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In 2018, the authors reported estimates of the number and proportion of cancers attributable to potentially modifiable risk factors in 2014 in the United States. These data are useful for advocating for and informing cancer prevention and control. Herein, based on up‐to‐date relative risk and cancer occurrence data, the authors estimated the proportion and number of invasive cancer cases (excluding nonmelanoma skin cancers) and deaths, overall and for 30 cancer types among adults who were aged 30 years and older in 2019 in the United States, that were attributable to potentially modifiable risk factors. These included cigarette smoking; second‐hand smoke; excess body weight; alcohol consumption; consumption of red and processed meat; low consumption of fruits and vegetables, dietary fiber, and dietary calcium; physical inactivity; ultraviolet radiation; and seven carcinogenic infections. Numbers of cancer cases and deaths were obtained from data sources with complete national coverage, risk factor prevalence estimates from nationally representative surveys, and associated relative risks of cancer from published large‐scale pooled or meta‐analyses. In 2019, an estimated 40.0% (713,340 of 1,781,649) of all incident cancers (excluding nonmelanoma skin cancers) and 44.0% (262,120 of 595,737) of all cancer deaths in adults aged 30 years and older in the United States were attributable to the evaluated risk factors. Cigarette smoking was the leading risk factor contributing to cancer cases and deaths overall (19.3% and 28.5%, respectively), followed by excess body weight (7.6% and 7.3%, respectively), and alcohol consumption (5.4% and 4.1%, respectively). For 19 of 30 evaluated cancer types, more than one half of the cancer cases and deaths were attributable to the potentially modifiable risk factors considered in this study. Lung cancer had the highest number of cancer cases (201,660) and deaths (122,740) attributable to evaluated risk factors, followed by female breast cancer (83,840 cases), skin melanoma (82,710), and colorectal cancer (78,440) for attributable cases and by colorectal (25,800 deaths), liver (14,720), and esophageal (13,600) cancer for attributable deaths. Large numbers of cancer cases and deaths in the United States are attributable to potentially modifiable risk factors, underscoring the potential to substantially reduce the cancer burden through broad and equitable implementation of preventive initiatives. [ABSTRACT FROM AUTHOR]

Background: Studies show that regular moderate to vigorous physical activity is associated with a lower risk of cardiovascular disease, certain cancers, and premature death, but few studies have examined associations of light-intensity physical activity (LPA) and mortality, especially among older adults.Objectives: The aim of this study was to investigate the association of LPA with the risks of death from all causes, cancer, cardiovascular diseases, and respiratory diseases among older adults in the Cancer Prevention Study-II Nutrition Cohort (CPS-II NC).Methods: Analyses included 123,232 participants in CPS-II NC, among whom 46,829 died during follow-up (1993-2014). Cox proportional hazards regression models were used to estimate hazard ratios (HR) and 95% confidence intervals (95% CI) for self-reported leisure time LPA associated with mortality.Results: Engaging in little or no LPA (<3 metabolic equivalent [MET]-h/week) was associated with a 16% higher risk of all-cause mortality (HR 1.16, 95% CI 1.12-1.20) compared to engaging in some LPA (3 to <9 MET-h/week) after adjusting for moderate to vigorous physical activity. However, there was no evidence of a dose-response relationship. A statistically significant interaction with age suggested that more LPA was associated with a lower risk of respiratory disease mortality only among participants aged ≥70 years (21+ vs. 3 to <9 MET-h/week, HR 0.78, 95% CI 0.66-0.91; pint = 0.003).Conclusions: In this prospective study of older adults, accumulating little/no leisure time LPA was associated with a higher risk of mortality. It is of substantial public health value to demonstrate the potential benefits of engaging in any activity, even if light in intensity, among older adults given the aging US population. [ABSTRACT FROM AUTHOR]

Background: Excess body weight is an established cause of postmenopausal breast cancer, but it is unknown if weight loss reduces risk.Methods: Associations between weight change and risk of breast cancer were examined among women aged 50 years and older in the Pooling Project of Prospective Studies of Diet and Cancer. In 10 cohorts, weight assessed on three surveys was used to examine weight change patterns over approximately 10 years (interval 1 median = 5.2 years; interval 2 median = 4.0 years). Sustained weight loss was defined as no less than 2 kg lost in interval 1 that was not regained in interval 2. Among 180 885 women, 6930 invasive breast cancers were identified during follow-up.Results: Compared with women with stable weight (±2 kg), women with sustained weight loss had a lower risk of breast cancer. This risk reduction was linear and specific to women not using postmenopausal hormones (>2-4.5 kg lost: hazard ratio [HR] = 0.82, 95% confidence interval [CI] = 0.70 to 0.96; >4.5-<9 kg lost: HR = 0.75, 95% CI = 0.63 to 0.90; ≥9 kg lost: HR = 0.68, 95% CI = 0.50 to 0.93). Women who lost at least 9 kg and gained back some (but not all) of it were also at a lower risk of breast cancer. Other patterns of weight loss and gain over the two intervals had a similar risk of breast cancer to women with stable weight.Conclusions: These results suggest that sustained weight loss, even modest amounts, is associated with lower breast cancer risk for women aged 50 years and older. Breast cancer prevention may be a strong weight-loss motivator for the two-thirds of American women who are overweight or obese. [ABSTRACT FROM AUTHOR]

The American Cancer Society (ACS) publishes the Diet and Physical Activity Guideline to serve as a foundation for its communication, policy, and community strategies and, ultimately, to affect dietary and physical activity patterns among Americans. This guideline is developed by a national panel of experts in cancer research, prevention, epidemiology, public health, and policy, and reflects the most current scientific evidence related to dietary and activity patterns and cancer risk. The ACS guideline focuses on recommendations for individual choices regarding diet and physical activity patterns, but those choices occur within a community context that either facilitates or creates barriers to healthy behaviors. Therefore, this committee presents recommendations for community action to accompany the 4 recommendations for individual choices to reduce cancer risk. These recommendations for community action recognize that a supportive social and physical environment is indispensable if individuals at all levels of society are to have genuine opportunities to choose healthy behaviors. This 2020 ACS guideline is consistent with guidelines from the American Heart Association and the American Diabetes Association for the prevention of coronary heart disease and diabetes as well as for general health promotion, as defined by the 2015 to 2020 Dietary Guidelines for Americans and the 2018 Physical Activity Guidelines for Americans. [ABSTRACT FROM AUTHOR]

