Vitamin D and Colorectal Cancer Risk – What is the Correlation?

MedicalResearch.com Interview with:

Stephanie J. Weinstein, M.S., Ph.D.  Metabolic Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH 

Dr. Weinstein

Stephanie J. Weinstein, M.S., Ph.D. 
Metabolic Epidemiology Branch, Division of Cancer Epidemiology and Genetics
National Cancer Institute, NIH  

MedicalResearch.com: What is the background for this study?  

Response: Vitamin D, known for its role in maintaining bone health, is hypothesized to lower colorectal cancer risk via several pathways related to cell growth and regulation. Previous prospective studies have reported inconsistent results for whether higher concentrations of circulating 25-hydroxyvitamin D, the accepted measure of vitamin D status, are linked to lower risk of colorectal cancer. The few randomized clinical trials of vitamin D supplementation and colorectal cancer completed thus far have not shown an effect; but study size, relatively short supplementation duration, and only moderate compliance may have contributed to their null findings.

To address inconsistencies in prior studies on vitamin D, and to investigate associations in population subgroups, we harmonized and analyzed participant-level data from over 5,700 colorectal cancer cases who had blood collected before colorectal cancer diagnosis, and 7,100 matched cancer-free controls. Study participants were drawn from 17 prospective cohorts from the United States, Europe, and Asia and were followed for an average of 5.5 years (range: 1 – 25 years). We used a single, widely accepted assay and laboratory for new vitamin D measurements and calibrated existing vitamin D measurements. In the past, substantial differences between assays made it difficult to integrate vitamin D data from different studies. Our novel calibration approach enabled us to explore risk systematically over the broad range of vitamin D levels seen internationally.  Continue reading

Lung Cancer Risk Drops Almost 40% Within 5 Years of Quitting Smoking

MedicalResearch.com Interview with:
Hilary Tindle, MD, MPH

“Used Cigarette Butts” by Indi Samarajiva is licensed under CC BY 2.0Associate Professor of Medicine and theWilliam Anderson Spickard, Jr., MD Chair in Medicine
Founding Director of ViTAL, the Vanderbilt Center for Tobacco, Addiction and Lifestyle
Division of Internal Medicine & Public Health and Vanderbilt Ingram Cancer Center (VICC)

MedicalResearch.com: What is the background for this study?

Response: Lung cancer is the most common cause of cancer related death for men and women ,and cigarette smoking is responsible for almost 9 of our every 10 lung cancers in the US. Lung cancer screening can reduce the risk of death from lung cancer by about 20% or even higher if screening is combined with quitting smoking.

We know that lung cancer risk is lower in people who quit smoking, compared to those who continue to smoke, but it was not clear how quickly this risk drops after quitting. Most prior studies on this subject assessed smoking status (current, former, never) at relatively few timepoints. By asking about smoking more frequently (every couple of years), we can get a better picture of a person’s true exposure to cigarette smoke and take into account periods where someone may have smoked more, less, or even quit altogether. Some people may start and stop multiple times over their lifetime.

Another question was exactly how long the risk of lung cancer stays elevated after quitting smoking. Again, by asking about smoking multiple times over someone’s lifetime, we get a better picture of how long they were truly smoke free.

MedicalResearch.com: What are the main findings?

  •  We analyzed data from the Framingham Heart Study Original and Offspring cohorts (almost 9000 people total) to study the risk of lung cancer after quitting smoking, and to determine if the risk of lung cancer ever goes back to that of someone who has never smoked (termed a “never smoker”). Study participants were followed for a median of almost 30 years, and were asked about smoking every 2-4 years.
  • We focused on heavier smokers, who had smoked more than 21 pack-years. (A “pack-year” is a way to quantify how much someone has been exposed to cigarette smoke. Pack years are the product of years of smoking times the amount smoked. For example, someone who smoked 1 pack of cigarettes per day for 20 years would have 20 pack years. Another person who smoked 2 packs per day for 10 years would also have 20 pack years.) As expected, the risks of lung cancer were highest among current smokers, followed by former smokers, followed by never smokers.
  • Compared to never smokers, former smokers had higher lung cancer risk: about 12 times higher within 10 years since quitting (YSQ), about 7 times higher from 10-15 YSQ, about 6 times higher from 15-25 YSQ, and over 3 times higher even after 25 YSQ.
  • Compared to current smokers, former smokers had lower lung cancer risk: 39% lower within 5 YSQ, which continued to drop over time.
  • Among all former smokers, about 4 in 10 lung cancers occurred after more than 15 YSQ, which is beyond the window of eligibility for current screening guidelines.

