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Background: Few prospective studies have examined biomarkers of glucose homeostasis or inflammation with prostate cancer risk by tumor stage or grade. Methods: We conducted a case-cohort study to examine associations of prediagnosis hemoglobin A1c (HbA1c), C-peptide, and C-reactive protein (CRP) with prostate cancer risk overall and stratified by tumor stage and grade. The study included 390 nonaggressive (T1-2, N0, M0, and Gleason score <8) and 313 aggressive cases (T3-4, or N1, or M1, or Gleason score 8-10) diagnosed after blood draw (1998-2001) and up to 2013, and a random subcohort of 1,303 cancer-free men at blood draw in the Cancer Prevention Study-II Nutrition Cohort. Prentice-weighted Cox proportional hazards regression models were used to estimate HRs and 95% confidence intervals (CI). Results: In the multivariable-adjusted model without body mass index, HbA1c was inversely associated with nonaggressive prostate cancer (HR per unit increase, 0.89; 95% CI, 0.80-1.00; P = 0.04). Analyses stratified by tumor stage and grade separately showed that HbA1c was inversely associated with low-grade prostate cancer (HR per unit increase, 0.89; 95% CI, 0.80-1.00) and positively associated with high-grade prostate cancer (HR per unit increase, 1.15; 95% CI, 1.01-1.30). C-peptide and CRP were not associated with prostate cancer overall or by stage or grade. Conclusions: The current study suggests that associations of hyperglycemia with prostate cancer may differ by tumor grade and stage. Impact: Future studies need to examine prostate cancer by tumor stage and grade, and to better understand the role of hyperglycemia in prostate cancer progression. [ABSTRACT FROM AUTHOR]

Alcoholic beverages are carcinogenic to humans. Globally, an estimated 4.1% of new cancer cases in 2020 were attributable to alcoholic beverages. However, the full cancer burden due to alcohol is uncertain because for many cancer (sub)types, associations remain inconclusive. Additionally, associations of consumption with therapeutic response, disease progression, and long-term cancer outcomes are not fully understood, public awareness of the alcohol-cancer link is low, and the interrelationships of alcohol control regulations and cancer risk are unclear. In December 2020, the U.S. NCI convened a workshop and public webinar that brought together a panel of scientific experts to review what is known about and identify knowledge gaps regarding alcohol and cancer. Examples of gaps identified include: (i) associations of alcohol consumption patterns across the life course with cancer risk; (ii) alcohol's systemic carcinogenic effects; (iii) alcohol's influence on treatment efficacy, patient-reported outcomes, and long-term prognosis; (iv) communication strategies to increase awareness of the alcohol-cancer link; and (v) the impact of alcohol control policies to reduce consumption on cancer incidence and mortality. Interdisciplinary research and implementation efforts are needed to increase relevant knowledge, and to develop effective interventions focused on improving awareness, and reducing harmful consumption to decrease the alcohol-related cancer burden. [ABSTRACT FROM AUTHOR]

Strategic planning is conducted by many organizations to systematically evaluate and assess their current state, establish or update their mission and/or goals, and identify strategies and activities to achieve the goals. The National Cancer Institute (NCI) Cohort Consortium is a collaborative network of 62 prospective cohort studies and their affiliated investigators that focus on cancer etiology and outcome research. The organization's membership grew markedly from 10 cohort studies at its inception in 2001 to 59 cohort studies at the time of the launch of the Consortium's strategic planning in 2017. This paper describes the strategic planning process that was conducted to establish organizational goals and to develop strategies and activities consistent with the Consortium's mission. The process involved a 2-year iterative approach combining surveys and in-person meetings. The resulting goals focus on communication, career development, research facilitation, scientific gaps, and common scientific challenges. The NCI Cohort Consortium's strategic plan and evaluation of its progress will advance new initiatives in cancer etiology and survivorship research. [ABSTRACT FROM AUTHOR]