Higher body mass index (BMI; weight (kg)/height (m)2) is associated with increased risk of pancreatic cancer in epidemiologic studies. However, BMI has usually been assessed at older ages, potentially underestimating the full impact of excess weight. We examined the association between BMI and pancreatic cancer mortality among 963,317 adults who were aged 30–89 years at their enrollment in Cancer Prevention Study II in 1982. During follow-up through 2014, a total of 8,354 participants died of pancreatic cancer. Hazard ratios per 5 BMI units, calculated using proportional hazards regression, declined steadily with age at BMI assessment, from 1.25 (95% confidence interval: 1.18, 1.33) in persons aged 30–49 years at enrollment to 1.13 (95% confidence interval: 1.02, 1.26) in those aged 70–89 years at enrollment (P for trend = 0.005). On the basis of a hazard ratio of 1.25 per 5 BMI units at age 45 years, we estimated that 28% of US pancreatic cancer deaths among persons born in 1970–1974 will be attributable to BMI ≥25.0—nearly twice the equivalent proportion of those born in the 1930s, a birth cohort with much lower BMI in middle age. These results suggest that BMI before age 50 years is more strongly associated with pancreatic cancer risk than BMI at older ages, and they underscore the importance of avoiding excess weight gain before middle age for preventing this highly fatal cancer. [ABSTRACT FROM AUTHOR]

Purpose: Histopathologic grade provides an integrated measure of biologic features which affects cancer prognosis. In invasive ductal breast cancer (IDBC), the grade of the ductal carcinoma in situ (DCIS) and invasive components are usually concordant, suggesting grade is established early in tumorigenesis and may be linked to etiologic factors. In this study, we used prospectively collected data from postmenopausal women in the Cancer Prevention Study-II (CPS-II) Nutrition Cohort to compare risk factor associations among low-grade and high-grade DCIS, as well as low-grade and high-grade IDBC.Methods: Among 73,825 cancer-free women at enrollment in the CPS-II Nutrition Cohort in 1992-1993 (mean age: 62.1 years), we verified 802 diagnosed with DCIS (C50 8500/2; n = 430 low-grade and 372 high-grade) and 3,125 with IDBC (C50 8500/3; n = 2,221 low-grade and 904 high-grade) through June 2013. Person-time contribution was conditional on screening mammograms self-reported on biennial surveys. Multivariable-adjusted joint Cox proportional hazards regression models were used to estimate hazard ratios (HR) and 95% confidence intervals (CI).Results: A personal history of benign breast disease was more strongly associated with higher risk of low-grade DCIS (HR = 2.20, 95% CI 1.81-2.67; p for heterogeneity = 0.0004) than high-grade DCIS. Consumption of two or more alcoholic drinks/day was only associated with a higher risk of low-grade IDBC (HR = 1.58, 95% CI 1.33-1.88; p for heterogeneity = 0.005).Conclusions: These results suggest heterogeneity by grade for breast cancer etiology. Identification of potential risk factor differences among low-grade and high-grade DCIS and IDBC may help to clarify associations, and ultimately, improve breast cancer risk prediction models. [ABSTRACT FROM AUTHOR]

Social isolation is associated with higher mortality in studies comprising mostly white adults, yet associations among black adults are unclear. In this prospective cohort study, we evaluated whether associations of social isolation with all-cause, cardiovascular disease, and cancer mortality differed by race and sex. Adults enrolled in Cancer Prevention Study II in 1982/1983 were followed for mortality through 2012 (n = 580,182). Sex- and race-specific multivariable-adjusted hazard ratios and 95% confidence intervals were estimated for associations of a 5-point social isolation score with risk of death. Social isolation was associated with all-cause mortality in all subgroups (P for trend ≤ 0.005); for the most isolated versus the least isolated, the hazard ratios were 2.34 (95% confidence interval (CI): 1.58, 3.46) and 1.60 (95% CI: 1.41, 1.82) among black men and white men, respectively (P for interaction = 0.40) and 2.13 (95% CI: 1.44, 3.15) and 1.84 (95% CI: 1.68, 2.01) among black women and white women, respectively (P for interaction = 0.89). The association did not differ between black men and black women (P for interaction = 0.33) but was slightly stronger in white women than in white men (P for interaction = 0.01). Social isolation was associated with cardiovascular disease mortality in each subgroup (P for trend < 0.03) but with cancer mortality only among whites (P for trend < 0.0001). Subgroup differences in the influence of specific social isolation components were identified. Identifying and intervening with socially isolated adults could improve health outcomes. [ABSTRACT FROM AUTHOR]

In the United States, it is estimated that more than 1.7 million people will be diagnosed with cancer, and more than 600,000 will die of the disease in 2018. The financial costs associated with cancer risk factors and cancer care are enormous. To substantially reduce both the number of individuals diagnosed with and dying from cancer and the costs associated with cancer each year in the United States, government and industry and the public health, medical, and scientific communities must work together to develop, invest in, and implement comprehensive cancer control goals and strategies at the national level and expand ongoing initiatives at the state and local levels. This report is the second in a series of articles in this journal that, together, describe trends in cancer rates and the scientific evidence on cancer prevention, early detection, treatment, and survivorship to inform the identification of priorities for a comprehensive cancer control plan. Herein, we focus on existing evidence about established, modifiable risk factors for cancer, including prevalence estimates and the cancer burden due to each risk factor in the United States, and established primary prevention recommendations and interventions to reduce exposure to each risk factor. [ABSTRACT FROM AUTHOR]