In the future, after additional study, guidelines may decide to extend the window of lung cancer screening beyond 15 YSQ. However, additional modeling studies are likely needed before making that determination. For now, anyone who qualifies for lung cancer screening based on age, pack years, and years since quitting, should have it.

MedicalResearch.com: What should readers take away from your report?

Response: If you currently smoke cigarettes, now is a great time to quit. The results of this study show that lung cancer risk drops almost 40% within 5 years since quitting, compared to people who continue to smoke.

If you already quit smoking, congratulations on taking that major step.

Whether you currently smoke, or if you quit smoking within the last 15 years, talk to your doctor to see if you are eligible for lung cancer screening. 

MedicalResearch.com: What recommendations do you have for future research as a result of this work?

 Response: We would like to see additional research from different groups to determine if the current lung cancer screening guidelines should potentially be altered to include those who quit more than 15 years ago. Again, this is a decision may require additional study, including an understanding of why some former smokers remain at elevated risk of lung cancer. Perhaps studying genetic variation could shed some light on this question.  

MedicalResearch.com: Is there anything else you would like to add?

Response: Yes, we would like to thank the NIH and particularly the NHLBI for supporting the Framingham Heart Study (FHS) and studies like it, and also to all the participants in the FHS for giving their information for decades, to the benefit of all Americans and the world. We consider studies such as the FHS to be “national treasures” in that they provide critical information for doctors and researchers to improve healthcare. The FHS is most often thought of as a cardiovascular dataset, but it also captures information on cancer. In the case of the current study, we re-analyzed information that was already collected, which is one of the efficient and low cost methods of conducting research. 

Citation:

 Hilary A Tindle, Meredith Stevenson Duncan, Robert A Greevy, Ramachandran S Vasan, Suman Kundu, Pierre P Massion, Matthew S Freiberg. Lifetime Smoking History and Risk of Lung Cancer: Results From the Framingham Heart Study. JNCI: Journal of the National Cancer Institute, 2018; DOI: 10.1093/jnci/djy041

 

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Protein Associated with Metastatic Breast Cancer

MedicalResearch.com Interview with:
Yingfei Wang, Ph.D. and Weibo Luo, Ph.D.
Department of Pathology
UT Southwestern Medical Center
Dallas TX 75390

MedicalResearch.com: What is the background for this study?

Response: Breast cancer is the most commonly diagnosed cancer in women. Tumor metastasis is frequently found in breast cancer patients and causes more than 90% of cancer death. There is currently no cure for this deadly disease. We have known that breast tumor is not supplied with sufficient oxygen (a phenomenon known as hypoxia), which makes breast cancer cells more aggressive and may be responsible for tumor recurrence, metastasis, and therapy resistance. Hypoxia-inducible factor (HIF) is a master regulator frequently detected in the hypoxic regions and switches on many oncogenes needed for breast cancer cells to grow and spread around the body. The role of HIF in gene regulation is precisely controlled and shutting down of HIF’s activity would be a promising strategy for the treatment of metastatic breast cancer.

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Combination EGFR + TNF Inhibition May Knock Out Most Lung Cancers

MedicalResearch.com Interview with:

Amyn Habib, M.D. Associate Professor, Neurology & Neurotherapeutics UT Southwestern Medical Center

Dr. Amyn Habib

Amyn Habib, M.D.
Associate Professor, Neurology & Neurotherapeutics
UT Southwestern Medical Center

MedicalResearch.com: What is the background for this study?

Response: The epidermal growth factor receptor (EGFR) is expressed in most lung cancers and could play an important role in driving the growth of lung cancer.  Drugs are available that can block the activity of the EGFR. However, EGFR inhibitors are successful in only a small subset of lung cancers that have a mutant form of the EGFR, and do not work in the majority of lung cancers that have the normal form of the EGFR.  Continue reading

Serotonin Receptors Tied To Weight Gain From Atypical Antipsychotic Medications

MedicalResearch.com Interview with:

Chen Liu, Ph.D. Assistant Professor Departments of Internal Medicine and Neuroscience Division of Hypothalamic Research The University of Texas Southwestern Medical Center Dallas, Texas 75390-9077

Dr. Chen Liu

Chen Liu, Ph.D.
Assistant Professor
Departments of Internal Medicine and Neuroscience
Division of Hypothalamic Research
The University of Texas Southwestern Medical Center
Dallas, Texas 75390-9077 

MedicalResearch.com: What is the background for this study?