Background: Some evidence suggests the association between body mass index (BMI) and pancreatic cancer risk is weaker among current smokers than among never smokers. Methods: We examined the association between BMI and pancreatic cancer mortality among adults who reported smoking status at enrollment into Cancer Prevention Study-II in 1982, including 420,543 never smokers, 282,244 former cigarette smokers, and 219,885 current cigarette smokers. After excluding the first 3 years of follow-up to reduce reverse causation, we calculated multivariable-adjusted hazard ratios (HR). Results: During the full follow-up period from 1985 to 2014, 7,904 participants died of pancreatic cancer. The HR per 5 BMI units was lower among current smokers [HR = 1.14; 95% confidence interval (CI), 1.07-1.20] than never smokers (HR = 1.22; 95% CI, 1.17-1.27), although this difference was not statistically significant (P = 0.06). BMI was significantly less strongly associated with pancreatic cancer mortality among current smokers reporting =20 cigarettes/day (HR = 1.10; 95% CI, 1.03-1.18) than among never smokers. During follow-up within 10 years of enrollment, when current smokers at enrollment were the most likely to have still been smoking, BMI was not associated with pancreatic cancer mortality among current smokers (HR = 1.02; 95% CI, 0.90-1.16, P = 0.03 for difference between current and never smokers). BMI HRs were similar among former and never smokers. Conclusions: These results support a weaker association between BMI and pancreatic cancer among current smokers than among never smokers. [ABSTRACT FROM AUTHOR]

Background: There is limited evidence of a potential inverse association between coffee, particularly caffeinated coffee, consumption and postmenopausal breast cancer risk, and few studies have examined this association by tumor hormone receptor status. To provide further evidence, we examined total, caffeinated, and decaffeinated coffee consumption in relation to postmenopausal invasive breast cancer incidence overall, and by tumor estrogen receptor (ER) and/or progesterone receptor (PR) subtype. Methods: Among 57,075 postmenopausal women in the Cancer Prevention Study-II Nutrition Cohort who were cancer free and reported coffee intake in 1999, we identified 2,980 women diagnosed with invasive breast cancer during follow-up through June 2015. Multivariable-adjusted Cox proportional hazards regression was used to compute hazard ratios (HR) and 95% confidence intervals (CI). Results: Neither total, caffeinated, nor decaffeinated coffee consumption was associated with invasive breast cancer risk; HRs (95% CIs) comparing consumption of =2 cups per day with <1 cup per month were 0.99 (0.89-1.11), 0.96 (0.87-1.06), and 1.06 (0.95-1.19), respectively. Similarly, coffee consumption was not associated with risk of hormone receptor-positive (ER+ or PR+) or hormone receptor-negative (ER- and PR-) breast tumors. Conclusions: These findings do not support an association between coffee consumption and invasive breast cancer risk among postmenopausal women. [ABSTRACT FROM AUTHOR]

Background: Energy balance-related factors, such as body mass index (BMI), diet, and physical activity, may influence colorectal cancer etiology through interconnected metabolic pathways, but their combined influence is less clear. Methods: We used reduced rank regression to derive three energy balance scores that associate lifestyle factors with combinations of prediagnostic, circulating levels of high-sensitivity C-reactive protein (hsCRP), C-peptide, and hemoglobin A1c (HbA1c) among 2,498 participants in the Cancer Prevention Study-II Nutrition Cohort. Among 114,989 participants, we verified 2,228 colorectal cancer cases. We assessed associations of each score with colorectal cancer incidence and by tumor molecular phenotypes using Cox proportional hazards regression. Results: The derived scores comprised BMI, physical activity, screen time, and 14 food groups, and explained 5.1% to 10.5% of the variation in biomarkers. The HR and 95% confidence interval (CI) for quartile 4 versus 1 of the HbA1c+C peptide-based score and colorectal cancer was 1.30 (1.15-1.47), the hsCRP-based score was 1.35 (1.19-1.53), and the hsCRP, C-peptide, and HbA1c-based score was 1.35 (1.19-1.52). The latter score was associated with non-CIMP tumors (HRQ4vsQ1: 1.59; 95% CI: 1.17-2.16), but not CIMP-positive tumors (Pheterogeneity = 0.04). Conclusions: These results further support hypotheses that systemic biomarkers of metabolic health--inflammation and abnormal glucose homeostasis--mediate part of the relationship between several energy balance-related modifiable factors and colorectal cancer risk. Impact: Results support cancer prevention guidelines for maintaining a healthful body weight, consuming a healthful diet, and being physically active. More research is needed on these clusters of exposures with molecular phenotypes of tumors. [ABSTRACT FROM AUTHOR]