The majority of leisure time is spent in sedentary behaviors such as television viewing. Studies have documented that prolonged leisure-time sitting is associated with higher risk of mortality—total, cardiovascular disease, cancer, and "all other causes"—but few have examined the "other" causes of death in detail. To examine associations of leisure-time sitting with risk of specific causes of death, we analyzed data from the Cancer Prevention Study II (CPS-II) Nutrition Cohort, a prospective US cohort including 127,554 men and women who were free of major chronic disease at study entry, and among whom 48,784 died during 21 years of follow-up (1993–2014; median follow-up, 20.3 years, interquartile range, 4.6 years). After multivariable adjustment, prolonged leisure-time sitting (≥6 vs. <3 hours per day) was associated with higher risk of mortality from all causes, cardiovascular disease (including coronary heart disease and stroke-specific mortality), cancer, diabetes, kidney disease, suicide, chronic obstructive pulmonary disease, pneumonitis due to solids and liquids, liver, peptic ulcer and other digestive disease, Parkinson disease, Alzheimer disease, nervous disorders, and musculoskeletal disorders. These findings provide additional evidence for associations between a broad range of mortality outcomes and prolonged sitting time. Given the pervasive nature of sitting in the contemporary lifestyle, this study further supports the recommendation that encouraging individuals to reduce sedentary time may provide health benefits. [ABSTRACT FROM AUTHOR]

Background: Alcohol consumption is associated with a higher risk of colorectal cancer, but to the authors' knowledge its influence on survival after a diagnosis of colorectal cancer is unclear. The authors investigated associations between prediagnosis and postdiagnosis alcohol intake with mortality among survivors of colorectal cancer.Methods: The authors identified 2458 men and women who were diagnosed with invasive, nonmetastatic colorectal cancer between 1992 (enrollment into the Cancer Prevention Study II Nutrition Cohort) and 2011. Alcohol consumption was self-reported at baseline and updated in 1997, 1999, 2003, and 2007. Postdiagnosis alcohol data were available for 1599 participants.Results: Of the 2458 participants diagnosed with colorectal cancer, 1156 died during follow-up through 2012. Prediagnosis and postdiagnosis alcohol consumption were not found to be associated with all-cause mortality, except for an association between prediagnosis consumption of <2 drinks per day and a slightly lower risk of all-cause mortality (relative risk [RR], 0.86; 95% confidence interval [95% CI], 0.74-1.00) compared with never drinking. Alcohol use was generally not associated with colorectal cancer-specific mortality, although there was some suggestion of increased colorectal cancer-specific mortality with postdiagnosis drinking (RR, 1.27 [95% CI, 0.87-1.86] for current drinking of <2 drinks/day and RR, 1.44 [95% CI, 0.80-2.60] for current drinking of ≥2 drinks/day).Conclusions: The results of the current study do not support an association between alcohol consumption and all-cause mortality among individuals with nonmetastatic colorectal cancer. The association between postdiagnosis drinking and colorectal cancer-specific mortality should be examined in larger studies of individuals diagnosed with nonmetastatic colorectal cancer. Cancer 2017;123:2006-2013. © 2017 American Cancer Society. [ABSTRACT FROM AUTHOR]

Background: Prospective cohort studies contribute importantly to understanding the role of lifestyle, genetic, and other factors in chronic disease etiology.Methods: The American Cancer Society (ACS) recruited a new prospective cohort study, Cancer Prevention Study 3 (CPS-3), between 2006 and 2013 from 35 states and Puerto Rico. Enrollment took place primarily at ACS community events and at community enrollment "drives." At enrollment sites, participants completed a brief survey that included an informed consent, identifying information necessary for follow-up, and key exposure information. They also provided a waist measure and a nonfasting blood sample. Most participants also completed a more comprehensive baseline survey at home that included extensive medical, lifestyle, and other information. Participants will be followed for incident cancers through linkage with state cancer registries and for cause-specific mortality through linkage with the National Death Index.Results: In total, 303,682 participants were enrolled. Of these, 254,650 completed the baseline survey and are considered "fully" enrolled; they will be sent repeat surveys periodically for at least the next 20 years to update exposure information. The remaining participants (n = 49,032) will not be asked to update exposure information but will be followed for outcomes. Twenty-three percent of participants were men, 17.3% reported a race or ethnicity other than "white," and the median age at enrollment was 47 years.Conclusions: CPS-3 will be a valuable resource for studies of cancer and other outcomes because of its size; its diversity with respect to age, ethnicity, and geography; and the availability of blood samples and detailed questionnaire information collected over time. Cancer 2017;123:2014-2024. © 2017 American Cancer Society. [ABSTRACT FROM AUTHOR]

Rationale: Tropospheric ozone (O3) is potentially associated with cardiovascular disease risk and premature death. Results from long-term epidemiological studies on O3 are scarce and inconclusive.Objectives: In this study, we examined associations between chronic ambient O3 exposure and all-cause and cause-specific mortality in a large cohort of U.S. adults.Methods: Cancer Prevention Study II participants were enrolled in 1982. A total of 669,046 participants were analyzed, among whom 237,201 deaths occurred through 2004. We obtained estimates of O3 concentrations at the participant's residence from a hierarchical Bayesian space-time model. Estimates of fine particulate matter (particulate matter with an aerodynamic diameter of up to 2.5 μm [PM2.5]) and NO2 concentrations were obtained from land use regression. Cox proportional hazards regression models were used to examine mortality associations adjusted for individual- and ecological-level covariates.Measurements and Main Results: In single-pollutant models, we observed significant positive associations between O3, PM2.5, and NO2 concentrations and all-cause and cause-specific mortality. In two-pollutant models adjusted for PM2.5, significant positive associations remained between O3 and all-cause (hazard ratio [HR] per 10 ppb, 1.02; 95% confidence interval [CI], 1.01-1.04), circulatory (HR, 1.03; 95% CI, 1.01-1.05), and respiratory mortality (HR, 1.12; 95% CI, 1.08-1.16) that were unchanged with further adjustment for NO2. We also observed positive mortality associations with both PM2.5 (both near source and regional) and NO2 in multipollutant models.Conclusions: Findings derived from this large-scale prospective study suggest that long-term ambient O3 contributes to risk of respiratory and circulatory mortality. Substantial health and environmental benefits may be achieved by implementing further measures aimed at controlling O3 concentrations. [ABSTRACT FROM AUTHOR]