Response: Atypical antipsychotics are second-generation antipsychotics (SGAs) that have been increasingly used to treat a variety of neuropsychiatric conditions such as schizophrenia, depression, and autism. Many patients taking these medications, however, are left in an agonizing dilemma.

On one hand, they rely on these drugs’ psychotropic effect for normal functioning in daily life. On the other, many SGAs, including the most widely prescribed olanzapine and clozapine, can cause a metabolic syndrome that is known for excessive weight gain, dyslipidemia, and type-2 diabetes_ENREF_2. Notably, while full-blown type 2 diabetes and morbid obesity typically take years to unfold in the general population, these conditions progress at a much faster pace (within months) following second-generation antipsychotics treatment. Other factors such as ethnicity, age, and sex can also aggravate SGA-induced metabolic syndrome. Together, these peculiar features strongly suggest a distinct etiology underlying SGA-induced metabolic syndrome that has yet been fully elucidated. Currently, there is no medication specifically targeting SGA-induced metabolic syndrome. For many youths and adults taking second-generation antipsychotics, metabolic complications are difficult to manage as lifestyle changes, nutritional consulting, and commonly used anti-diabetic medications only provide limited relief.

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Holes in Cigarette Filters Linked To Increase in Lung Adenocarcinomas

MedicalResearch.com Interview with:
Peter G. Shields, M.D.
Deputy Director, Comprehensive Cancer Center
James Cancer Hospital
Professor, College of Medicine
Julius F. Stone Chair in Cancer Research
The Ohio State University Columbus, OH

MedicalResearch.com: What do we know about the health effects of cigarette filters? 
Response:  The issue is that the design of the filters makes a cigarette even more dangerous, which can be regulated by the FDA. The issue is not about having a filter, but how they are made. And now we are changing the dialogue to the design of virtually all cigarettes. The holes on the filter are likely one reason the cigarettes of today are more dangerous.

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NSAIDS May Increase Mortality From Endometrial Cancer

MedicalResearch.com Interview with:

Theodore Brasky, PhD Research Assistant Professor Center of Excellence in Regulatory Tobacco Science Epidemiology College of Public Health The Ohio State University

Dr. Theodore Brasky

Theodore Brasky, PhD
The Ohio State University
Comprehensive Cancer Center

MedicalResearch.com: What is the background for this study? What are the main findings?

Response: There is a significant amount of data to suggest that long-term, regular use of nonsteroidal anti-inflammatory drugs (NSAIDS; examples include aspirin and ibuprofen) are associated with reduced risks of several cancers. Although the data across studies are inconsistent, one such candidate is endometrial cancer, which is the most common gynecologic cancer. There is good evidence that the use of these medications is associated with improved prognosis among patients diagnosed with colon cancer. Despite the importance of inflammation in endometrial cancer progression, very few have examined whether use of NSAIDs is associated with risk of death or recurrence from the disease. The study we published is the first of its kind to examine NSAID use comprehensively and in a study of over 4,000 patients.

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Study Links Well-Water Arsenic To Increased Bladder Cancer Risk in New England

MedicalResearch.com Interview with:

Dr. Debra Silverman Sc.D Branch Chief and Senior Investigator in the Occupational and Environmental Epidemiology Branch, Division of Cancer Epidemiology & Genetics National Cancer Institute

Dr. Debra Silverman

Dr. Debra Silverman Sc.D
Branch Chief and Senior Investigator in the Occupational and Environmental Epidemiology Branch, Division of Cancer Epidemiology & Genetics
National Cancer Institute

MedicalResearch.com: What is the background for this study? What are the main findings?

Dr. Silverman: We know that bladder cancer mortality rates have been elevated in northern New England for at least five decades. Incidence patterns in Maine, New Hampshire and Vermont are similar—about 20% higher than those for the United States overall. Elevated rates have been observed in both men and women, suggesting the role of a shared environmental etiologic factor.

A unique feature of northern New England is that a high proportion of the population uses private wells as their primary source of drinking water. The well water may contain low-to-moderate levels of arsenic. There are two possible sources of this arsenic contamination:

  • Naturally occurring arsenic from geological sources (released from rock deep in the earth)
  • Leaching of arsenic-based pesticides used on food crops many years ago. From the 1920s through the 1960s there was extensive agricultural use of arsenic-based pesticides. These compounds were used on food crops such as blueberries, apples and potatoes. Residue from the treatments may have leached into the ground water.

Intake of water containing high levels of arsenic is an established cause of bladder cancer, largely based on studies conducted in highly exposed populations. However, emerging evidence suggests that low-to-moderate levels of exposure may also increase bladder cancer risk.

