be important for addressing disparities in cancer care and treatment and ensuring that all people benefit from continued advancements in cancer treatment.

Cancer Incidence by Race and Ethnicity

Overall cancer incidence rates decreased for all racial and ethnic groups between 2013 and 2018, with the largest decreases among AIAN and Black people (Figure 1). This decrease eliminated a disparity in overall cancer incidence for Black people, who had the highest rate of new cancers in 2013 but had a similar cancer incidence rate as White people in 2018. Among the four leading types of cancer, rates of new lung and bronchus and colon and rectum cancer decreased across all racial and ethnic groups from 2013 to 2018. Rates of new prostate cancer cases decreased for Black, Hispanic, and AIAN people, while they remained fairly stable for White and Asian and Pacific Islander people over the period. The decreases narrowed disparities in colon and rectum and prostate cancer incidence rates for Black people over the period. New female breast cancer rates also decreased for AIAN and Black people, while there were small increases in the breast cancer incidence rate for other groups.

Overall, White and Black people have the highest rates of new cancers. Within the U.S., there were over 1.7 million new cancer cases reported in 2018, or 436 new cancer cases for every 100,000 people. White people had the highest rate of new cancers at 437 per 100,000 people, followed by Black people at 427 per 100,000 people, while cancer incidence rates were lower among Hispanic, Asian and Pacific Islander, and AIAN people. Although Asian and Pacific Islander (API) men and women have the lowest overall cancer incidence and mortality, they have among the highest liver and stomach cancer rates , roughly double the rates for White people.

Patterns of cancer incidence by race and ethnicity vary across cancer types. Female breast, prostate, lung and bronchus, and colon and rectum cancers had the highest rates of new cancers in 2018. Although White or Black people had the highest incident rates across these cancer types, patterns of incidence by race and ethnicity varied by type (Figure 2):

• Female breast cancer . Like cancers overall, White people had the highest rate of new female breast cancers (128 per 100,000 females), followed by Black people (121 per 100,000 females). Other racial/ethnic groups had lower incidence rates, particularly AIAN people, whose new female breast cancer rate was roughly half the rate for White people at 65 per 100,000 females.
• Prostate cancer . Black people had the highest rate of new prostate cancers at 164 per 100,000 males, followed by White people at 99 per 100,000 males and Hispanic people at 80 per 100,000 males. Asian and Pacific Islander and AIAN people were substantially less likely to have a new prostate cancer case, as their rates were more than three times lower than the rate for Black people.
• Lung and bronchus cancer. Rates of new lung and bronchus cancer were similar for White and Black people at 55 and 54 per 100,000 people, respectively, while rates were lower for other groups and lowest for Hispanic people at 27 per 100,000.
• Colon and rectum cancer. Black people had the highest rate of new colon and rectum cancer (40 per 100,000 people), followed by White and Hispanic people, at 36 and 33 per 100,000, respectively. The lowest rate of new colon and rectum cancers was among AIAN people at 26 per 100,000 people.

Across all cancers and for each cancer type there are differences in incidence rates within racial and ethnic groups, such as by gender, geographic location, and country of origin. For example, overall cancer incidence rates were higher for men than women among White, Black, Hispanic, and AIAN people in 2018, while they were higher for women among Asian and Pacific Islander people. Black men have the highest rates of age-adjusted lung cancer incidence among all groups. In general, rural populations have higher incidence of preventable cancers and higher mortality compared to their urban counterparts, although cancer incidence is higher in urban areas for some types of cancer, such as breast and prostate cancer . Research further shows a similar pattern for people of color in rural areas, who generally have higher cancer incidence and mortality for preventable cancers compared to their urban counterparts. Other research has found that Black women in rural counties had higher incidence of regional cervical cancer than those in urban counties, and White women in rural counties had higher incidence than those in urban counties for cervical cancer at every stage, while there were no rural-urban differences among Hispanic women. Research also shows that, within racial and ethnic groups, there is wide variation in cancer incidence between U.S.-born and foreign-born people living in the U.S. For example, studies show that foreign-born Hispanic and Asian people have higher incidence of gastric cancer than their U.S. born counterparts, largely due to increased infection from H. pylori , which is endemic to multiple Latin American and Asian countries. However, compared to foreign-born Latino people, U.S.-born Latino people have higher rates of breast, colorectal, prostate, lung, and liver cancers, and U.S.-born Chinese and Filipina people have higher breast and colorectal cancer incidence compared to their foreign-born counterparts.