Introduction: There is limited research on associations of moderate-to-vigorous physical activity (MVPA) and sitting with risk of myeloid neoplasms (MN) or MN subtypes. We examined these associations in the Cancer Prevention Study-II Nutrition Cohort. Methods: Among 109,030 cancer-free participants (mean age 69.2, SD 6.1 years) in 1999, 409 were identified as having been diagnosed with a MN [n = 155 acute myeloid leukemia (AML), n = 154 myelodysplastic syndromes (MDS), n = 100 other ML] through June 2013. Cox proportional hazards regression was used to calculate multivariable adjusted hazard ratios (HR) and 95% confidence intervals (CI) for associations of MVPA (MET-h/wk) and sitting (h/d) with risk of all MN, myeloid leukemia only, MDS, and AML. Results: Compared with insufficient MVPA [>0-<7.5 metabolic equivalent hours/week (MET)-h/wk], the HR (95% CI) for meeting physical activity guidelines (7.5-<15 MET-h/wk MVPA) and risk of MN was 0.74 (95% CI, 0.56-0.98) and for doubling guidelines (15-<22.5 MET-h/wk) was 0.75 (0.53-1.07); however, there was no statistically significant association for higher MVPA (22.5+ MET-h/wk, HR, 0.93; 95% CI, 0.73-1.20). Similarly, meeting/doubling guidelines was associated with lower risk of MDS (HR, 0.57; 95% CI, 0.35-0.92/HR, 0.51; 95% CI, 0.27-0.98), but there was no association for 22.5+ MET-h/wk (HR, 0.93; 95% CI, 0.63-1.37). MVPA was not associated with risk of myeloid leukemia or AML. Sitting time was not associated with risk of any outcome. Conclusions: These results suggest that there may be a nonlinear association between MVPA and risk of MDS and possibly other MN. [ABSTRACT FROM AUTHOR]

Background: Acrylamide, an industrial chemical and probable human carcinogen, can be formed in primarily carbohydrate-containing foods during high-heat cooking or processing. Most epidemiologic studies show no associations of dietary acrylamide intake with most cancer outcomes, but limited prospective evidence suggests a positive association with renal cell carcinoma (RCC). Methods: In 1999, 102,154 men and women from the Cancer Prevention Study-II Nutrition Cohort completed a questionnaire on diet, lifestyle, and cancer risk factors and were followed through June 30, 2013. Cox proportional hazards regression was used to estimate the HR and 95% confidence interval (CI) for the association between estimated dietary acrylamide intake and risk of RCC. Results: After 1,137,441 person-years of follow-up, 412 cases of invasive RCC occurred. In multivariable-adjusted models, there was no association between acrylamide intake and risk of RCC (HR = 1.09; 95% CI, 0.82-1.43) for the highest versus lowest quartile of intake. Associations were not modified by sex or smoking history. Conclusions: We found no associations between dietary acrylamide exposure and risk of invasive RCC. Impact: The findings from this large, prospective analysis do not support a positive association between higher dietary acrylamide intake and RCC risk. [ABSTRACT FROM AUTHOR]

Cohort studies have been central to the establishment of the known causes of cancer. To dissect cancer etiology in more detail--for instance, for personalized risk prediction and prevention, assessment of risks of subtypes of cancer, and assessment of small elevations in risk--there is a need for analyses of far larger cohort datasets than available in individual existing studies. To address these challenges, the NCI Cohort Consortium was founded in 2001. It brings together 58 cancer epidemiology cohorts from 20 countries to undertake large-scale pooling research. The cohorts in aggregate include over nine million study participants, with biospecimens available for about two million of these. Research in the Consortium is undertaken by >40 working groups focused on specific cancer sites, exposures, or other research areas. More than 180 publications have resulted from the Consortium, mainly on genetic and other cancer epidemiology, with high citation rates. This article describes the foundation of the Consortium; its structure, governance, and methods of working; the participating cohorts; publications; and opportunities. The Consortium welcomes new members with cancer-oriented cohorts of 10,000 or more participants and an interest in collaborative research. [ABSTRACT FROM AUTHOR]