To explore possible reasons for the excess incidence of bladder cancer in northern New England, we conducted a large, comprehensive population-based case-control study in Maine, New Hampshire and Vermont. We examined the role of known and suspected bladder cancer risk factors, with a focus on private well water consumption and arsenic levels in drinking water.

The major cause of bladder cancer is cigarette smoking. Some occupational exposures (e.g., exposure to metalworking fluids such as that experienced by metalworkers and some types of machine operators) are also associated with elevated risk. However, smoking and occupational exposures do not appear to explain the New England bladder cancer excess.

This study was funded and carried out by researchers in the NCI Division of Cancer Epidemiology and Genetics in collaboration with the Geisel School of Medicine at Dartmouth, the Departments of Health for Maine, New Hampshire, and Vermont, and the US Geological Survey.

We reported that heavy consumption of drinking water from private dug wells (which are shallow—less than 50 feet deep—and susceptible to contamination from manmade sources than drilled wells), established prior to 1960 (when arsenic-based pesticides were widely used), may have contributed to the longstanding bladder cancer excess in northern New England.

We saw that cumulative arsenic exposure from all water sources showed an increasing risk with increasing exposure (exposure-response relationship). Among the highest exposed participants, risk was twice that of the lowest exposure group. (Cumulative arsenic exposure is a measure of the average daily arsenic intake by number of days of arsenic exposure.)

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Hepatitis C Raises Risk of HPV Head and Neck Cancers

MedicalResearch.com Interview with:

Harrys A. Torres, MD, FACP, FIDSA Associate Professor Director of Hepatitis C Clinic Department of Infectious Diseases, Infection Control and Employee Health The University of Texas MD Anderson Cancer Center Houston TX 77030

Dr. Harrys Torres

Harrys A. Torres, MD, FACP, FIDSA
Associate Professor
Director of Hepatitis C Clinic
Department of Infectious Diseases, Infection Control and Employee Health
The University of Texas MD Anderson Cancer Center
Houston TX 77030

Medical Research: What is the background for this study? What are the main findings?

Dr. Torres: Hepatitis C virus (HCV) is an oncogenic virus and is associated with an increased risk of liver cancer and certain types of non-Hodgkin lymphomas. In 2009, at MD Anderson Cancer Center, we set up the first clinic in the United States, and probably in the world, specifically devoted to managing HCV infection in cancer patients. In the clinic, we expected to see a number of patients with liver cancers and non-Hodgkin’s lymphoma, as these have documented associations with HCV. Unexpectedly, we saw a high number of HCV-infected patients with head and neck cancers, and wondered whether there was an undiscovered association between having the infection and head and neck cancers. To explore this, we conducted a case-control study using 409 head and neck cancer subjects (164 oropharyngeal, 245 non-oropharyngeal [oral cavity, nasopharynx, larynx] cancers) and 694 control subjects with other smoking-associated cancers (378 lung, 168 esophagus, and 148 urinary bladder cancers), and compared the prevalence of HCV infection in the two groups. We observed a high prevalence of HCV infection in oropharyngeal (14%) and non-oropharyngeal (20%) cancer patients when compared to control subjects (6.5%). After adjusting for confounders such as smoking, alcohol intake, and socioeconomic status, HCV-infected individuals were 2.04 times more likely to have oropharyngeal cancers and 2.85 times more likely to have non-oropharyngeal cancers. Of note, HCV was associated only with patients with oropharyngeal cancers that tested positive for human papilloma virus, which is one of the main virus linked with increased risk of oropharyngeal cancers.

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Early Breast Cancer Screening Recommended For Survivors of Childhood Hodgkin’s Lymphoma

MedicalResearch.com Interview with:

David Hodgson, MD, MPH, FRCPC Associate Professor University of Toronto

Dr. David Hodgson

David Hodgson, MD, MPH, FRCPC
Associate Professor
University of Toronto
Toronto, ON Canada  

MedicalResearch.com: What is the background for this study?

Dr. Hodgson: We know that treatment for childhood Hodgkin lymphoma can cause some side effects that arise years after treatment is  finished. In particular, radiotherapy given to the chest of adolescent females increases the risk of developing breast cancer in young adult survivors. But there are very little data about whether the early initiation of breast cancer screening will prevent breast cancer deaths in these survivors, and what kinds of screening is optimal. This is important because less than half of these young survivors are undergoing breast cancer screening, and in some jurisdictions early screening is not covered by insurance.