Cancer Mortality by Race and Ethnicity

Overall cancer mortality rates decreased for all racial and ethnic groups, with the largest decrease among Black people, but Black people continued to have the highest cancer mortality rate in 2018 (Figure 3). Between 2013 and 2018, the difference between the overall cancer mortality rate for Black and White people narrowed, but Black people remained at higher risk for cancer death. Among the leading four types of cancer death, mortality rates for female breast cancer decreased for White, Black, and Hispanic people and increased for Asian and Pacific Islander and AIAN people. Colon and rectum and lung and bronchus cancer mortality rates decreased across all racial and ethnic groups, while prostate cancer mortality rates decreased for Black and AIAN people but remained fairly stable for White and Asian and Pacific Islander people. Decreases over the period narrowed disparities in mortality for Black people for colon and rectum, lung and bronchus, and prostate cancer, although they remained at higher risk for dying from colon and rectum and prostate cancer compared to White people. The decreases largely eliminated the difference in lung and bronchus mortality rates between Black and White people, while the difference in breast cancer mortality rates remained largely stable.

Black people are at the highest risk for cancer death even though White people have the highest rate of new cancers. This increased mortality risk partly reflects a later stage of disease at diagnosis among Black patients, although Black patients additionally have lower stage-specific survival for most cancer types. In 2018, Black people had the highest cancer mortality rate at 169 per 100,000 people, followed by White people at 150 per 100,000 (Figure 4). Rates were lower for Hispanic, AIAN, and Asian and Pacific Islander people. As is the case for cancer incidence rates, racial and ethnic patterns of cancer mortality vary by cancer type:

• Female breast cancer . Black people had the highest rate of female breast cancer deaths (27 per 100,000 females) followed by White people (19 per 100,000 females), despite White people having the highest rate of new female breast cancers. Female breast cancer death rates for other groups were half or less than the rate for Black people.
• Prostate cancer . Consistent with having the highest incidence of prostate cancer, Black people also had the highest rate of prostate cancer deaths, at 37 per 100,000 males, more than twice as high as the rates for all other groups, which ranged from 9.2 per 100,000 males for Asian and Pacific Islander people to 17.7 per 100,000 males for White people.
• Lung and bronchus cancer. Like patterns in cancer incidence rates, Black and White people are at similar risk for lung and bronchus cancer death, with a mortality rate of 36 per 100,000 people for both groups. These rates are higher than rates for other groups, and more than double the rate for Hispanic people (15 per 100,000 people).
• Colon and rectum cancer. Racial/ethnic patterns of colon and rectum cancer mortality rates also were similar to incidence patterns with Black people having the highest colon and rectum cancer death rate (17 per 100,000 people), followed by White people at 13 per 100,000 people and a slightly lower rate for Hispanic people at 11 per 100,000 people. Asian and Pacific Islander people had the lowest rate of death due to colon and rectum cancer at 9 per 100,000 people.

As is the case for cancer incidence, across all cancers and for each cancer type there are differences in cancer mortality rates within racial and ethnic groups, such as by gender, country of origin, and geographic location. Across racial and ethnic groups, men have higher rates of cancer death compared to women. Notably, there exists variation in cancer mortality between U.S.-born and foreign-born Black people living in the U.S. For example, one study found that U.S.-born Black people experienced higher cancer mortality for cervical, lung and bronchus, colorectal, and prostate cancers compared to Black individuals from the Caribbean. Similarly, compared to foreign-born Latino people, U.S.-born Latino people have worse survival rates for breast, colorectal, prostate, lung, and liver cancers. In contrast, compared to foreign-born Asian people, U.S.-born Asian people experience lower mortality rates across multiple cancers, including breast, colon and rectum, and prostate cancers.

Cancer Screening, Diagnosis, and Treatment by Race and Ethnicity

Research shows that the overall rate of cancer screening is lower among Black, Hispanic, Asian, and AIAN populations compared to their White counterparts, but people of color are more likely than White people to receive certain types of screening. Reasons for these variations in screening patterns across different groups are not well understood. Research suggests that outside of health insurance coverage and geographic differences, participation in cancer screening is related to multiple factors, such as provider recommendation , shared decision-making between patients and providers, perceptions of cancer screening , and gender differences in cancer screening behaviors, which may vary across communities .

