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Discovering the causes of cancer and the means of prevention

Scientific Highlights July - October 2016

Posted on December 05, 2016

Cancer Topics

All Cause Mortality

Body Mass Index (also under Obesity)

Analysis of data pooled from 189 studies, representing over 10.5 million people from 32 countries, demonstrated body mass index (BMI) outside of the normal range (20-24.9) is associated with increased risk of mortality. The finding held across all areas of the world, with the absolute increases in risk for obese and moderately obese men higher than those among obese and moderately obese women, respectively. When the analysis was limited to never-smokers and excluded deaths in the first five years of follow-up, there was an increase in premature mortality among even overweight (BMI 25-29.9) persons, compared to those in the normal range. (Global BMI Mortality Collaboration. Body-mass index and all-cause mortality: Individual-participant-data meta-analysis of 239 prospective studies in four continents. Lancet 2016). Read more in BMI Outside Normal Range Associated with Increased Risk of Mortality (Research News Highlight).

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Bladder

APOBEC-Signature Mutations

Investigators explored the contribution of two common germline variants in the APOBEC3 region. SNP rs1014971 was associated with bladder cancer risk, increased APOBEC3B expression, and enrichment with APOBEC-signature mutations in bladder tumors. In contrast, a 30-kb deletion that eliminates APOBEC3B and creates an APOBEC3A-APOBEC3B chimera was not important in bladder cancer, whereas it was associated with breast cancer risk and enrichment with APOBEC-signature mutations in breast tumors. In vitro, APOBEC3B expression was predominantly induced by treatment with a DNA-damaging drug in bladder cancer cell lines, and APOBEC3A expression was induced as part of the antiviral interferon-stimulated response in breast cancer cell lines. These findings suggest a tissue-specific role of environmental oncogenic triggers, particularly in individuals with germline APOBEC3 risk variants. (Middlebrooks CD, Banday AR, Matsuda K, et al.  Association of germline variants in the APOBEC3 region with cancer risk and enrichment with APOBEC-signature mutations in tumorsNat Genet 2016). Read more in Genetic and environmental factors influence APOBEC mutagenesis in tumors.

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Breast

Birth Cohort Effects

In a study that simultaneously compared birth cohort effects among both younger and older women in Asian and Western populations, investigators found that rapidly rising cohort-specific breast cancer rates have narrowed the historic disparity between Chinese and U.S. non-Hispanic white women, particularly in regions with the lowest baseline rates and among older women. (Sung H, Rosenberg PS, Chen WQ, et al. The impact of breast cancer-specific birth cohort effects among younger and older Chinese populations. Int J Cancer 2016)

Genetics

Previous genome-wide association studies identified two independent breast cancer susceptibility loci represented by single nucleotide polymorphisms (SNPs) rs13281615 and rs11780156 at 8q24. A fine-mapping study identified three additional independent association signals in women of European ancestry, represented by rs35961416, rs7815245, and rs2033101. Integrative analysis using functional genomic data from several sources implied that SNPs rs7815245 in Signal 3, and rs1121948 in Signal 5 (in linkage disequilibrium with rs11780156), were putatively functional variants for two of the five independent association signals. (Shi J, Zhang Y, Zheng W, et al. Fine-scale mapping of 8q24 locus identifies multiple independent risk variants for breast cancer. Int J Cancer 2016)

Genetic Susceptibility Locus

A genome-wide association study identified a single nucleotide polymorphism (SNP) rs11249433 at 1p11.2 associated with breast cancer risk. To fine-map this locus, investigators genotyped 92 SNPs in a 900 kb region flanking rs11249433 in 45,276 breast cancer cases and 48,998 controls of European, Asian and African ancestry from 50 studies in the Breast Cancer Association Consortium. The strongest association observed was for the original identified index SNP rs11249433 and risk for ER-positive breast cancer. (Horne HN, Chung CC, Zhang H, et al. Fine-mapping of the 1p11.2 breast cancer susceptibility locus. PLoS One 2016)

Genetic Susceptibility and Terminal Duct Lobular Unit Involution

Reduced levels of terminal duct lobular unit (TDLU) involution, as reflected by higher numbers of TDLUs and acini per TDLU, have been associated with higher breast cancer risk. Previously, younger age at menarche and older age at menopause have been related to lower levels of TDLU involution. A pooled analysis of a priori selected single nucleotide polymorphisms (SNPs) and standardized TDLU involution measures demonstrated that a subset of SNPs previously found to be related to ages at menarche or menopause was also associated with standardized measures of TDLU involution, suggesting some shared genetic mechanisms. (Oh H, Bodelon C, Palakal M, et al. Ages at menarche- and menopause-related genetic variants in relation to terminal duct lobular unit involution in normal breast tissue. Breast Cancer Res Treat 2016)