Background: Several studies have examined association between human papillomaviruses (HPV) and esophageal cancer, but results have been inconsistent. This is the first prospective study to investigate associations between α, ß and γ HPV detection in the oral cavity and risk of esophageal cancer. Methods: We conducted a nested case-control study among 96,650 cancer-free participants in the American Cancer Society Cancer Prevention Cohort and the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial. Incident esophageal cancer cases (n = 125) were identified during an average 3.9 years of follow-up. Three controls per case (n = 372) were selected and matched on age, sex, race/ethnicity, and time since mouthwash collection. α, ß, and γ HPV DNA in oral samples were detected using a next-generation sequencing assay. Conditional logistic regression models were used to estimate OR and 95% confidence intervals (CIs), adjusting for smoking and alcohol consumption. Statistical significance was evaluated using permutation test. Results: Prevalence of oral α, ß, and γ HPV was 18.4%, 64.8%, and 42.4% in cases and 14.3%, 55.1%, and 33.6% in controls, respectively. Oral HPV16 detection was not associated with esophageal cancer (OR = 0.54, 95% CI, 0.1-4.84) and none of the esophageal squamous cell carcinoma cases (n = 28) were HPV16 positive. Some oral HPV types were more common in cases than controls; however, none of the associations were statistically significant. Conclusions: Although HPVs in the oral cavity are very common, this study showed no evidence of association between oral HPVs and esophageal cancer. Impact: Oral HPVs may not contribute to risk of esophageal cancer. [ABSTRACT FROM AUTHOR]

Background: The oral microbiota play a central role in oral health, and possibly in carcinogenesis. Research suggests that coffee and tea consumption may have beneficial health effects. We examined the associations of these common beverages with the oral ecosystem in a large cross-sectional study. Methods: We assessed oral microbiota in mouthwash samples from 938 participants in two U.S. cohorts using 16S rRNA gene sequencing. Coffee and tea intake were assessed from food frequency questionnaires. We examined associations of coffee and tea intake with overall oral microbiota diversity and composition using linear regression and permutational MANOVA, respectively, and with taxon abundance using negative binomial generalized linear models; all models adjusted for age, sex, cohort, body mass index, smoking, ethanol intake, and energy intake. Results: Higher tea intake was associated with greater oral microbiota richness (P = 0.05) and diversity (P = 0.006), and shifts in overall community composition (P = 0.002); coffee was not associated with these microbiome parameters. Tea intake was associated with altered abundance of several oral taxa; these included Fusobacteriales, Clostridiales, and Shuttleworthia satelles (higher with increasing tea) and Bifidobacteriaceae, Bergeyella, Lactobacillales, and Kingella oralis (lower with increasing tea). Higher coffee intake was only associated with greater abundance of Granulicatella and Synergistetes. Conclusions: In the largest study to date of tea and coffee consumption in relation to the oral microbiota, the microbiota of tea drinkers differed in several ways from nondrinkers. [ABSTRACT FROM AUTHOR]

Background: Prior studies of prostate cancer survivors suggest that smoking might be associated with higher prostate cancer-specific mortality (PCSM) after diagnosis with prostate cancer. However, most of these studies were small, and questions remain regarding this association's strength and whether it persists after adjustment for stage and Gleason score. Methods: This analysis included men diagnosed with nonmetastatic prostate cancer between enrollment in the Cancer Prevention Study II Nutrition Cohort in 1992-1993 and June 2013. Cigarette smoking was self-reported at enrollment and updated in 1997 and every 2 years thereafter. Analyses of pre-diagnosis and post-diagnosis smoking included 9,781 and 9,111 prostate cancer cases, respectively, with vital status follow-up through 2014. Results: There were 672 deaths from prostate cancer in analyses of pre-diagnosis smoking and 554 in analyses of post-diagnosis smoking. In multivariable-adjusted Cox proportional hazards regression models including stage and Gleason score, both current smoking before diagnosis [HR = 1.50; 95% confidence interval (CI), 1.06-2.13] and current smoking after diagnosis (HR = 1.71; 95% CI, 1.09-2.67) were associated with higher PCSM compared to never smoking. Prostate cancer survivors who quit smoking <20 years before diagnosis were also at significantly higher risk of PCSM (HR = 1.29; 95% CI, 1.04-1.61). Conclusions: This large prospective study suggests that current smoking both before and after diagnosis of prostate cancer is associated with higher PCSM, even after accounting for stage and Gleason score. [ABSTRACT FROM AUTHOR]