• Mammograms . Since implementation of the Affordable Care Act coverage expansions, the share of people who have gone without a recent mammogram fell for some groups but did not change for other groups. Between 2012 (the latest year data are available prior to implementation of the ACA coverage expansions in 2014) and 2020, the share of people in the groups recommended for screening by the U.S. Preventive Services Task Force (USPSTF) who did not receive a recent mammogram fell for White, Black, and Hispanic people. There was no significant change for other groups. Hispanic people had the largest decrease, with the share falling by 11 percentage points from 32% to 21%, and Black people had a 7 percentage point decline from 22% to 15% (Figure 5). In contrast, White people had a smaller 2 percentage point decrease from 24% to 22%. The larger decrease for Hispanic people reversed a disparity and resulted in them being less likely than White people to go without a recent mammogram as of 2020 (21% vs. 22%). The share of Black people who did not receive a mammogram was already slightly lower than White people as of 2012 (22% vs. 24%), and this difference widened to 15% vs. 22% as of 2020. While this improvement likely, in part, reflects the implementation of focused interventions to decrease disparities in breast cancer screening, research also suggests that Black and Hispanic women are more likely than White women to overestimate their screening history . Native Hawaiian and Other Pacific Islander (NHOPI) people also were less likely than White people to go without a recent mammogram as of 2020, while Asian and AIAN people were more likely to go without a mammogram.
• Pap smears. The share of people in the recommended groups for screening who did not receive a recent pap smear did not significantly change for most groups between 2012 and 2020. However, it increased from 17% to 22% for White people and from 31% to 36% for Asian people. As of 2020, Black people were less likely than White people to go without a recent pap smear (17% vs. 22%), while all other groups were more likely to have not received one, with the largest difference for Asian people (36% vs. 22%). However, research has found that Black women compared to all groups are the least likely to receive human papillomavirus (HPV) co-testing with pap smears.
• Colorectal screening. The share of people in the recommended groups for screening who were not up-to-date with colorectal cancer screening decreased for most groups between 2012 and 2020. Native Hawaiian and Other Pacific Islander (NHOPI) people had the largest decrease, with the share falling by 18 percentage points from 46% to 28%, followed by Hispanic people who had a decrease of 10 percentage points, from 47% to 37%. As of 2020, Hispanic, Asian, and AIAN people were more likely than White people to not be up to date with colorectal cancer screening tests, while there were no significant differences between White and Black people in the recommended screening group.
• Other research suggests that African American people face disparities in receipt of prostate screening relative to their increased risk. Similarly, eligible Black adults are less likely to undergo lung cancer screening compared to all other groups and less likely to complete subsequent annual screening for lung cancer compared to White patients. Individuals in rural areas, in general, are less likely to receive cancer screening compared to their urban counterparts, though these findings are mixed for different racial and ethnic groups.

Data suggest that the COVID-19 pandemic contributed to decreases or delays in cancer screening. Overall, health care use and spending dropped precipitously in the spring of 2020 when many social distancing measures were put in place to mitigate the spread of coronavirus. While health care use and spending began to rebound as the year progressed, overall spending remained down as of December 2020 due to a decrease in utilization of non-COVID medical care. Analysis from the Centers for Disease Control and Prevention (CDC) found that, during California’s stay-at-home order, cervical cancer screening rates among approximately 1.5 million women in the Kaiser Permanente Southern California (KPSC) network decreased approximately 80% compared with baseline. The decrease was similar across all racial/ethnic groups in the KPSC network and returned to near normal after reopening. According to an analysis of electronic health records by Epic Health Research Network, average weekly screenings for breast, colon, and cervical cancers dropped by 94%, 86%, and 94%, respectively, during January 20–April 21, 2020, relative to the averages before January 20, 2020. A follow-up study conducted in July 2020 showed that weekly screening rates were rising but had not yet reached pre-pandemic levels. Other research found that between January-June 2020, breast and cervical cancer screening rates fell among low-income women, with the highest decreases among AIAN, Asian and Pacific Islander, and Hispanic people. Subsequent research in Washington State found similar trends with greater reductions in breast cancer screening for communities of color compared to their White counterparts, and larger fall offs in screening for women in rural areas compared to urban areas during the pandemic. More recent research in Massachusetts found that over the remainder of 2020, while overall cancer screening appeared to have recovered (and even increased compared to pre-pandemic for all cancer screening, except for colonoscopy), the pandemic accentuated racial disparities in mammography for Black and Hispanic patients.