Standardized Terminal Duct-Lobular Unit Involution Measures Predict Risk

Lesser degrees of terminal duct-lobular unit (TDLU) involution predict higher breast cancer risk; however, standardized measures to quantitate levels of TDLU involution have only recently been developed. Investigators assessed whether three standardized measures of TDLU involution, with high intra/inter pathologist reproducibility in normal breast tissue, accurately predicted subsequent breast cancer risk among 99 women with benign breast disease. Standardized quantitative measures of TDLU counts and acini counts approximated by TDLU span measures or visually assessed in categories are independently associated with breast cancer risk. Visual assessment of TDLU numbers and acini content, which are highly reproducible between pathologists, could help identify women at high risk for subsequent breast cancer among the million women diagnosed annually with BBD in the US. (Figueroa JD, Pfeiffer RM, Brinton LA, et al. Standardized measures of lobular involution and subsequent breast cancer risk among women with benign breast disease: A nested case-control studyBreast Cancer Res Treat 2016)

Tamoxifen and Risk of Contralateral Breast Cancer

Using data from community healthcare settings (Kaiser Permanente Institute for Health Research - Colorado and Kaiser Permanente Northwest Center for Health Research - Oregon), investigators found that tamoxifen therapy was associated with reduced risk of contralateral breast cancer (CBC) during treatment and after its cessation, with risk progressively decreasing as tamoxifen therapy duration increased. If adjuvant endocrine therapy is indicated for breast cancer treatment, these findings in concert with trial data suggest that women should be encouraged to complete the full course.  (Gierach GL, Curtis RE, Pfeiffer RM, et al. Association of adjuvant tamoxifen and aromatase inhibitor therapy with contralateral breast cancer risk among U.S. women with breast cancer in a general community setting. JAMA Oncol 2016; Epub Oct 6, 2016)

Tissue Microvessel Density

In a study of 218 women referred for breast biopsy, increased microvessel density in breast tissue was associated with breast cancer, independently of mammographic density, consistent with magnetic resonance imaging findings suggestive of its possible value as a radiological cancer biomarker. (Felix AS, Lenz P, Pfeiffer R, et al. Relationships between mammographic density, tissue microvessel density, and breast biopsy diagnosis. Breast Cancer Res 2016)

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Cervix

Biomarkers

EDITORIAL:  Wentzensen N, Silver MI. Biomarkers for cervical cancer prevention programs: The long and winding road from discovery to clinical use. J Low Genit Tract Dis 2016.

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Endometrium

Body Mass Index, Physical Activity, and Television Time

Data on 580 women with endometrial cancer in the NIH-AARP Diet and Health Study suggest that higher post-diagnosis body mass index (BMI) and TV viewing may be associated with higher mortality risk among EC patients, but that there may be complicated interrelationships between lifestyle factors of BMI, physical activity, and TV viewing and the mediating role of health status that need to be clarified. (Arem H, Pfeiffer RM, Moore SC, et al. Body mass index, physical activity, and television time in relation to mortality risk among endometrial cancer survivors in the NIH-AARP Diet and Health Study cohort. Cancer Causes Control 2016; Epub Oct 11, 2016)

Inflammation Markers

In a nested case-control study within the PLCO Screening Trial, baseline serum levels of 64 inflammation-related biomarkers were measured for 284 incident endometrial cancer cases and 284 matched controls. Several inflammation markers were prospectively associated with endometrial cancer, including adipokines, pro- and anti-inflammatory cytokines, angiogenic factors, and acute phase proteins. Inverse associations with anti-inflammatory markers (IL13, IL21), other inflammation markers/mediators (CCL3, IL1B, IL23), and a robust positive association between VEGFA and endometrial cancer risk were independent of BMI and estradiol, suggesting that these factors may influence risk through other mechanisms. (Trabert B, Eldridge RC, Pfeiffer RM, et al.  Pre-diagnostic circulating inflammation markers and endometrial cancer risk in the Prostate, Lung, Colorectal and Ovarian Cancer (PLCO) Screening Trial. Int J Cancer 2016; Epub Oct 22, 2016)