Background: Although some familial cancer syndromes include biliary tract cancers (BTCs; cancers of the gallbladder, intrahepatic and extrahepatic bile ducts, and ampulla of Vater), the few studies that have examined the relationships between family history of cancer (FHC) and BTCs have reported inconclusive findings. The objective of this study was to investigate the associations of FHC with risk of BTC in the Biliary Tract Cancers Pooling Project (BiTCaPP). Methods: We used Cox proportional hazards regressions models to estimate HRs and 95% confidence intervals for associations between FHC (any, first-degree, in female relative, in male relative, relative with gastrointestinal cancer, and relative with hormonally related cancer) and BTC risk by anatomic site within the biliary tract, adjusting for sex and race/ethnicity. Sensitivity analyses were conducted that restricted to studies reporting cholecystectomy data and to people without a history of cholecystectomy. Results: Data on FHC were available from 12 prospective studies within BiTCaPP, which collectively contributed 2,246 cases (729 gallbladder, 345 intrahepatic and 615 extrahepatic bile duct, and 385 ampulla of Vater cancers) with 21,706,107 person-years of follow-up. A marginal, inverse association between FHC and gallbladder cancer was driven to the null when analysis was restricted to studies reporting cholecystectomy data and to people without a history of cholecystectomy. FHC was not associated with risk of BTC at the other anatomic sites. Conclusions: These findings do not support an association between FHC and BTCs. Impact: In a study of 1.5 million people, FHC is not a risk factor for BTCs. [ABSTRACT FROM AUTHOR]

Background: The presence of circulating antibodies to the p53 tumor suppressor protein is a potential early detection colorectal cancer biomarker. However, studies of prediagnostic measures of p53 seropositivity in relation to colorectal cancer risk are limited. Methods: We conducted a nested case-control study of serum p53 autoantibodies and risk of colorectal cancer within the Cancer Prevention Study-II Nutrition Cohort. Among cohort participants who were cancer free at the time of blood collection, 392 were subsequently diagnosed with colorectal cancer over 11 years of follow-up. Two controls were matched to each case on birth date, blood draw date, race, and sex. Autoantibodies to p53 were detected in 41 of the 392 cases (10.5%) and 49 of the 774 controls (6.3%). Results: Participants who were seropositive for p53 antibodies before diagnosis were more likely to be subsequently diagnosed with colorectal cancer [RR = 1.77; 95% confidence interval (CI), 1.12-2.78]. This association was strongest within 3 years of diagnosis (RR = 2.26; 95% CI, 1.06-4.83). An association was also suggested when colorectal cancer was diagnosed 4 to <6 years after p53 measurement (RR = 1.84; 95% CI, 0.89-3.79), but not 6 or more years later (RR = 1.15; 95% CI, 0.44-2.99). Conclusions: If these results are confirmed, serum p53 antibodies may be useful on a panel of early detection markers for colorectal cancer. Impact: Individuals who were seropositive for p53 antibodies were twice as likely to develop colorectal cancer within the next 3 years compared with those who were seronegative. This marker is a good candidate for inclusion on an early detection marker panel for colorectal cancer. [ABSTRACT FROM AUTHOR]

Background: Associations of coffee consumption with cancer mortality are inconsistent for many types of cancer, and confounding by smoking is an important concern. Methods: Cox proportional hazards regression was used to estimate multivariable-adjusted HRs for coffee consumption associated with death from all cancers combined and from specific cancer types among 922,896 Cancer Prevention Study-II participants ages 28-94 years who completed a four-page questionnaire and were cancer free at baseline in 1982. Results: During follow-up through 2012, there were 118,738 cancer-related deaths. There was a nonlinear association between coffee consumption and all-cancer death among current smokers and former smokers and no association among never smokers. Among nonsmokers, a 2 cup/day increase in coffee consumption was inversely associated with death from colorectal [HR = 0.97; 95% confidence interval (CI) 0.95-0.99], liver [HR = 0.92; 95% CI, 0.88-0.96], and female breast (HR = 0.97; 95% CI, 0.94-0.99) cancers, and positively associated with esophageal cancer-related death (HR = 1.07; 95% CI, 1.02-1.12). For head and neck cancer, a nonlinear inverse association was observed starting at 2-3 cups per day (HR = 0.72; 95% CI, 0.55-0.95), with similar associations observed at higher levels of consumption. Conclusions: These findings are consistent with many other studies that suggest coffee drinking is associated with a lower risk of colorectal, liver, female breast, and head and neck cancer. The association of coffee consumption with higher risk of esophageal cancer among nonsmokers in our study should be confirmed. Impact: These results underscore the importance of assessing associations between coffee consumption and cancer mortality by smoking status. [ABSTRACT FROM AUTHOR]