Research suggests that people of color receive later stage diagnoses for some types of cancer compared to their White counterparts. For many cancers, stage of diagnosis may be one of the most important predictors of survival, where people diagnosed at earlier stages have better survival outcomes. For certain cancers, disparities in stage of diagnosis despite comparable screening rates may be related to screening guidelines not accounting for earlier onset and increased age-specific cancer incidence for different groups, as well as disparities in quality of screening techniques and delays in diagnostic evaluation . Furthermore, national surveys do not distinguish between screening and follow-up mammograms, which may contribute to overestimates of screening. Recent analysis from the American Cancer Society finds that, among people diagnosed with cancers for which screening is recommended (lung, colorectum, female breast, cervix, and prostate), Black people generally had the lowest proportion of localized-stage cancer and the highest proportion of distant-stage cancer compared with other racial and ethnic groups, except for prostate cancer, for which AIAN men had the highest proportion of distant-stage disease. Black people were also more likely than other groups to be diagnosed with advanced disease for most other cancer types. Other research shows that, compared to White patients, Black patients present with more advanced disease at diagnosis across prostate, breast, and cervical cancers. Research further shows that, across multiple tumor types, Black patients present with higher-grade and more aggressive disease compared to White patients, and among those with endometrial cancer, Black patients are more likely to have subtypes associated with worse outcomes. Hispanic people are more likely than White people to be diagnosed with distant stage lung cancer , yet have lower lung cancer mortality compared to both Black and White people. Prior work has also found that compared to White patients, AIAN patients have more advanced disease at diagnosis and worse survival outcomes for multiple cancers. For skin cancers, Black patients have the highest percentage of late-stage melanoma and increased mortality compared to White patients, likely secondary to a higher proportion of later stage diagnoses, although other studies have found that increased mortality rates persist even for earlier stage diagnoses .

Racial disparities in cancer care and treatment have also been identified, particularly for diagnostic and treatment delays, which contribute to worse survival outcomes. Evidence suggests that Black patients are less likely than White patients to receive stage-appropriate treatment or guideline-concordant care across multiple types of invasive cancers. Compared to White patients, Black patients are less likely to receive a lung cancer screening after receiving a referral, are less likely to receive a provider recommendation for surgery for lung cancer, and are more likely to refuse surgery after it is recommended. Black people also are treated less frequently with chemotherapy and radiation for colorectal cancer. Furthermore, research has found lower rates of provider recommendation for colorectal screening for Black patients compared to their White counterparts. For breast and gynecological cancers , Black and Hispanic women are less likely than White women to receive certain evidence-based workup procedures or guideline recommended treatments. Other work has found that, compared to White women with similar treatment plans, Black women more often have delays in breast cancer treatment initiation. Research has similarly found that compared to White patients, Black and Hispanic patients have increased delays in receipt of surgery for breast cancer. While less studied, work has found that Asian women have a higher rate of receiving no follow-up after abnormal breast cancer screening compared to White women, with these differences being starkest among Filipina and Vietnamese women.

People of color are also more likely to report unmet needs for cancer care, including supportive care. Across communities of color, unmet socioeconomic and supportive care needs are linked to poor cancer therapy adherence . Even after adjusting for differences in socioeconomic status and health system access, research finds that U.S.-born Black people and foreign-born Latino and Asian people are more likely to perceive an unmet need in cancer care than U.S.-born White people. Furthermore, Hispanic cancer survivors report worse quality of life and unmet supportive care needs (including information about disease, psychological support, pain management, and treatment side effects) compared to White cancer survivors. Similar work has identified a high prevalence of unmet needs in physical health concerns, emotional support, and daily activity challenges for Asian and Pacific Islander cancer survivors and a shortage of patient navigators and support groups for AIAN cancer survivors.

Factors Contributing to Racial Cancer Disparities

Research suggests that racial cancer disparities are driven by a combination of inequities in health coverage and access to care, social and economic factors, and care and treatment that are rooted in racism and discrimination. Moreover, some research suggests that hereditary risk and genetic determinants for specific subtypes of cancer, in addition to environmental influences on genetic expression, may also explain a portion of disparities.

People of color are more likely than their White counterparts to be uninsured and to face other barriers to accessing health care that may limit access to cancer screening, care, and treatment. Data show that people of color are less likely to have health insurance and more likely to face barriers to accessing care, such as not having a usual source of care. Research shows that, overall, uninsured people are more likely than those with insurance to go without needed medical care due to cost and less likely to receive preventive care and services. Research further shows that financial barriers and lack of health insurance prevent adequate cancer care and management and are associated with lower screening , delays in diagnosis, decreased receipt of cancer therapies, and lower treatment adherence . One study found that Hispanic and African American women were more likely than White women to experience delays in receiving adjuvant chemotherapy for breast cancer, and that insurance status was an important factor contributing to these delays. Research also finds that Black and Hispanic cancer patients are more likely than White patients to forego needed cancer treatment because of problems with transportation and that Black patients are more likely to report health care costs as a barrier to cancer care follow-up. Other work shows that lack of doctor recommendations, increased health literacy risks, and competing priorities (working multiple jobs, needing to reschedule physician appointments, and low family income) contribute to differences in receipt of breast cancer screening and pap smear testing among Black and Hispanic women. Among AIAN people, decreased availability of endoscopic services within Indian Health Service and tribal facilities, in addition to underfunded referral systems may contribute to more limited screening compared to the rest of the U.S. population.