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Esophagus

Survival Advantage of Prior Diagnosis of Barrett’s Esophagus

A case-case study to compare the clinical presentation, medical history, and survival of esophageal adenocarcinoma (EA) with and without a prior diagnosis of Barrett’s esophagus (BE) was conducted using data from the Surveillance, Epidemiology and End Results Medicare database. EA cases occurring among individuals previously diagnosed with BE presented with less advanced disease, were more likely to undergo surgery and less likely to receive chemotherapy and radiotherapy, and had better overall mean survival than the large majority of EA cases that occur without a prior BE diagnosis. (Cook MB, Drahos J, Wood S, et al. Pathogenesis and progression of oesophageal adenocarcinoma varies by prior diagnosis of Barrett's oesophagus. Br J Cancer 2016; Epub Oct 25, 2016)

Vitamin B (Also under Stomach)

B vitamins, which play an essential role in DNA synthesis and methylation, were found to have a possible protective effect against esophageal and gastric cancers in data from the General Population Nutrition Intervention Trial in Linxian, China. Subjects included 498 esophageal squamous cell carcinomas (OSCCs), 255 gastric cardia adenocarcinomas (GCAs), and an age- and sex-matched sub-cohort of 947 individuals. Baseline serum riboflavin and vitamin B12 were inversely associated with risk of esophageal cancer, while higher flavin mononucleotide levels were significantly associated with increased risk of esophageal and gastric cancer. (Ren J, Murphy G, Fan J, et al. Prospective study of serum B vitamins levels and oesophageal and gastric cancers in China. Sci Rep 2016; Epub Oct 17)

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Gallbladder

Inflammatory and Other Immune Markers

Most gallbladder cancer (GBC) cases arise in the context of gallstones, which cause inflammation, but few gallstone patients develop GBC. Investigators assessed 65 immune-related markers in serum and bile from 41 GBC cases and 127 gallstone patients from Shanghai, China, followed by a replication study among 35 GBC cases and 31 gallstone controls from Chile. Among 15 markers elevated in both serum and bile from GBC versus gallstone patients in the Shanghai study, six were also significantly elevated in serum from Chile (CCL20, C-reactive protein, CXCL8, CXCL10, resistin, serum amyloid A). Further research on these markers may guide translational efforts to identify individuals at high risk of developing GBC. (Koshiol J, Castro F, Kemp TJ, et al. Association of inflammatory and other immune markers with gallbladder cancer: Results from two independent case-control studies. Cytokine 2016)

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Genetics

Nonsynonymous Mutations and Immune Checkpoint Inhibitor Responses

Immune checkpoint inhibitor treatment represents a promising clinical approach and has been shown to be effective in a subset of melanoma, non-small cell lung cancer (NSCLC), and kidney cancers. Recent studies have suggested that the number of nonsynonymous mutations (NsM) can be used to select melanoma and NSCLC patients most likely to benefit from checkpoint inhibitor treatment. An assessment of NsM across 7,757 tumor samples drawn from 26 cancers sequenced in The Cancer Genome Atlas (TCGA) Project found that more than 30% of bladder, colon, gastric, and endometrial cancers have NsM counts above an empirically-derived threshold that was confirmed in melanoma and NSCLC. These data could inform the prioritization of tumor types for possible clinical trials to investigate further indications for effective use of immune checkpoint inhibitors. (Colli LM, Machiela MJ, Myers TA, et al. Burden of nonsynonymous mutations among tcga cancers and candidate immune checkpoint inhibitor responses. Cancer Res 2016)

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Kidney

Analgesic Use

An investigation of renal cell carcinoma (RCC) risk and analgesic use in the U.S. Kidney Cancer Study and the PLCO Screening Trial suggests that acetaminophen use may be associated with increased RCC risk. Use of NSAIDs and aspirin was not associated with RCC risk in either of the two studies. Updating a recent meta-analysis with these findings also supported an association between acetaminophen use and kidney cancer and RCC specifically, with comparable summary estimates for cohort and case-control studies. (Karami S, Daughtery SE, Schwartz K, et al. Analgesic use and risk of renal cell carcinoma: A case-control, cohort and meta-analytic assessment. Int J Cancer 2016)

Functional Characterization of a Susceptibility Locus

Genome-wide association studies have identified multiple renal cell carcinoma susceptibility loci. Investigators used regional imputation and bioinformatics analysis of the 12p12.1 locus to identify the single-nucleotide polymorphism rs7132434 as a potential functional variant which upregulates BHLHE41 expression which, in turn, induces IL-11, a member of the IL-6 cytokine family. (Bigot P, Colli LM, Machiela MJ, et al. Functional characterization of the 12p12.1 renal cancer-susceptibility locus implicates BHLHE41. Nat Commun 2016)