MedicalResearch.com: What are the main findings?

Dr. Hodgson: Because there has not been, and likely never will be, a large randomized screening trial for these patients, we used all the available information about their breast cancer risk, other health issues and the effectiveness of screening, and created a mathematical model that allows us to estimate the number of breast cancer deaths prevented by starting screening at age 25 for women who had received chest RT as teenagers. We found that one would have to invite about 260 survivors to early mammographic screening to prevent one breast cancer death, which compares favorably to other accepted reasons for breast cancer screening. Using MRI for screening, approximately 80 women would have to be invited to prevent one breast cancer death, because MRI is so much more sensitive than mammography. One of the problems with MRI, however, is that a substantial number of women will have “false positive” tests – abnormal findings that are not really cancer.

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Genetics Study Points To Different Pathways For Melanoma Risk

MedicalResearch.com Interview with:

Nancy E. Thomas, MD PhD Department of Dermatology, University of North Carolina Chapel Hill, NC 27599

Dr. Nancy E. Thomas

Nancy E. Thomas, MD PhD
Department of Dermatology, University of North Carolina
Chapel Hill, NC 27599

Medical Research: What is the background for this study?

Dr. Thomas: Melanoma had been thought for some time to arise from at least two causal pathways, a ‘chronic sun exposure pathway’ and a ‘nevus pathway’. However, the role of inherited genetic variation in development of melanoma along these pathways had not previously been studied. Thus, we chose to examine the association of SNPs in putative low-penetrance melanoma susceptibility loci with histologic markers of divergent pathways.

Medical Research: What are the main findings?

Dr. Thomas: Within the large Genes, Environment and Melanoma Study, we investigated the relationship of germline variants in newly identified low-penetrance melanoma risk loci to histologic markers of divergent causal pathways in melanoma. We present strong evidence that the IRF4 rs12203592*T genotype is positively associated with chronic sun exposure-related melanoma and inversely associated with nevus-related melanoma. We also found that the IRF4 rs12203592 genotype is linked to the bi-model age distribution known to occur in melanoma and which is related to the divergent pathways. IRF4 rs12203592 is a functional variant known to affect IRF4 expression in human skin and melanoma cell lines. We conclude that IRF4rs12203592 is likely, at least in part, to determine pathway-specific risk for melanoma development.

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No Increase Risk of Breast Cancer Recurrence With Antidepressants While On Tamoxifen

Reina Haque, PhD, MPH Research scientist Department of Research & Evaluation Kaiser Permanente Southern California Pasadena Calif

Dr. Haque

MedicalResearch.com Interview with:
Reina Haque, PhD, MPH

Research scientist
Department of Research & Evaluation
Kaiser Permanente Southern California
Pasadena Calif

Medical Research: What is the background for this study? What are the main findings?

Dr. Haque: Tamoxifen is a commonly prescribed generic drug taken by women with breast cancer to reduce their chances of developing a recurrence. Tamoxifen is recommended for five years, but has notable side effects, including hot flashes, night sweats and depression. Since hormone replacement therapy is not recommended to alleviate these symptoms in breast-cancer survivors, antidepressants have been increasingly prescribed for relief. Almost half of the 2.4 million breast-cancer survivors in the U.S. take antidepressants.

However, previous studies have suggested that antidepressants reduce tamoxifen’s effectiveness in lowering subsequent breast-cancer risk. This study was conducted to determine whether taking tamoxifen and antidepressants (in particular, paroxetine) concomitantly is associated with an increased risk of recurrence or contralateral breast cancer.
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Young Black Colon Cancer Patients Have Greater Risk of Recurrence

Harry H. Yoon, MD Mayo Clinic Rochester, MN 55905MedicalResearch.com Interview with:
Harry H. Yoon, MD
Mayo Clinic
Rochester, MN 55905

Medical Research: What is the background for this study? What are the main findings?

Dr. Yoon: In the U.S., the survival of patients with colon cancer is known to differ by race, with individuals of black race having worse outcomes than those of white race.

However, it has been difficult to tease apart why the differences in survival exist.

It is generally believed that social or other non-biologic factors (eg, decreased access to care, suboptimal treatment) contribute to the discrepancy.  It’s also known that differences in the general medical condition of patients could affect how long a patient lives.

However, it is unknown whether there are race-based differences in the biology of colon tumors themselves.  This biology can be reflected in the genetic composition of tumors, as well as by whether and how quickly the cancer returns after the patient has undergone surgery and chemotherapy.