Background: Calcium intake may be important for bone health, but its effects on other outcomes, including cardiovascular disease (CVD) and cancer, remain unclear. Recent reports of adverse cardiovascular effects of supplemental calcium have raised concerns. Objective: We investigated associations of supplemental, dietary, and total calcium intakes with all-cause, CVD-specific, and cancer-specific mortality in a large, prospective cohort. Design: A total of 132,823 participants in the Cancer Prevention Study II Nutrition Cohort, who were followed from baseline (1992 or 1993) through 2012 for mortality outcomes, were included in the analysis. Dietary and supplemental calcium information was first collected at baseline and updated in 1999 and 2003. Multivariable-adjusted Cox proportional hazards models with cumulative updating of exposures were used to calculate RRs and 95% CIs for associations between calcium intake and mortality. Results: During a mean follow-up of 17.5 y, 43,186 deaths occurred. For men, supplemental calcium intake was overall not associated with mortality outcomes (P-trend > 0.05 for all), but men who were taking ≥1000 mg supplemental calcium/d had a higher risk of all-cause mortality (RR: 1.17; 95% CI: 1.03, 1.33), which was primarily attributed to borderline statistically significant higher risk of CVD-specific mortality (RR: 1.22; 95% CI: 0.99, 1.51). For women, supplemental calcium was inversely associated with mortality from all causes [RR (95% CI): 0.90 (0.87, 0.94), 0.84 (0.80, 0.88), and 0.93 (0.87, 0.99) for intakes of 0.1 to <500, 500 to <1000, and ≥1000 mg/d, respectively; P-trend < 0.01]. Total calcium intake was inversely associated with mortality in women (P-trend < 0.01) but not in men; dietary calcium was not associated with all-cause mortality in either sex. Conclusions: In this cohort, associations of calcium intake and mortality varied by sex. For women, total and supplemental calcium intakes are associated with lower mortality, whereas for men, supplemental calcium intake ≥1000 mg/d may be associated with higher all-cause and CVD-specific mortality. [ABSTRACT FROM AUTHOR]

Purpose: Physical activity is hypothesized to lower the risk of ovarian cancer, but current evidence for an association is limited and inconclusive. The purpose of this study was to examine moderate-to-vigorous physical activity, walking, and leisure-time sitting in relation to incident ovarian cancer, overall and by histologic subtype.Methods: Moderate-vigorous recreational physical activity (MET-hours/week), recreational walking, and leisure-time sitting were examined in relation to epithelial ovarian cancer in the American Cancer Society Cancer Prevention Study II Nutrition Cohort, a US cohort followed for cancer incidence from 1992 to 2011. Exposure information was collected via self-administered questionnaires. Cox proportional hazards regression was used to estimate multivariable-adjusted relative risks (RRs) and 95% confidence intervals (CIs) of total, serous, and nonserous ovarian cancer according to MET-hours/week, hours/week of walking, and hours/day of sitting.Results: Among 63,972 postmenopausal women, 651 cases of ovarian cancer were identified during follow-up. Neither MET-hours/week nor walking was associated with risk. However, ≥6 h/day of sitting, compared to <3, was associated with higher risk of ovarian cancer (RR 1.44, 95% CI 1.12-1.85), particularly for serous cancer (RR 1.52, 95% CI 1.06-2.16), although statistical heterogeneity by histology was not detected (p = 0.36).Conclusions: Results from this study do not support an association between physical activity and ovarian cancer, whereas prolonged sitting may be associated with higher risk. Additional large studies are needed to further assess possible etiologic differences by histologic subtype. [ABSTRACT FROM AUTHOR]

The International Agency for Research on Cancer recently classified outdoor air pollution and airborne particulate matter as carcinogenic to humans. However, there are gaps in the epidemiologic literature, including assessment of possible joint effects of cigarette smoking and fine particulate matter (particulate matter less than or equal to 2.5 µm in diameter) on lung cancer risk. We present estimates of interaction on the additive scale between these risk factors from Cancer Prevention Study II, a large prospective US cohort study of nearly 1.2 million participants recruited in 1982. Estimates of the relative excess risk of lung cancer mortality due to interaction, the attributable proportion due to interaction, and the synergy index were 2.19 (95% confidence interval (CI): −0.10, 4.83), 0.14 (95% CI: 0.00, 0.25), and 1.17 (95% CI: 1.00, 1.37), respectively, using the 25th and 75th percentiles as cutpoints for fine particulate matter. This suggests small increases in lung cancer risk among persons with both exposures beyond what would be expected from the sum of the effects of the individual exposures alone. Although reductions in cigarette smoking will achieve the greatest impact on lung cancer rates, these results suggest that attempted reductions in lung cancer risk through both tobacco control and air quality management may exceed expectations based on reducing exposure to either risk factor alone. [ABSTRACT FROM PUBLISHER]

Little is known about the risk of non-Hodgkin lymphoma (NHL) in nonsmokers who are exposed to environmental tobacco smoke (ETS). Previous research on NHL and ETS has not included men or examined doses of ETS exposure during childhood. The Cancer Prevention Study II Nutrition Cohort collected information on smoking habits and exposure to ETS during childhood and adulthood. Among 61,326 never-smoking men and women, 884 incident cases of NHL were identified between 1992 and 2009. Multivariable-adjusted relative risks and 95% confidence intervals were calculated using Cox proportional hazards regression to identify associations between ETS and NHL risk. Compared with no exposure to ETS as a child or an adult, childhood and/or adult ETS exposure was not associated with NHL overall. There was a positive association between the number of smokers in the house as a child (P for trend = 0.05) and exposure to 6 or more hours per week of ETS as an adult (relative risk = 2.37, 95% confidence interval: 1.12, 5.04) with follicular lymphoma risk. Adult ETS exposure was associated with a lower risk of diffuse large B-cell lymphoma (relative risk = 0.68, 95% confidence interval: 0.48, 0.97). This study suggests that adult and childhood ETS exposure may affect the risk of NHL, and that the associations differ by histological subtype. [ABSTRACT FROM PUBLISHER]