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Liver

Insulin Resistance

Insulin resistance likely increases the risk of chronic liver disease (CLD) and liver cancer, but long-term prospective studies with measured fasting glucose and insulin are lacking. Data from a prospective study of Finnish male smokers with follow-up time up to 22 years showed that baseline elevated fasting glucose and insulin, and insulin resistance were independently associated with risk of liver cancer and CLD mortality, suggesting a potentially important etiologic role for insulin and glucose dysregulation, even in the absence of diagnosed diabetes. (Loftfield E, Freedman ND, Lai GY, et al. Higher glucose and insulin levels are associated with risk of liver cancer and chronic liver disease mortality among men without a history of diabetes. Cancer Prev Res (Phila) 2016)

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Lung

Novel Genetic Susceptibility Locus

Epidemiologically related traits may share genetic risk factors, and pleiotropic analysis could identify individual loci associated with these traits. A pleiotropic analysis of genome-wide association studies of lung cancer and cardiovascular disease risk factors (blood lipids, type 2 diabetes, body mass index, and smoking) found that 6p22.1 (rs6904596, ZNF184) was associated with both lung cancer and blood triglycerides. The association was replicated in a lung cancer meta-analysis. The shared genetic risk factors between the two traits contributed to the uncovering of a hitherto unidentified genetic locus for lung cancer. (Zuber V, Marconett CN, Shi J, et al. Pleiotropic analysis of lung cancer and blood triglycerides. J Natl Cancer Inst 2016)

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Lymphoma

HIV (Also under Sarcoma)

The biology of HIV-associated cancers may differ depending on immunologic and virologic context during development. Therefore, an understanding of the burden of Kaposi sarcoma (KS) and non-Hodgkin lymphoma (NHL) relative to antiretroviral therapy (ART), virologic suppression, and CD4 count is important. Patients with KS and NHL from eight clinical cohorts were identified among patients with HIV. Over time, KS and NHL occurred at higher CD4 counts and lower HIV RNA values, and KS occurred more frequently after ART initiation. These changes were driven by an increasing proportion of patients with HIV who received effective ART, had higher CD4 counts, and had suppressed HIV RNA and not by increases in cancer risk within these subgroups. An improved understanding of HIV-associated cancer pathogenesis and outcomes in the context of successful ART is therefore important. (Yanik EL, Achenbach CJ, Gopal S, et al. Changes in clinical context for Kaposi's sarcoma and non-Hodgkin lymphoma among people with HIV infection in the United States. J Clin Oncol 2016)

Medical Conditions

The authors used a novel method—"medical condition-wide association study, or MedWAS"—to comprehensively evaluate medical risk factors for non-Hodgkin lymphoma (NHL) documented in the Surveillance, Epidemiology, and End Results (SEER)-Medicare data. They found 55 conditions variously associated with NHL. Examples included well-established associations of human immunodeficiency virus, solid organ transplantation, and hepatitis C virus with increased diffuse large B-cell lymphoma (DLBCL) risk, and autoimmune conditions with DLBCL and marginal zone lymphoma (MZL), along with some novel associations for NHL overall and NHL subtypes. (Engels EA, Parsons R, Besson C, et al. Comprehensive evaluation of medical conditions associated with risk of non-Hodgkin lymphoma using Medicare claims ("MedWAS"). Cancer Epidemiol Biomarkers Prev 2016)

Whole Exome Sequencing

Hodgkin lymphoma shows strong familial aggregation but no major susceptibility genes have been identified to date. Applying whole genome sequencing to members of Hodgkin lymphoma-prone families, investigators identified a causal mutation in the KDR gene, which is a type III receptor tyrosine kinase, the main mediator of vascular endothelial growth factor induced proliferation, survival, and migration. While independent validation is needed, this mutation may increase downstream tumor cell proliferation activity and might be a candidate for targeted therapy. (Rotunno M, McMaster ML, Boland J, et al. Whole exome sequencing in families at high risk for Hodgkin lymphoma: Identification of a predisposing mutation in the KDR gene. Haematologica 2016)

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Obesity

Body Mass Index (also under All Cause Mortality)