Background: Obesity is an established risk factor for renal cell carcinoma (RCC). Although genome-wide association studies (GWAS) of RCC have identified several susceptibility loci, additional variants might be missed due to the highly conservative selection. Methods: We conducted a multiphase study utilizing three independent genome-wide scans at MD Anderson Cancer Center (MDA RCC GWAS and MDA RCC OncoArray) and National Cancer Institute (NCI RCC GWAS), which consisted of a total of 3,530 cases and 5,714 controls, to investigate genetic variations in obesity-related genes and RCC risk. Results: In the discovery phase, 32,946 SNPs located at ±10 kb of 2,001 obesity-related genes were extracted from MDA RCC GWAS and analyzed using multivariable logistic regression. Proxies (R² > 0.8) were searched or imputation was performed if SNPs were not directly genotyped in the validation sets. Twenty-one SNPs with P < 0.05 in both MDA RCC GWAS and NCI RCC GWAS were subsequently evaluated in MDA RCC OncoArray. In the overall meta-analysis, significant (P < 0.05) associations with RCC risk were observed for SNP mapping to IL1RAPL2 [rs10521506-G: OR meta = 0.87 (0.81-0.93), Pmeta = 2.33 × 10-5], PLIN2 [rs2229536-A: ORmeta = 0.87 (0.81-0.93), Pmeta = 2.33 × 10-5], SMAD3 [rs4601989-A: ORmeta = 0.86 (0.80-0.93), Pmeta = 2.71 × 10-4], MED13L [rs10850596-A: ORmeta = 1.14 (1.07-1.23), Pmeta = 1.50 × 10-4], and TSC1 [rs3761840-G: ORmeta = 0.90 (0.85-0.97), Pmeta = 2.47 × 10-3]. We did not observe any significant cis-expression quantitative trait loci effect for these SNPs in the TCGA KIRC data. Conclusions: Taken together, we found that genetic variation of obesity-related genes could influence RCC susceptibility. Impact: The five identified loci may provide new insights into disease etiology that reveal importance of obesity-related genes in RCC development. [ABSTRACT FROM AUTHOR]

Background: Cigarette price increases effectively prevent smoking initiation and reduce cigarette consumption among young smokers. However, the impact of cigarette prices on smoking cessation among older smokers is less clear, particularly for those aged 65 years and older, a group that is at highest risk of smoking-related disease and will almost double in the United States between 2012 and 2050. Methods: Biennial questionnaires administered between 1997 and 2013 assessed smoking status for 9,446 Cancer Prevention Study-II Nutrition Cohort participants who were =50 years old and lived in Washington, DC, and 48 states. For each interval between biennial questionnaires, change in price per pack and average price level per pack were calculated. The separate associations between these price variables and smoking cessation during the same time interval were determined. Results: In multivariable-adjusted models, each $1.00 price increase was associated with a 9% higher rate of quitting [rate ratio (RR) = 1.09; 95% confidence interval (CI), 1.04-1.14). Each $1.00 increase in average price was associated with a 6% higher rate of quitting (RR = 1.06; 95% CI, 1.02-1.10). The association with average price was strongest among smokers aged 65 years and older (RR = 1.07; 95% CI, 1.04-1.11) and, for price change, for smokers with no major prevalent disease (RR = 1.13; 95% CI, 1.07-1.19). Conclusions: These results suggest that increasing cigarette prices will promote quitting even among smokers aged 65 years and older. Impact: Increasing cigarette prices through higher taxes could reduce smoking rates among older adults and decrease risk of smoking-related cancers and diseases in this high-risk group. [ABSTRACT FROM AUTHOR]

The association between leisure-time physical activity (LTPA) and male breast cancer risk is unclear. In the Male Breast Cancer Pooling Project, with 449 cases and 13,855 matched controls, we used logistic regression with study stratification to generate adjusted ORs and 95% confidence intervals (CI) for LTPA tertiles and male breast cancer risk. Compared with low LTPA, medium and high LTPA were not associated with male breast cancer risk (OR, 1.01; 95% CI, 0.79-1.29; 0.90, 0.69-1.18, respectively). In jointeffects analyses, compared with the referent of high body mass index (BMI; ⩾25 kg/m2)/low LTPA, neither medium nor high PA was associated with risk among high BMI men, but normal BMI men (<25 kg/m2) with low or medium LTPA were at a nonsignificant ~16% reduced risk and those with high LTPA were at a 27% reduced risk (OR, 0.73; 95% CI, 0.50-1.07). Physical activity alone may not confer protection against male breast cancer risk. [ABSTRACT FROM AUTHOR]