Beyond health coverage and access to care, discrimination and bias within the health care system may contribute to cancer disparities. A significant and longstanding body of  research  suggests that provider and institutional bias and discrimination are drivers of racial health disparities, contributing to racial differences in diagnosis, prognosis, and treatment decisions and differences in experiences obtaining health care. For example, KFF survey data show that Black and Hispanic adults are more likely to report some negative experiences with health care providers, including providers not believing they were telling the truth or refusing to provide pain medication or other treatments they thought they needed. Furthermore, recent research has found that Black patients are over twice as likely as White patients to have at least one negative descriptor in the history and physical notes of their electronic health record. Research finds that women perceiving racial or ethnic-based medical discrimination were less likely to be screened for colorectal and breast cancer compared to those not perceiving discrimination. Other studies have not found a link between race-based discrimination and receipt of cancer screening but have found that perceived discrimination due to other reasons such as age or gender is associated with decreased receipt of pap smears and mammography.

Research also points to the role of communication and interactions between providers and patients in driving disparities. This work suggests that enhancing providers’ ability to provide  culturally and linguistically appropriate care , as well as  increasing diversity of the health care workforce , may help address health disparities. For example, research shows that limited health literacy and limited English proficiency is associated with a decreased likelihood of breast and colorectal cancer screening among Chinese Americans. Other work finds that disparities in cancer screening among immigrants reflect a combination of cultural beliefs and attitudes, lack of knowledge, and barriers to access, which the authors conclude highlight the importance of developing culturally sensitive interventions to increase cancer screening uptake among these communities. Experiences suggest that socio-culturally and individually-tailored education and outreach , community level interventions which often rely on community health workers or religious leaders , and changes at the health systems level , such as direct referral to cancer screening from primary care providers and increased clinical equipment and staffing, may improve cancer screening and follow-up for people of color.

Disparities in exposure to risk factors, due largely to underlying social and economic inequities, drive cancer disparities. For example, historic housing policies, including redlining, and ongoing economic inequities have resulted in residential segregation that pushed many low-income people and people of color into segregated urban neighborhoods. Many of these neighborhoods have dense industrial facilities that result in high exposure to harmful air toxins. Reflecting these patterns, research finds higher exposure to air toxins that pose cancer risks in neighborhoods with concentrated shares of African American people compared to neighborhoods with higher shares of White people. Similarly, in California, higher exposure to pesticides is associated with increased rates of testicular germ cell cancer, particularly among Latino people. Beyond exposure to environmental risks, certain health behaviors may influence cancer risks and outcomes, such as smoking, obesity, alcohol consumption, and limited physical activity. These individual health behaviors are often shaped by broader social and economic factors, such as access to healthy food, financial ability to purchase food, availability of green space, and time to engage in leisure activities. Data show that AIAN and Black adults are more likely than White adults to smoke, while Asian and Hispanic adults have lower smoking rates. Moreover, Black, AIAN, NHOPI, and Hispanic adults are more likely to be obese than White adults, while Asian adults are less likely to be obese. Research further suggests that Latino and African American people are more likely than their White counterparts to have multiple behavioral risks that may contribute to cancer risk. However, research also finds that Black patients diagnosed with lung cancer are less likely to be chronic smokers compared to White patients and that, even at lower levels of smoking, Black and AIAN patients have higher rates of lung cancer compared to White patients, suggesting that smoking may not be the main driver of lung cancer disparities for these groups. Increased prevalence of comorbidities among people of color, such as diabetes, may also influence disparities in cancer survival and treatment outcomes. Moreover, foreign-born Asian and Latino people may face an increased risk for specific cancers associated with infection with cancer-associated pathogens that have higher incidence in their countries of origin.

While socioeconomic and health care access factors are primary drivers of cancer disparities, research also suggests that hereditary risk and genetic determinants for specific cancer subtypes may explain a portion of disparities. Some genetic determinants may influence susceptibility due to genetic variants or cancer-driven gene mutations in obesity, chronic inflammation, and immune responses. Research further suggests that environmental influences on gene expression may play a role in explaining racial disparities in cancer incidence and progression. For breast cancer, American Cancer Society analyses consistently find that Black people have the second highest incidence rate for female breast cancers after White people, but disproportionately higher rates of triple negative breast cancers and increased likelihood of being diagnosed with high-grade and metastatic breast cancer compared to all other groups. Hormone receptor status for breast cancers is a significant factor contributing to survival disparities, with triple negative breast cancers being less likely to be detected through screening and associated with worse prognosis, high frequency of metastasis, and lower survival compared to other breast cancer subtypes. Research has linked a higher prevalence of triple negative breast cancers among Black women to West African ancestry and specific birthplace . However, prior research has noted that tumor biological differences may contribute less to racial disparities in cancer outcomes compared to health care access barriers, and that there are no racial differences in efficacy of local or systemic therapy for breast, lung, or colorectal cancers.