Higher dietary intakes of flavonoids and proanthocyanidins have been associated with a lower risk of several cancers. Few prospective epidemiologic studies have examined individual flavonoids and proanthocyanidins in relation to prostate cancer. We examined these associations in a prospective US cohort of 43,268 men with a mean age of 70 years who completed detailed self-administered questionnaires in 1999–2000. During a mean follow-up of 7.8 years, 3,974 total prostate cancers, including 567 high-grade cases and 362 advanced cases, were ascertained. Cox proportional hazards regression models were used to calculate multivariable-adjusted relative risks and 95% confidence intervals. Residual energy-adjusted total flavonoids (for fifth quintile vs. first quintile, relative risk = 1.11, 95% confidence interval: 1.01, 1.23; P for trend = 0.02) and several subclasses were positively associated with overall prostate cancer risk, mostly limited to the top quintile and the first 2 years of follow-up. The associations for total flavonoids, flavan-3-ols, and proanthocyanidins with high-grade prostate cancer risk varied by follow-up time. During follow-up from 2002 to 2009, we observed suggestive inverse trends with higher total flavonoids (P for trend = 0.05) and proanthocyanidins (P for trend = 0.04) with high-grade prostate cancer, but not with advanced prostate cancer. Although evidence is limited, a possible role of total flavonoids and proanthocyanidins in prostate cancer tumor progression deserves further study. [ABSTRACT FROM PUBLISHER]

Tubal sterilization is a common form of contraception in the United States and is hypothesized to be associated with a lower risk of breast cancer. However, prior observational studies have reported inconsistent results. We investigated the association between tubal sterilization and breast cancer risk among 77,249 postmenopausal, cancer-free women in the Cancer Prevention Study II (CPS-II) Nutrition Cohort, enrolled in 21 states in the United States during 1992–1993. During 15 years of follow-up through June 30, 2007, 4,084 invasive breast cancer cases were diagnosed. Multivariable Cox proportional hazard regression was used to estimate hazard ratios and 95% confidence intervals. A meta-analysis including the CPS-II Nutrition Cohort results with other published results from 4 case-control studies and 3 prospective studies was conducted to provide a summary estimate for the association between tubal sterilization and breast cancer risk. In the CPS-II Nutrition Cohort, tubal sterilization was not associated with breast cancer incidence (multivariable-adjusted hazard ratio = 1.08, 95% confidence interval: 0.97, 1.20). Associations stratified by year of tubal sterilization, age, and time since surgery were also null. The meta-analysis also found no association between tubal sterilization and breast cancer risk (odds ratio = 0.97, 95% confidence interval: 0.84, 1.09). Tubal sterilization does not appear to be associated with breast cancer risk. [ABSTRACT FROM PUBLISHER]

Epidemiologic studies suggest that coffee intake is associated with reduced risk of oral/pharyngeal cancer. The authors examined associations of caffeinated coffee, decaffeinated coffee, and tea intake with fatal oral/pharyngeal cancer in the Cancer Prevention Study II, a prospective US cohort study begun in 1982 by the American Cancer Society. Among 968,432 men and women who were cancer free at enrollment, 868 deaths due to oral/pharyngeal cancer occurred during 26 years of follow-up. Cox proportional hazards regression was used to estimate multivariable-adjusted relative risk. Intake of >4 cups/day of caffeinated coffee was associated with a 49% lower risk of oral/pharyngeal cancer death relative to no/occasional coffee intake (relative risk = 0.51, 95% confidence interval: 0.40, 0.64) (1 cup/day = 237 ml). A dose-related decline in relative risk was observed with each single cup/day consumed (Ptrend < 0.001). The association was not modified by sex, smoking status, or alcohol use. An inverse association for >2 cups/day of decaffeinated coffee intake was suggested (relative risk = 0.61, 95% confidence interval: 0.37, 1.01). No association was found for tea drinking. In this large prospective study, caffeinated coffee intake was inversely associated with oral/pharyngeal cancer mortality. Research is needed to elucidate biologic mechanisms whereby coffee might help to protect against these often fatal cancers. [ABSTRACT FROM PUBLISHER]

Radon is a known cause of human lung cancer. Previously, the authors observed a significant positive association between mean county-level residential radon concentrations and lung cancer mortality in the Cancer Prevention Study II (CPS-II), a large prospective study of nearly 1.2 million participants recruited in 1982 by the American Cancer Society. There was also a significant positive association with mortality from chronic obstructive pulmonary disease. Because it is unclear whether radon is associated with mortality from other malignant or nonmalignant disease, the authors examined the association between radon and nonrespiratory mortality in the CPS-II. Mean county-level residential radon concentrations (mean = 53.5 (standard deviation: 38.0) Bq/m3) were linked to participants by their zip code at enrollment. Cox proportional hazards regression models were used to estimate adjusted hazard ratios and 95% confidence intervals for all-cause (excluding lung cancer and respiratory mortality) and cause-specific mortality associated with radon concentrations. A total of 811,961 participants in 2,754 counties were analyzed, including 265,477 deaths through 2006. There were no clear associations between radon and nonrespiratory mortality in the CPS-II. These findings suggest that residential radon is not associated with any other mortality beyond lung cancer or chronic obstructive pulmonary disease. [ABSTRACT FROM AUTHOR]