In addition, it is unknown whether race-based differences in biology may be related to the age of the patient at the time of diagnosis.  Blacks with colorectal cancer typically have an earlier age of onset than whites do.

A major barrier to addressing these questions are that there are very few large populations of colon cancer patients where everyone had the same disease stage and received uniform treatment, and where patients were monitored for years afterward specifically to see whether the cancer returned.  It is much harder to measure whether cancer has returned (ie, cancer recurrence), as compared to simply knowing whether a patient is alive or dead.  This difference is important, because knowing about cancer recurrence sheds more light on cancer biology than only knowing about patient survival, since many factors unrelated to cancer biology (eg., heart disease) can affect whether a person is alive or dead.

The most reliable data on cancer recurrence (not just patient survival) generally comes from patients who have enrolled in a clinical trial.  In the Alliance N0147 trial, all patients had the same cancer stage (ie, stage III), underwent surgery and received standard of care chemotherapy (ie, “FOLFOX”) after surgery.  Patients had uniform, periodic monitoring after chemotherapy to see if the cancer returned.

In other words, examining racial outcomes in this cohort largely eliminates some of the key factors (eg, decreased access to care, suboptimal treatment) that are believed to contribute to racial discrepancies, and provides a unique opportunity to determine if differences in cancer biology between races may exist.

This study was done to see if colon cancers are genetically different based on race, and whether race-based differences exist in cancer recurrence rates.

The study found that tumors from whites, blacks, and Asians were different in terms of the frequency of mutations in two key cancer-related genes, BRAF and KRAS.  Tumors from whites were twice as likely to have mutated BRAF (14% in whites compared to 6% in Asians and 6% in blacks).  Tumors from blacks had the highest frequency of KRAS mutations (44% in blacks compared to 28% in Asians and 35% in whites).  Tumors from Asians were the mostly likely to have normal copies of both genes (67% in Asians compared to 50% in blacks and 51% in whites).

Next, the study found that the colon cancers among blacks had more than double the risk of cancer recurrence, compared to whites.  However, this discrepancy was only evident among young patients (ie, aged less than 50 years).  Almost 50% of younger black patients experienced colon cancer recurrence within 5 years, compared to ~30% of black patients over age 50, or compared to white or Asian patients regardless of age. The worse outcome among young blacks remained evident even after adjusting for many potential confounding factors, such as tumor grade, the number of malignant nodes, or the presence of BRAF or KRASmutations.  Because this question was examined in a clinical trial cohort of uniform stage and treatment, the role of multiple important potential confounders was diminished.

To our knowledge, this is the first report indicating that colon cancers from young black individuals have a higher chance of relapsing after surgery and chemotherapy, compared to those from white individuals.

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Breast Cancer Pattern Likely To Change as Population Ages

Philip S. Rosenberg, PhD Biostatistics Branch, Senior Investigator Division of Cancer Epidemiology and Genetics National Cancer Institute, 9609 Medical Center Drive Bethesda, MD 20892MedicalResearch.com Interview with:
Philip S. Rosenberg, PhD
Biostatistics Branch, Senior Investigator
Division of Cancer Epidemiology and Genetics
National Cancer Institute, 9609 Medical Center Drive
Bethesda, MD 20892 

Medical Research: What is the background for this study? What are the main findings?

Dr. Rosenberg: It has been previously reported that breast cancer burden (number of new cases diagnosed in a year) is expected to rise in the future, mostly due to the aging of the female population in the US.

Also, it has been established that the age-adjusted breast cancer incidence rates (cases per 100,000 women per year) are increasing for invasive ER-positive cancers overall and decreasing for ER-negative cancers overall. When taken together, these two trends tend balance each other out, resulting in a somewhat flat breast cancer incidence rate overall. 

Though the overall trends for invasive breast cancer have been previously reported, this study uses a more refined forecasting method by including recent birth cohort patterns to forecast breast cancer to 2030 by age group, estrogen receptor-status, and invasive vs. in situ tumors.

New in this report are the findings for in situ tumors and the more granular break down by age, ER status, and invasive vs. in situ tumors both for rate and burden (number of cases).
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Aspirin and Ibuprofen May Reduce Bowel Cancer Risk in Lynch Syndrome

Aung Ko Win, MBBS MPH PhD Research Fellow NHMRC Early Career Clinical Research Fellow Centre for Epidemiology and Biostatistics Melbourne School of Population and Global Health The University of Melbourne VIC 3010 AustraliaMedicalResearch.com Interview with:
Aung Ko Win, MBBS MPH PhD

Research Fellow
NHMRC Early Career Clinical Research Fellow
Centre for Epidemiology and Biostatistics
Melbourne School of Population and Global Health
The University of Melbourne VIC 3010
Australia

Medical Research: What is the background for this study?