Background: The glycemic potential and energy density (ED) of diet may influence endometrial cancer risk. Although glycemic load (GL) is considered a probable risk factor for endometrial cancer, no studies have evaluated the association of total dietary ED with risk. Methods: We evaluated associations of ED, GL, and glycemic index (GI) with postmenopausal endometrial cancer incidence. Analyses included 30,997 postmenopausal women from the Cancer Prevention Study II Nutrition Cohort with no previous history of cancer or diabetes, who provided information on diet, lifestyle, and medical history in 1999 and were followed for cancer incidence through June 2013. Multivariable-adjusted HRs and 95% confidence intervals were estimated for quartiles (Q) of total dietary ED, GL, and GI in relation to endometrial cancer incidence using Cox proportional hazards regression models. Results: During a median follow-up time of 13.6 years, 425 endometrial cancer cases were identified. Median dietary ED was 1.5 kcal/g [interquartile range (IQR) = 1.3-1.7 kcal/g]. Median (IQR) GL and GI were 113.7 (100.5-126.8) and 52.5 (50.4-54.5), respectively. After adjustment for age, use of hormone replacement therapy, physical activity, and body mass index (kg/m²), neither ED, GL, nor GI were associated with endometrial cancer risk. Conclusions: We found no associations of ED, GL, or GI with endometrial cancer risk. Impact: These results do not support an association between total dietary ED, GL, or GI and risk of postmenopausal endometrial cancer. [ABSTRACT FROM AUTHOR]

Background: The relationship between excess body weight and prostate cancer risk is unclear. However, some evidence suggests that waist circumference, which provides a measure of central adiposity, may be positively associated with more advanced stages or grades of prostate cancer. Methods: The association between waist circumference and prostate cancer was investigated among 46,094 men enrolled in the Cancer Prevention Study II Nutrition Cohort, of whom 5,711 were diagnosed with this cancer between 1997 and 2013. Using Cox proportional hazards regression, we examined associations of weight circumference with total and high-grade prostate cancer incidence and with prostate cancer mortality. Results: In both categorical and continuous analyses, waist circumference was not associated with total or high-grade (Gleason score = 8) prostate cancer incidence or with prostate cancer mortality regardless of whether body mass index was adjusted for in the statistical model. Waist circumference was inversely associated with low-grade (Gleason score < 8) prostate cancer, but the association was not statistically significant after adjustment for body mass index. Conclusions: Our results suggest that central adiposity, as measured by waist circumference, is not significantly associated with prostate cancer incidence or mortality. Impact: Compared with men in other studies with significant results, men in our study were considerably older, suggesting that age may influence the association between waist circumference and prostate cancer. [ABSTRACT FROM AUTHOR]

Background: Coffee consumption has been reported to be inversely associatedwith hepatocellular carcinoma (HCC), themost common type of liver cancer. Caffeine has chemopreventive properties, but whether caffeine is responsible for the coffee-HCC association is not well studied. In addition, few studies have examined the relationship by sex, and no studies have examined whether there is an association between coffee and intrahepatic cholangiocarcinoma (ICC), the second most common type of liver cancer. Methods: In the Liver Cancer Pooling Project, a consortium of U.S.-based cohort studies, data from 1,212,893 individuals (HCC, n = 860; ICC, n = 260) in nine cohorts were pooled. Multivariable- adjusted hazard ratios (HR) and 95% confidence intervals (CI) were estimated using proportional hazards regression. Results: Higher coffee consumption was associated with lower risk of HCC (HR>3 cups/day vs. non-drinker, 0.73; 95% CI, 0.53-0.99; Ptrend cups/day = <0.0001). More notable reduced risk was seen among women than men (Pinteraction = 0.07). Women who consumed more than three cups of coffee per day were at a 54% lower risk of HCC (HR, 0.46; 95% CI, 0.26-0.81), whereas men had more modest reduced risk of HCC (HR, 0.93; 95% CI, 0.63-1.37). The associations were stronger for caffeinated coffee (HR>3 cups/day vs. non-drinker, 0.71; 95% CI, 0.50-1.01) than decaffeinated coffee (HR, 0.92; 95% CI, 0.55-1.54). There was no association between coffee consumption and ICC. Conclusions: These findings suggest that, in a U.S. population, coffee consumption is associated with reduced risk of HCC. Impact: Further research into specific coffee compounds and mechanisms that may account for these associations is needed. [ABSTRACT FROM AUTHOR]