Background A recent pooled analysis of randomized trials of daily aspirin for prevention of vascular events found a substantial reduction (relative risk [RR] = 0.63, 95% confidence interval [CI] = 0.49 to 0.82) in overall cancer mortality during follow-up occurring after 5 years on aspirin. However, the magnitude of the effect of daily aspirin use, particularly long-term use, on cancer mortality is uncertain. Methods We examined the association between daily aspirin use and overall cancer mortality among 100 139 men and women with no history of cancer in the Cancer Prevention Study II Nutrition Cohort. Cox proportional hazards regression models were used to estimate multivariable-adjusted relative risks (RRs) and 95% confidence intervals (CIs). Results Between 1997 and 2008, 5138 participants died from cancer. Compared with no use, daily aspirin use at baseline was associated with slightly lower cancer mortality, regardless of duration of daily use (for <5 years of use, RR = 0.92, 95% CI = 0.85 to 1.01; for ≥5 years of use, RR = 0.92, 95% CI = 0.83 to 1.02). Associations were slightly stronger in analyses that used updated aspirin information from periodic follow-up questionnaires and included 3373 cancer deaths (for <5 years of use, RR = 0.84, 95% CI = 0.76 to 0.94; for ≥5 years of use, RR = 0.84, 95% CI = 0.75 to 0.95). Conclusion These results are consistent with an association between recent daily aspirin use and modestly lower cancer mortality but suggest that any reduction in cancer mortality may be smaller than that observed with long-term aspirin use in the pooled trial analysis. [ABSTRACT FROM PUBLISHER]

Although several studies have shown a lower risk of non-Hodgkin lymphoma (NHL) in alcohol drinkers compared with nondrinkers, the dose-response relation and potential differences between former and current drinking and across beverage types and subtypes are unclear. The authors examined associations of alcohol intake with risk of NHL and NHL subtypes in the Cancer Prevention Study II Nutrition Cohort, a prospective study of US men and women aged 50–74 years. Between 1992 and 2007, there were 1,991 incident NHL cases among 143,124 participants. Multivariable-adjusted relative risks and 95% confidence intervals were computed using Cox proportional hazards regression. Compared with nondrinkers, the relative risk of NHL associated with former drinking was 0.90 (95% confidence interval (CI): 0.75, 1.10); the relative risks associated with current intakes of <1, 1–2, and >2 drinks/day were 0.93 (95% CI: 0.83, 1.03), 0.91 (95% CI: 0.78, 1.06), and 0.78 (95% CI: 0.65, 0.93), respectively. Associations did not differ by sex (P-interaction = 0.45) or beverage type (P-difference = 0.22). Alcohol intake was more strongly associated with B-cell lymphoma (P-trend = 0.005) than with T-cell lymphoma (P-trend = 0.76), and associations were similar among B-cell lymphoma subtypes. In this prospective study, current heavy alcohol intake was associated with a reduced risk of NHL. Associations did not differ by beverage type and were slightly stronger for B-cell tumors than for T-cell tumors. [ABSTRACT FROM PUBLISHER]

Background: Lung cancer and cardiovascular disease (CVD) mortality risks increase with smoking, secondhand smoke (SHS), and exposure to fine particulate matter < 2.5 μm in diameter (PM2.5) from ambient air pollution. Recent research indicates that the exposure-response relationship for CVD is nonlinear, with a steep increase in risk at low exposures and flattening out at higher exposures. Comparable estimates of the exposure-response relationship for lung cancer are required for disease burden estimates and related public health policy assessments.Objectives: We compared exposure-response relationships of PM2.5 with lung cancer and cardiovascular mortality and considered the implications of the observed differences for efforts to estimate the disease burden of PM2.5.Methods: Prospective cohort data for 1.2 million adults were collected by the American Cancer Society as part of the Cancer Prevention Study II. We estimated relative risks (RRs) for increments of cigarette smoking, adjusting for various individual risk factors. RRs were plotted against estimated daily dose of PM2.5 from smoking along with comparison estimates for ambient air pollution and SHS. Results: For lung cancer mortality, excess risk rose nearly linearly, reaching maximum RRs > 40 among long-term heavy smokers. Excess risks for CVD mortality increased steeply at low exposure levels and leveled off at higher exposures, reaching RRs of approximately 2-3 for cigarette smoking. Conclusions: The exposure-response relationship associated with PM2.5 is qualitatively different for lung cancer versus cardiovascular mortality. At low exposure levels, cardiovascular deaths are projected to account for most of the burden of disease, whereas at high levels of PM2.5, lung cancer becomes proportionately more important. [ABSTRACT FROM AUTHOR]

The obesity epidemic is attributed in part to reduced physical activity. Evidence supports that reducing time spent sitting, regardless of activity, may improve the metabolic consequences of obesity. Analyses were conducted in a large prospective study of US adults enrolled by the American Cancer Society to examine leisure time spent sitting and physical activity in relation to mortality. Time spent sitting and physical activity were queried by questionnaire on 53,440 men and 69,776 women who were disease free at enrollment. The authors identified 11,307 deaths in men and 7,923 deaths in women during the 14-year follow-up. After adjustment for smoking, body mass index, and other factors, time spent sitting (≥6 vs. <3 hours/day) was associated with mortality in both women (relative risk = 1.34, 95% confidence interval (CI): 1.25, 1.44) and men (relative risk = 1.17, 95% CI: 1.11, 1.24). Relative risks for sitting (≥6 hours/day) and physical activity (<24.5 metabolic equivalent (MET)-hours/week) combined were 1.94 (95% CI: 1.70, 2.20) for women and 1.48 (95% CI: 1.33, 1.65) for men, compared with those with the least time sitting and most activity. Associations were strongest for cardiovascular disease mortality. The time spent sitting was independently associated with total mortality, regardless of physical activity level. Public health messages should include both being physically active and reducing time spent sitting. [ABSTRACT FROM PUBLISHER]

The article discusses a research study about the association between waist circumference (WC) and all-cause mortality in a large U.S. cohort. The researchers found high levels of association of WC with an approximately two-fold higher risk of mortality in men and women after adjustment of body mass index (BMI) and other risk factors. Among men, normal, overweight and obese BMI categories, the study found a positive association between WC and mortality.