Response: At least 1 in 1,000 people in the population have a mutation in one of the mismatch repair genes that causes Lynch syndrome. These people have a very high risk of bowel cancer (colorectal cancer): if nothing is done, about half would develop the disease. The main risk reduction method for these people is to have regular colonoscopy screening every year. Almost nothing is known whether or not lifestyle factors and medications can modify the risk of bowel cancer for people with Lynch syndrome.

A study was conducted to investigate the associations between aspirin and ibuprofen intake and the risk of bowel cancer, by studying 1,858 people with Lynch syndrome who were recruited into the Colon Cancer Family Registry from Australia, New Zealand, Canada and the USA. This is the largest study to date investigating the associations between aspirin, ibuprofen and bowel cancer risk for people with Lynch syndrome. Continue reading

Tubal Ligation May Limit Spread Of Endometrial Cancer

MedicalResearch.com Interview with:
Ashley S. Felix, PhD

Bethesda, MD

MedicalResearch: What is the background for this study? What are the main findings?

Dr. Felix: Endometrial cancer prognosis is strongly affected by disease stage, or the extent of spread from the primary site. Endometrial cancers can spread via the lymph nodes, blood vessels, through the uterine wall, or through the fallopian tube into the peritoneal cavity. The last of these mechanisms is poorly understood, but appears to be a more common mode of spread for aggressive histologic subtypes of endometrial cancer. We hypothesized that women who previously underwent tubal ligation (TL) and later developed endometrial cancer would have lower stage disease, possibly by blocking passage of tumor cells along the fallopian tubes. Further, we hypothesized that TL would be associated with better prognosis, due to its relationship with lower stage.

We found that women in our study who previously had tubal ligation were more likely to have lower stage endometrial cancer compared with women who did not report a previous tubal ligation. Specifically, tubal ligation was inversely associated with stage III and stage IV cancer across all subtypes of the disease, including aggressive histologic subtypes. Further, in statistical models of tubal ligation, tumor stage, and mortality, we observed no independent association with improved survival, suggesting that tubal ligation impacts mortality mainly through its effects on stage.

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Lymph Node Cancer Metastases Do Not Require Growth of New Blood Vessels

Timothy P. Padera, PhD Edwin L. Steele Laboratories Department of Radiation Oncology MGH Cancer Center, Massachusetts General Hospital and Harvard Medical School Boston, Massachusetts 02114MedicalResearch.com Interview with:
Timothy P. Padera, PhD
Edwin L. Steele Laboratories
Department of Radiation Oncology
MGH Cancer Center, Massachusetts General Hospital and Harvard Medical School
Boston, Massachusetts 02114

MedicalResearch: What is the background for this study? What are the main findings?

Dr. Padera: Systemic therapy benefits cancer patients with lymph node metastases; however all phase III clinical trials to date of antiangiogenic therapy have failed in the adjuvant setting. We have previously reported the lack of efficacy of antiangiogenic therapies in pre-clinical models of spontaneous lymphatic metastasis, however there were no mechanistic data to explain these observations. Here, we developed a novel chronic lymph node window model to facilitate new discoveries in the mechanisms of growth and spread of lymph node metastases. Our new data provide pre-clinical evidence along with supporting clinical evidence that angiogenesis does not occur in the growth of metastatic lesions in the lymph node. These results reveal a mechanism of treatment resistance to antiangiogenic therapy in adjuvant setting, particularly those involving lymph node metastases.

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Molecule May Help Ovarian Cancer Patients Overcome Chemotherapy Resistance

Wei Zhang, Ph.D., Professor Department of Pathology Director, Cancer Genomics Core Lab University of Texas MD Anderson Cancer Center Houston, Texas 77030MedicalResearch.com Interview with:
Wei Zhang, Ph.D., Professor

Department of Pathology
Director, Cancer Genomics Core Lab
University of Texas MD Anderson Cancer Center
Houston, Texas 77030

Medical Research: What is the background for this study? What are the main findings?

Dr. Zhang: Epithelial ovarian cancer remains the most lethal gynecological malignancy. The 5-year survival rate for patients with advanced ovarian cancer is only 30-40%, and acquired resistance to platinum is considered a major factor in disease relapse. A major challenge in cancer treatment is the resilient ability of cancer cells to repair DNA damage caused by chemotherapy agents.  In this study, we found that adding a molecule called miR-506 to standard chemotherapy can help cells overcome drug resistance, so that the chemotherapy drugs remain effective against ovarian cancer. This research supports a new combination approach, which may substantially benefit patients with this deadly disease.