Current screening guidelines for some cancers may also contribute to disparities by not accounting for differences in cancer risk across communities. Cancer screening guidelines have been developed based on clinical trials that largely underrepresented communities of color and, as such, may not reflect variations in cancer incidence and risk factors among different groups. In 2020, the American Thoracic Society released a statement noting that lung cancer screening guidelines do not recognize disparities in smoking behaviors or lung cancer risk and suggesting that researchers, providers, and professional organizations should consider an approach that includes eligibility assessments for high-risk individuals who are excluded under the guidelines. Research showed that under these USPSTF screening guidelines African American and Hispanic people were less likely than White people to be eligible for lung cancer screening despite having equal or greater risk of lung cancer compared to White smokers. Although the screening guidelines were updated in March 2021, this research further found that while the shares of people eligible for screening increased across groups, these disparities persisted. Moreover, some researchers have suggested that separate prostate cancer screening guidelines should be utilized for African American men given their higher rates of incidence and mortality, pointing to the lack of racial diversity in the studies upon which existing guidelines are based. For breast cancer, work has suggested promoting screening before the age of 50 to reduce mortality disparities, given the younger age of onset and higher incidence of certain cancer types among Black women. The USPSTF currently recommends breast cancer screening prior to the age of 50 as a Grade C guideline, which means it is suggested providers offer or provide this service for selected patients depending on individual circumstances. For colon cancer, there have similarly been efforts to lower the age to begin screening to 45 years for Black patients. As of May 2021, USPSTF guidelines were updated to begin colorectal cancer screening at age 45 as a Grade B recommendation , meaning it is suggested that providers offer the service to all eligible people. This change was made to reflect increasing colorectal cancer incidence at a younger age in the general U.S. population and higher rates among Black and AIAN people.

Underrepresentation of Black and Hispanic adults and other people of color in oncology clinical trials may contribute to cancer treatment and mortality disparities. Research has identified multiple barriers to participation in clinical trials for people of color, including lack of understanding and information about trials, fear and stigma of participating, and time and resource constraints associated with trial participation (including financial burden, time commitment, transportation, and compensation). Furthermore, research suggests that physicians are less likely to discuss clinical trials with patients of color and that trials may exclude a significant portion of Black patients due to co-existing comorbidities or lab cutoffs. Research has found that when offered to participate, at least half of patients offered participation in a clinical trial do participate, and that Black patients participate in clinical trials at similar rates compared to White patients. Moreover, previously limited coverage of clinical trial participation by Medicaid may have exacerbated underrepresentation in trials, given that people of color are disproportionately covered through Medicaid. In 2021, the Centers for Medicare and Medicaid Services issued new requirements for all states to cover routine patient costs associated with clinical trial participation. However, Medicaid does not cover ancillary costs of trial participation, such as those related to childcare and employment. Medicaid does offer a separate non-emergency medical transportation benefit , while the Food and Drug Administration does not consider reimbursement for travel expenses to and from clinical trial sites or associated costs.

Looking Ahead

Overall, the data suggest that continued efforts within and beyond the health care system will be important to reduce ongoing racial disparities in cancer, many of which are rooted in systemic racism. Within the health care system, these may include ongoing efforts to reduce gaps in health insurance, increase access to care, and eliminate discrimination and bias. Beyond the health care system, addressing broader social and economic factors, including exposure to environmental risks and disparities in behavioral risks will also be important. Furthermore, there are ongoing discussions about reevaluating the implications of current cancer screening guidelines for disparities and whether to adjust guidelines or screening approaches to account for higher prevalence and risk for cancers among different communities. Moving forward, increasing diversity among oncology clinical trials and within the health care workforce will also be important for addressing disparities in cancer care and treatment, and ensuring that all people benefit from continued advancements in cancer treatment.

• Racial Equity and Health Policy
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• American Indian/Alaska Native

Also of Interest

• Web Event: Understanding and Addressing Racial Disparities in Cancer Outcomes, Care, and Treatment
• Use of Race in Clinical Diagnosis and Decision Making: Overview and Implications

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Metabolic Regulation of Exosome Biogenesis as a Determinant of Cancer Cell Metastasis

Principal investigator: mark antonyak, co-pi: robert weiss.