Background: Time spent sitting is distinctly different from accumulating too little physical activity and may have independent deleterious effects. Few studies have examined the association between sitting time and site-specific cancer incidence. Methods: Among 69,260 men and 77,462 women who were cancer-free and enrolled in the American Cancer Society Cancer Prevention Study II Nutrition Cohort, 18,555 men and 12,236 women were diagnosed with cancer between 1992 and 2009. Extended Cox proportional hazards regression was used to estimate multivariable-adjusted relative risks (RR) and 95% confidence intervals (CI) of leisure-time spent sitting with total and site-specific cancer incidence. Results: Longer leisure-time spent sitting, after adjustment for physical activity, BMI, and other factors, was associated with risk of total cancer in women (RR = 1.10; 95% CI, 1.04â€"1.17 for ≥6 hours vs. <3 hours per day), but not men (RR = 1.00; 95% CI, 0.96â€"1.05). In women, sitting time was associated with risk of multiple myeloma (RR = 1.65; 95% CI, 1.07â€"2.54), invasive breast cancer (RR = 1.10; 95% CI, 1.00â€"1.21), and ovarian cancer (RR = 1.43; 95% CI, 1.10â€"1.87). There were no associations between sitting time and site-specific cancers in men. Conclusion: Longer leisure-time spent sitting was associated with a higher risk of total cancer risk in women, and specifically with multiple myeloma, breast, and ovarian cancers, but sitting time was not associated with cancer risk in men. Further research is warranted to better understand the differences in associations between men and women. Impact: For women, these findings support American Cancer Society guidelines for cancer prevention to reduce sitting time when possible. [ABSTRACT FROM AUTHOR]

The article offers information on the research "Tobacco and Alcohol in Relation to Male Breast Cancer: An Analysis of the Male Breast Cancer Pooling Project Consortium." Topics discussed include use of unconditional logistic regression to estimate study design-specific study and confidence intervals (CI), association of cigarette smoking status, smoking pack-years, and age with male breast cancer risk, and etiologic factors for male breast cancer.

The article discusses a research on the association between circulating polyomavirus antibody levels and risk of non-hodgkin lymphoma (NHL). It mentions three human polyomaviruses have been classified as probable carcinogens. It mentions associations between polyomavirus antibodies and NHL incidence were studies using data from the American Cancer Society Cancer Prevention Study. It mentions human polyomavirus antibody do not predict a higher NHL risk in immunocompetent individuals.

The article presents a study regarding establishment of the Cancer Prevention Study II Nutrition Cohort Colorectal Tissue Repository, from which archived surgical tissues were collected to better understand colorectal cancer etiology and prognosis. The study reveals that the most important elements in forming a repository include having the cases' hospital contact & surgical accession information. Also the study mentions that the repository can be used as resource for colorectal cancer studies.

The articles discusses a study which examined the association of total recreational physical activity, walking and leisure-time sitting with postmenopausal breast cancer incidence. Topics covered include relations of estrogen receptor (ER) status, body mass index (BMI), adult weight gain, and postmenopausal hormones (PMH) use to cancer incidence, and an inverse association between physical activity and postmenopausal breast cancer.

The article presents the study which examined the association between single-nucleotide polymorphisms (SNP) in or near β-carotene 15,15'-monooxygenase 1 (BCMO1) and breast cancer risk in the National Cancer Institute's (NCI) Breast and Prostate Cancer Cohort Consortium (BPC3). Also cited are the major carotenoids in the U.S. like lycopene, lutein and zeaxanthin (3-5), as well as the effects of menopausal status, smoking status, and alcohol intake to breast cancer.

The article discusses the association of hay fever and asthma to colorectal cancer mortality and incidence based on the findings of the Cancer Prevention Study I (CPS-I) conducted from 1959 to 1972, CPS-II conducted from 1982 to 2008, and the CPS-II Nutrition Cohort conducted from 1993 to 2007. Topics covered include the highlights of the CPS-1, CPS-II and CPS-II Nutrition Cohort, the statistical analyses used in determining the association, and the analyzed Iowa Women's Health Study (IWHS).