Analysis of data pooled from 189 studies, representing over 10.5 million people from 32 countries, demonstrated body mass index (BMI) outside of the normal range (20-24.9) is associated with increased risk of mortality. The finding held across all areas of the world, with the absolute increases in risk for obese and moderately obese men higher than those among obese and moderately obese women, respectively. When the analysis was limited to never-smokers and excluded deaths in the first five years of follow-up, there was an increase in premature mortality among even overweight (BMI 25-29.9) persons, compared to those in the normal range. (Global BMI Mortality Collaboration. Body-mass index and all-cause mortality: Individual-participant-data meta-analysis of 239 prospective studies in four continents. Lancet 2016). Read more in BMI Outside Normal Range Associated with Increased Risk of Mortality (Research News Highlight).

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Pancreas

Functional Characterization of Risk Locus

Genome-wide association studies (GWAS) have identified multiple common susceptibility loci for pancreatic cancer. Through fine-mapping and functional analysis of one such locus residing in a 610 kb gene desert on chr13q22.1 (marked by rs9543325), investigators identified a putative functional insertion/deletion variant at chr13q22.1 that associates with decreased DIS3 expression in carriers of pancreatic cancer risk-increasing alleles, and could therefore affect nuclear RNA processing and/or decay. (Hoskins JW, Ibrahim A, Emmanuel MA, et al. Functional characterization of a chr13q22.1 pancreatic cancer risk locus reveals long-range interaction and allele-specific effects on DIS3 expression. Hum Mol Genet 2016)

Microbiome

The relationship of oral microbiota with subsequent risk of pancreatic cancer was examined in a large nested case-control study within two prospective cohort studies. Using prediagnostic oral wash samples, carriage of oral pathogens, Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitans, were associated with higher risk of pancreatic cancer. Phylum Fusobacteria and its genus Leptotrichia were associated with decreased pancreatic cancer risk.  (Fan X, Alekseyenko AV, Wu J, et al. Human oral microbiome and prospective risk for pancreatic cancer: a population-based nested case-control study. Gut 2016; Epub Oct 14, 2016)

New Genetic Susceptibility Variants

Genome-wide association studies (GWAS) have identified common pancreatic cancer susceptibility variants at 13 chromosomal loci in individuals of European descent. To identify new variants, we performed imputation based on 1000 Genomes (1000G) Project data and association analysis using 5,107 case and 8,845 control subjects from 27 cohort and case-control studies that participated in the PanScan I-III GWAS. This analysis, in combination with a two-staged replication in additional subjects from the PANcreatic Disease ReseArch (PANDoRA) and Pancreatic Cancer Case-Control (PanC4) Consortia uncovered three new pancreatic cancer risk signals marked by single nucleotide polymorphisms (SNPs) rs2816938 at chromosome 1q32.1, rs10094872 at 8q24.21, and rs35226131 at 5p15.33. These SNPs represent independent risk variants at previously identified pancreatic cancer risk loci on chr1q32.1 (NR5A2), chr8q24.21 (MYC) and chr5p15.33 (CLPTM1L-TERT). (Zhang M, Wang Z, Obazee O, et al. Three new pancreatic cancer susceptibility signals identified on chromosomes 1q32.1, 5p15.33 and 8q24.21. Oncotarget 2016;)

Prior Radiation Therapy

Among 23,982 five-year survivors of testicular cancer (TC) diagnosed between 1947 and 1991, doses from radiotherapy to the pancreas were estimated for 80 pancreatic cancer patients and 145 matched controls. Cumulative incidence of second primary pancreatic cancer was 1.1% at 30 years after TC diagnosis. A dose-response relationship exists between radiation to the pancreas and subsequent cancer risk, and persists for over 20 years. These excesses, although small, should be considered when radiotherapy with exposure to the pancreas is considered for newly diagnosed patients. Additional data on chemotherapy are needed. (Hauptmann M, Børge Johannesen T, Gilbert ES, et al. Increased pancreatic cancer risk following radiotherapy for testicular cancer. Br J Cancer 2016)