DESCRIPTION (provided by applicant):

The studies outlined in this proposal focus on the mechanisms by which aggressive breast cancer cells generate large numbers of exosomes with unique cargo, together with a total secretome that significantly enhances their potential for metastatic spread. They are based on exciting developments in the cancer biology field which show that exosomes, a major class of extracellular vesicles (EVs), play important roles in a number of aspects of cancer progression. These include the ability of exosomes to confer tumor cells with the capability to show resistance to chemotherapeutic reagents as well as to immune therapy, together with their roles in promoting metastatic spread. We recently discovered that the downregulation of SIRT1 by aggressive breast cancer cells has an important influence on the numbers of exosomes that they generate, the nature of the exosome cargo, as well as the composition of their total secretome. This is due to the NAD+-dependent deacetylase/deacylase Sirtuin (SIRT1) playing a key role in maintaining normal lysosomal function through a novel mechanism that ensures the proper expression of a major subunit of the vacuolar ATPae (v-ATPase). We also have recently found that the formation and shedding of exosomes appear to be dependent on the elevations in glutamine metabolism characteristic of breast cancer cells (i.e. their ‘glutamine addiction’). These findings now raise important questions regarding how the dependence of aggressive breast cancer cells on glutamine metabolism influences and/or works together with the down-regulation of SIRT1 expression/activation to regulate lysosomal function and exosome biogenesis, thus producing a secretome that stimulates cancer cell invasiveness and helps drive the metastatic process. The different laboratories participating in this proposal will take advantage of their multi-disciplinary expertise in biochemical and chemical biology approaches in probing cancer cell metabolism and exosome biogenesis, high-resolution imaging, 3D spheroid culture and tumor organoids, and the use of mouse models, in probing three key aspects of the mechanisms driving breast cancer metastasis. These are: 1) Examining the relationship between SIRT1 down-regulation, elevated glutamine metabolism and the generation exosomes with unique cargo by aggressive breast cancer cells. 2) Understanding how SIRT1 down-regulation impacts vacuolar ATPase expression to generate a secretome capable of promoting cancer cell invasiveness. 3) Determining how SIRT1 expression/activity affects exosome production, cell invasiveness and metastatic spread in breast cancer models. The expectation is that these studies will lead to the identification of exciting new treatment strategies for the devastating effects of aggressive breats cancers, and ultimately, for other metastatic diseases.

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Leading Change in Cancer Clinical Research, Because Our Patients Can’t Wait

May 31, 2024 , by W. Kimryn Rathmell, M.D., Ph.D., and Shaalan Beg, M.D.

Greater use of technologies that can increase participation in cancer clinical trials is just one of the innovations that can help overcome some of the bottlenecks holding up progress in clinical research. 

Thanks to advances in technology, data science, and infrastructure, the pace of discovery and innovation in cancer research has accelerated, producing an impressive range of potential new treatments and other interventions that are being tested in clinical studies . The extent of the innovative ideas that might help people live longer, improve our ability to detect cancer early, or otherwise transform care is staggering. 

Our understanding of tumor biology is also evolving, and those gains in knowledge are being translated into the continued discovery of targets for potential interventions  and the development of novel types of treatments. Some of these therapies are producing unprecedented clinical responses  in studies, including in traditionally difficult-to-treat cancers. 

These advances have contributed to a record number of Food and Drug Administration (FDA) approvals in recent years with, arguably, the most notable approvals being those for drugs that can be used for any cancer, regardless of where it is in the body . 

In some instances, the activity of new agents has been so profound that clinical investigators are having to rethink their criteria for implementation in patient care and their definitions of treatment response. 

For example, although HER2 has been a known therapeutic target in breast cancer for many decades, the new antibody-drug conjugates  (ADCs) that target HER2 have proven to be vastly more effective than the original HER2-targeted therapies. This has forced researchers to rethink fundamental questions about how these ADCs are used in patient care: Can they be effective in people whose tumors have lower expression of HER2 than we previously thought was needed ? And, if so, do we need to redefine how we classify HER2-positive cancer? 

As more innovative therapies like ADCs hit the clinic at a far more rapid cadence than ever before, the research community is being inundated with such fundamentally important questions.

However, the remarkable progress we're experiencing with novel new therapies is tempered by a critical bottleneck: the clinical research infrastructure can’t be expected to keep pace in this new landscape. 

Currently, many studies struggle to enroll enough participants. At the same time, there are patients who don’t have ready access to studies from which they might benefit. Furthermore, ideas researchers have today for studies of innovative new interventions might not come to fruition for 2 or 3 years, or even longer—years that people with cancer don’t have. 

The key to overcoming this bottleneck is to invite innovation to help reshape our clinical trials infrastructure. And here’s how we plan to accomplish that.

Testing Innovation in Cancer Clinical Trials

A transformation in cancer clinical research is already underway. That transformation has been led in part by the success of novel precision oncology approaches, such as those tested in the NCI-MATCH trial .