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Breast Cancer Risk Reduction of Prophylactic Salpingo-Oophorectomy May Be Overestimated For Some BRCA1 Carriers

Bernadette A.M. Heemskerk-Gerritsen, Ph.D.		 Department of Medical Oncology Erasmus MC Cancer Institute Roterdam, the NetherlandsMedicalResearch.com Interview with:
Bernadette A.M. Heemskerk-Gerritsen, Ph.D.
Department of Medical Oncology
Erasmus MC Cancer Institute
Roterdam, the Netherlands

Medical Research: What is the background for this study? What are the main findings?

Dr. Heemskerk-Gerritsen: Women with a BRCA1 or BRCA2 mutation have substantially higher risks of developing both primary and contralateral breast cancer (BC) and ovarian cancer than women from the general population. Options to reduce these increased cancer risks include risk-reducing mastectomy (RRM) and/or risk-reducing salpingo-oophorectomy (RRSO). The latter intervention obviously reduces the risk of developing ovarian cancer, but has been reported also to reduce the risk of developing a subsequent breast cancer with approximately 50%. However, studies on the efficacy of risk-reducing surgery in BRCA1/2 mutation carriers are confined to observational studies, thus challenging several methodological issues. Consequently, previous studies on breast cancer risk-reduction after RRSO may have been influenced by bias associated with selection of study subjects, bias associated with start of follow-up, or by confounding, and breast cancer risk-reduction may have been overestimated.

In the current study, we revisited the association between risk-reducing salpingo-oophorectomy and breast cancer risk in BRCA1/2 mutation carriers, focusing on the impact of different analytical methods and potential types of bias.

First, we replicated the analyses of four previously performed studies, to examine if our Dutch cohort was comparable with the cohorts used in the previous studies. We replicated the approximately 50% breast cancer risk reduction after RRSO in the Dutch cohort.

Second, we estimated the effect of RRSO on breast cancer risk in the Dutch cohort using a revised analytical approach for observational studies in BRCA1/2 mutation carriers in order to minimize bias as much as possible. Using this method of analysis, we found no evidence of first BC risk-reduction after RRSO in BRCA1/2 mutation carriers.

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‘Chemobrain’: Cognitive Impairment May Be a Form Of Cancer-Related PTSD

Dr. Kerstin Hermelink Senior psychologist  Dept. of Gynecology and Obstetrics Ludwig Maximilian University of MunichMedicalResearch.com Interview with:
Dr. Kerstin Hermelink
Senior psychologist
Dept. of Gynecology and Obstetrics
Ludwig Maximilian University of Munich

MedicalResearch: What is the background for this study? What are the main findings?

Dr. Hermelink: Many breast cancer patients report problems of cognitive functioning that interfere considerably with their professional and private lives. In the last two decades, a number of studies have confirmed that subgroups of breast cancer patients show at least subtle cognitive impairment. Initially, the condition has entirely been attributed to chemotherapy effects and has therefore colloquially been named “chemobrain”. Meanwhile, however, cognitive impairment has also been found in patients who were managed without chemotherapy and, surprisingly, even in patients who had not yet received any systemic treatment at all.

Several hypotheses on the causation of cognitive impairment that occurs already pretreatment have been put forward; for instance, biological effects of the cancer itself might affect cognitive functioning, or there might be shared genetic vulnerability for cancer and cognitive impairment. None of these hypotheses have been empirically confirmed; thus, pretreatment cognitive impairment is as yet unexplained.

Our study was designed to investigate the effects of cancer-related post-traumatic stress on cognitive function in breast cancer patients before the start of treatment. Stress has a substantial influence on cognitive functioning, and post-traumatic stress disorder (PTSD) is associated with impairment of cognitive function. While the incidence of full diagnosis of stress disorder is low among breast cancer patients, many of these patients show symptoms of PTSD, with a peak shortly after diagnosis.

We did not find an elevated risk of overall cognitive impairment in pretreatment breast cancer patients compared with matched non-cancer controls; however, the cancer patients scored worse than the controls on a small fraction of the cognitive indices that were used. Performance on these indices was indeed robustly associated with PTSD symptoms.

Our results therefore indicate that pretreatment cognitive impairment in breast cancer patients may be largely caused by the stress of being diagnosed with cancer.

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