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Prostate

Body Mass Index

Evidence suggests that obesity in adulthood is associated with increased risk of "clinically significant" prostate cancer. However, studies of body mass index (BMI) across the adult life course and prostate cancer risks remain limited. Data from a prospective cohort of 69,873 men in the Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial showed that BMI at age 20 years, 50 years, and baseline questionnaire (mean age = 63 years) were associated with increased risks of fatal prostate cancer. In five BMI trajectories identified, fatal prostate cancer risk was increased in men who had a normal BMI or who were overweight at age 20 years and developed obesity by baseline compared with men who maintained a normal BMI. Aggressive and nonaggressive prostate cancer were not associated with BMI, and modest inverse associations were seen for total prostate cancer. The results suggest that BMI trajectories during adulthood that result in obesity lead to an elevated risk of fatal prostate cancer. (Kelly SP, Graubard BI, Andreotti G, et al. Prediagnostic body mass index trajectories in relation to prostate cancer incidence and mortality in the PLCO Cancer Screening Trial. J Natl Cancer Inst 2016; Epub Oct 20)

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Resources

PLCO Tissue Resource

The Prostate, Lung, Colorectal and Ovarian (PLCO) Cancer Screening Trial undertook a large-scale effort to create a public resource of pathology tissues from PLCO participants who developed a cancer during the trial. Formalin-fixed paraffin-embedded tissue blocks were obtained from pathology laboratories on a loan basis for central processing of tissue microarrays, with additional free-standing tissue cores collected for nucleic acid extraction. The methods and protocols developed for this effort, and the detailed description of this resource provided in this article will be useful for those seeking to use PLCO pathology tissue specimens for their research and may also inform future tissue collection efforts in other settings. (Zhu CS, Huang WY, Pinsky PF, et al. The Prostate, Lung, Colorectal and Ovarian Cancer (PLCO) Screening Trial pathology tissue resource. Cancer Epidemiol Biomarkers Prev 2016)

Record Linkage

EDITORIAL: Major JM, Penberthy L, McGlynn KA. Data systems and record linkage: Considerations for pharmacoepidemiologic studies examining cancer risk. Ann Epidemiol 2016; Epub Aug 31).

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Sarcoma

HIV (Also under Lymphoma)

The biology of HIV-associated cancers may differ depending on immunologic and virologic context during development. Therefore, an understanding of the burden of Kaposi sarcoma (KS) and non-Hodgkin lymphoma (NHL) relative to antiretroviral therapy (ART), virologic suppression, and CD4 count is important. Patients with KS and NHL from eight clinical cohorts were identified among patients with HIV. Over time, KS and NHL occurred at higher CD4 counts and lower HIV RNA values, and KS occurred more frequently after ART initiation. These changes were driven by an increasing proportion of patients with HIV who received effective ART, had higher CD4 counts, and had suppressed HIV RNA and not by increases in cancer risk within these subgroups. An improved understanding of HIV-associated cancer pathogenesis and outcomes in the context of successful ART is therefore important. (Yanik EL, Achenbach CJ, Gopal S, et al. Changes in clinical context for Kaposi's sarcoma and non-Hodgkin lymphoma among people with HIV infection in the United States. J Clin Oncol 2016)

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Stomach

Vitamin B (Also under Esophagus)

B vitamins, which play an essential role in DNA synthesis and methylation, were found to have a possible protect effect against esophageal and gastric cancers in data from the General Population Nutrition Intervention Trial in Linxian, China. Subjects included 498 esophageal squamous cell carcinomas (OSCCs), 255 gastric cardia adenocarcinomas (GCAs), and an age- and sex-matched sub-cohort of 947 individuals. Baseline serum riboflavin and vitamin B12 were inversely associated with risk of esophageal cancer, while higher flavin mononucleotide levels were significantly associated with increased risk of esophageal and gastric cancer. (Ren J, Murphy G, Fan J, et al. Prospective study of serum B vitamins levels and oesophageal and gastric cancers in China. Sci Rep 2016; Epub Oct 17)

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Tobacco

Light and Intermittent Smoking

Light and/or intermittent smokers have been the fastest growing segment of cigarette smokers in the U.S. over the past two decades. Defining their behavioral characteristics is a critical public health priority. Based on pooled data from three large national surveys, light and/or intermittent smokers differed in smoking, drug use and mental health behaviors from heavier-daily, former and never smokers. Notable differences by level of smoking frequency and intensity were observed for nicotine dependence, age of smoking initiation and race/ethnicity. (Reyes-Guzman CM, Pfeiffer RM, Lubin J, et al. Determinants of light and intermittent smoking in the U.S.: Results from three pooled national health surveys. Cancer Epidemiol Biomarkers Prev 2016; Epub Oct 19, 2016)

Smokeless Tobacco

COMMENTARY: Freedman ND. Smokeless Tobacco-An Important Contributor to Cancer, but More Work Is Needed. Am J Epidemiol 2016; Epub Oct 15, 2016.

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