Epidemiologic evidence suggests that cancer incidence is associated with diabetes as well as certain diabetes risk factors and treatments. This consensus statement of experts assembled jointly by the American Diabetes Association and the American Cancer Society reviews the state of science concerning 1) the association between diabetes and cancer incidence or prognosis; 2) risk factors common to both diabetes and cancer; 3) possible biologic links between diabetes and cancer risk; and 4) whether diabetes treatments influence the risk of cancer or cancer prognosis. In addition, key unanswered questions for future research are posed. CA Cancer J Clin 2010. © 2010 American Cancer Society, Inc. [ABSTRACT FROM AUTHOR]

Several studies have shown a positive association between acculturation and obesity in Hispanics. We sought to examine the association in a sample of urban Hispanic women. Using data collected in the Chicago Breast Health Project, we used logistic regression to examine the association of obesity (BMI ≥ 30 kg/m2) with language acculturation and years in the US in a sample of 388 Hispanic women. Women self-reported the number of years they had lived in the US (mean 17.6) as well as their preferred language across several domains, which was used to calculate a language acculturation score. Nearly all the women (98%) were born outside the US with the majority (65%) born in Mexico and the majority of women (69%) had low language acculturation, i.e., answered “only Spanish” in every domain. Over half of the women were obese (56%). In multivariable analysis, odds of obesity was twice as high among women living in the US for greater than 20 years compared to those in the US for 10 years or less (OR/year = 2.07, 95% CI 1.25–3.42). In contrast, low language acculturation was not associated with odds of obesity (OR = 1.14, 95% CI 0.70–1.86). While greater years in the US increased odds of obesity among Hispanic women, no association of obesity with language acculturation was found. These results suggest that mechanisms other than language contribute to the immigration effect. [ABSTRACT FROM AUTHOR]

A letter to the editor is presented in response to the article "Weight Cycling and Cancer Incidence in a Large Prospective US Cohort" by V. L. and colleagues in the 2015 issue.

The authors reflect on the progress of efforts to find a cure for cancer in the U.S. They note the human and economic costs of cancer. They also cite the factors that make the progress in the fight against cancer complicated, including demographic trends, susceptibility to treatment and multiple molecular variants of cancer with different prognosis. They state that the reduction of cigarette smoking in the U.S. is one of the biggest successes to date in the primary prevention of cancer and other chronic diseases during the last 50 years.

Background & Aims: Folate intake has been inversely associated with colorectal cancer risk in several prospective epidemiologic studies. However, no study fully assessed the influence of the high levels of folate that are frequently consumed in the United States as a result of mandatory folate fortification, which was fully implemented in 1998, and the recent increase in use of folate-containing supplements. There is evidence that consumption of high levels of folic acid, the form of folate used for fortification and in supplements, has different effects on biochemical pathways than natural folates and might promote carcinogenesis. Methods: We investigated the association between folate intake and colorectal cancer among 43,512 men and 56,011 women in the Cancer Prevention Study II (CPS-II) Nutrition Cohort; 1023 were diagnosed with colorectal cancer between 1999 and 2007, a period entirely after folate fortification began. Cox proportional hazards regression was used to calculate multivariate hazards ratios (RR) and 95% confidence interval (CI). Results: Intake of high levels of natural folate (RRQ5vsQ1 = 0.86; 95% CI: 0.70–1.06; P trend = .12) or folic acid (RRQ5vsQ1 = 0.84; 95% CI: 0.68–1.03; P trend = .06) were not significantly associated with risk of colorectal cancer. Total folate intake was significantly associated with lower risk (RRQ5vsQ1 = 0.81; 95% CI: 0.66–0.99; P trend = .047). Conclusions: Intake of high levels of total folate reduces risk of colorectal cancer; there is no evidence that dietary fortification or supplementation with this vitamin increases colorectal cancer risk. [ABSTRACT FROM AUTHOR]

Method. Two hundred fifty-six 20-40 year-old Latinas were randomly assigned to the intervention (n=127) or control group (n=129). Data were collected at a baseline and eight-months after randomization. Results. Compared to women who attended 0-2 sessions, those who attended at least three of the 16 sessions reported lower dietary fat (p<.001) and improved BSE proficiency (p<.001). However, there were no differences in fiber intake at eight months. Women who attended at least three sessions were more likely to be lower in acculturation. Conclusions. The optimal length for health-risk reduction interventions is unknown. Our results suggest that, while participation is associated with improved outcomes, fewer sessions than traditionally offered in most behavioral interventions may be sufficient to effect initial behavior change. [ABSTRACT FROM AUTHOR]

Objectives: Secretory leukocyte protease inhibitor (SLPI) is an innate-immunity protein displaying antimicrobial and anti-inflammatory properties that is found in high concentrations in saliva. The role of extracellular salivary SLPI in head and neck squamous cell carcinoma (HNSCC) remains unclear. Thus, we aimed to evaluate the association between SLPI and HNSCC risk in the Cancer Prevention Study II Nutrition Cohort.Materials and Methods: Among 53,180 men and women with no history of cancer who provided an oral rinse between 2001 and 2002, 60 were subsequently diagnosed with incident HNSCC between specimen collection and June 2009. In this nested case-control study, archived oral supernatants were evaluated using the Human SLPI Quantikine ELISA Kit for all 60 cases and 180 controls individually matched on gender, race, date of birth, and date of oral rinse collection. Conditional logistic regression was used to estimate HNSCC risk.Results: Overall, pre-diagnostic salivary SLPI was associated with a non-statistically significant higher risk of HNSCC (OR=1.6, 95% CI=0.9-3.0). Among never smokers, high SLPI was associated with a non-statistically significant lower risk (OR=0.5, 95% CI=0.1-1.9), whereas among ever smokers, high SLPI was associated with a statistically significant higher risk (OR=2.1, 95% CI=1.0-4.3) of HNSCC, compared to low SLPI.Conclusion: While results from this study suggest that higher concentrations of salivary SLPI might increase the risk of HNSCC among ever smokers, more research is needed to verify these findings and define the mechanisms by which SLPI and smoking influence the etiology of HNSCC. [ABSTRACT FROM AUTHOR]

This article presents a study on temporal trends in smoking-related mortality in the U.S. from 1959 to 2010. Mortality risks were compared according to sex and self-reported smoking status in two cohort studies and five pooled contemporary cohort studies. The study concludes that risk of smoking-related mortality continues to increase among women and the increased risks are nearly identical for men and women.