This innovative study ushered in novel ways of recruiting participants and involving oncologists at centers big and small. And NCI-MATCH has spawned several successor studies that are incorporating and building on its innovations and achievements.

An innovation that emerged from the COVID pandemic was the increase of remote work, even in the clinical trials domain. Indeed, staffing shortages have caused participation in NCI-funded trials to decline. In response, NCI is piloting a Virtual Clinical Trials Office to offer remote support staff to participating study sites. This support staff includes research nurses, clinical research associates, and data specialists, all of whom will help NCI-Designated Cancer Centers and community practices engaged in clinical research activities.

Such technology-enabled services can allow us to reimagine how clinical trials are designed and run. This includes developing technologies and processes for remotely identifying clinical trial participants, shipping medications to participants at home, having imaging performed in the health care settings where our patients live, and empowering local physicians to participate in clinical trials.

We also need mechanisms to test and implement innovations in designing and conducting clinical studies. 

The Pragmatica-Lung Cancer Treatment Trial , an innovative phase 3 study launched by  NCI’s National Clinical Trials Network (NCTN) , was designed to be easy to launch, enroll participants, and interpret its results. 

NCI recently established Clinical Trials Innovation Unit (CTIU) to pressure test a variety of innovations. The CTIU, which includes leadership from FDA and NCTN, is already working on future innovations, including those that will streamline data collection and apply novel approaches to clinical studies, all with the goal of making them less burdensome to run and easier for patients to participate.

Data-Driven Solutions

The era of data-driven health care is here, providing still more opportunities to transform cancer clinical research. 

The emergence of artificial intelligence (AI) solutions, large language models, and informatics brings real potential for wholesale changes in how we match patients to clinical studies, assess side effects, and monitor events like disease progression. 

Recognizing this potential, NCI is offering funding opportunities and other resources that will fuel the development of AI tools for clinical research, allow us to carefully test their usefulness, and ultimately deploy them across the oncology community. 

Creating Partnerships and Expanding Health Equity

To be sure, none of this will be, or can be, done by NCI alone. All these innovations require partnerships. We will increase our engagement with partners in the public- and private-sectors, including other government agencies and nonprofits. 

That includes high-level engagement with the Office of the National Coordinator for Health Information Technology (ONC), with input from FDA, Centers for Medicare & Medicaid Services, and Centers for Disease Control and Prevention.

Dr. W. Kimryn Rathmell, M.D., Ph.D.

NCI Director

One example of such a partnership is the USCDI+ Cancer program . Conducted under the auspices of the ONC, this program will further the aims of the White House's reignited Cancer Moonshot SM by encouraging the adoption and utilization of interoperable cancer health IT standards, providing resources to support cancer-specific use cases, and promoting alignment between federal partners. 

And just as importantly, the new partnerships we create must include those with patients, advocates, and communities in ways we have never considered before.

A central feature of this community engagement must involve intentional efforts to expand health equity, to create study designs that are inclusive and culturally appropriate. Far too many marginalized communities and populations today are further harmed by studies that fail to provide findings that apply to their unique situations and needs.

Very importantly, the future will require educating our next generation of clinical investigators and empowering them with the tools that enable new ways of managing clinical studies. By supporting initiatives spearheaded by FDA and professional groups like the American Society of Clinical Oncology, NCI is making it easier for community oncologists to participate in clinical trials and helping clarify previously misunderstood regulatory requirements. 

These efforts must also ensure that we have a clinical research workforce that is representative of the people it is intended to serve. Far too many structural barriers have prevented this from taking place in the past, and it’s time for that to change. 

Expanding our capacity doesn’t mean doing more of the same, it means challenging ourselves to work differently. This will let us move forward to a new state, one in which clinical research is integrated in everyday practice. It is only with more strategic partnerships and increased inclusivity that we can open the doors to seeing clinical investigation in new ways, with new standards for success.

A Collaborative Effort

Shaalan Beg, M.D.

Senior Advisor for Clinical Research

To make the kind of progress we all desire, we have to recognize that our clinical studies system needs to evolve.

There was a time when taking years to design, launch, and complete a clinical trial was acceptable. It isn’t acceptable anymore. We are in an era where we have the tools and the research talent to make far more rapid progress than we have in the past. 

And we can do that by engaging with many different communities and stakeholders in unique and dynamic ways—making them partners in our effort to end cancer as we know it.

Together, our task is to capitalize on this work so we can move faster and enable cutting-edge research that benefits as many people as possible. 

We also know that there are more good ideas in this space, and part of this transformation includes grass roots efforts to drive systemic change. So, we encourage you to share your ideas on how we can transform clinical research. Because achieving this goal can’t be done by any one group alone. We are all in this together. 

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