Objective: To evaluate the association of parity, number of live births, and age at first birth with mortality using multivariable-adjusted Cox proportional hazards regression models.Design: Observational cohort.Setting: Not applicable.Patient(s): A total of 424,797 women.Intervention(s): None.Main Outcome Measure(s): All-cause and cause-specific mortality.Result(s): During median follow-up of 24.93 years, 238,324 deaths occurred. Parous, compared with nulliparous, women had lower rates of all-cause (hazards ratio [HR] = 0.94, 95% confidence interval [CI] 0.93-0.96) mortality, driven by heart disease and overall cancer mortality. A linear trend was found for more births and diabetes mortality (P<.001) with having ≥6 births, compared with 2, associated with an HR of 1.28 (95% CI 1.15-1.43). Compared with age at first birth from 20-22 years, age at first birth <20 years was associated with higher mortality rates overall (HR = 1.04, 95% CI 1.02-1.06), driven by heart disease and chronic obstructive pulmonary disease mortality; whereas, ≥35 years was associated with higher overall cancer mortality (HR = 1.13, 95% CI 1.06-1.20).Conclusion(s): Although parity was associated with a slight reduction in rates of all-cause mortality resulting in a minimal impact on average lifespan, the higher diabetes mortality in grand multiparous women might warrant continuous monitoring, particularly for abnormal glucose metabolism, among these women. [ABSTRACT FROM AUTHOR]

The overall 5-year relative survival rate for all cancers combined is now 68%, and there are over 16.9 million survivors in the United States. Evidence from laboratory and observational studies suggests that factors such as diet, physical activity, and obesity may affect risk for recurrence and overall survival after a cancer diagnosis. The purpose of this American Cancer Society guideline is to provide evidence-based, cancer-specific recommendations for anthropometric parameters, physical activity, diet, and alcohol intake for reducing recurrence and cancer-specific and overall mortality. The audiences for this guideline are health care providers caring for cancer survivors as well as cancer survivors and their families. The guideline is intended to serve as a resource for informing American Cancer Society programs, health policy, and the media. Sources of evidence that form the basis of this guideline are systematic literature reviews, meta-analyses, pooled analyses of cohort studies, and large randomized clinical trials published since 2012. Recommendations for nutrition and physical activity during cancer treatment, informed by current practice, large cancer care organizations, and reviews of other expert bodies, are also presented. To provide additional context for the guidelines, the authors also include information on the relationship between health-related behaviors and comorbidities, long-term sequelae and patient-reported outcomes, and health disparities, with attention to enabling survivors' ability to adhere to recommendations. Approaches to meet survivors' needs are addressed as well as clinical care coordination and resources for nutrition and physical activity counseling after a cancer diagnosis., (© 2022 The Authors. CA: A Cancer Journal for Clinicians published by Wiley Periodicals LLC on behalf of American Cancer Society.)

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., (©2021 The Authors; Published by the American Association for Cancer Research.)

Background: Alcohol consumption is an established risk factor for several cancer types, but there are no contemporary published estimates of the state-level burden of cancer attributed to alcoholic beverage consumption. Such estimates are needed to inform public policy and cancer control efforts. We estimated the proportion and number of incident cancer cases and cancer deaths attributable to alcohol consumption by sex in adults aged ≥30 years in all 50 states and the District of Columbia in 2013-2016., Methods: Age-, sex-, and state-specific cancer incidence and mortality data (2013-2016) were obtained from the US Cancer Statistics database. State-level, self-reported age and sex stratified alcohol consumption prevalence was estimated using the 2003-2006 Behavioral Risk Factor Surveillance System surveys and adjusted with state sales data., Results: The proportion of alcohol-attributable incident cancer cases ranged from 2.9 % (95 % confidence interval: 2.7 %-3.1 %) in Utah to 6.7 % (6.4 %-7.0 %) in Delaware among men and women combined, from 2.7 % (2.5 %-3.0 %) in Utah to 6.3 % (5.9 %-6.7 %) in Hawaii among men, and from 2.7 % (2.4 %-3.0 %) in Utah to 7.7 % (7.2 %-8.3 %) in Delaware among women. The proportion of alcohol-attributable cancer deaths also varied considerably across states: from 1.9 % to 4.5 % among men and women combined, from 2.1% to 5.0% among men, and from 1.4 % to 4.4 % among women. Nationally, alcohol consumption accounted for 75,199 cancer cases and 18,947 cancer deaths annually., Conclusion: Alcohol consumption accounts for a considerable proportion of cancer incidence and mortality in all states. Implementing state-level policies and cancer control efforts to reduce alcohol consumption could reduce this cancer burden., (Copyright © 2021 Elsevier Ltd. All rights reserved.)

Background: Excess body weight is an established cause of postmenopausal breast cancer, but it is unknown if weight loss reduces risk., Methods: Associations between weight change and risk of breast cancer were examined among women aged 50 years and older in the Pooling Project of Prospective Studies of Diet and Cancer. In 10 cohorts, weight assessed on three surveys was used to examine weight change patterns over approximately 10 years (interval 1 median = 5.2 years; interval 2 median = 4.0 years). Sustained weight loss was defined as no less than 2 kg lost in interval 1 that was not regained in interval 2. Among 180 885 women, 6930 invasive breast cancers were identified during follow-up., Results: Compared with women with stable weight (±2 kg), women with sustained weight loss had a lower risk of breast cancer. This risk reduction was linear and specific to women not using postmenopausal hormones (>2-4.5 kg lost: hazard ratio [HR] = 0.82, 95% confidence interval [CI] = 0.70 to 0.96; >4.5-<9 kg lost: HR = 0.75, 95% CI = 0.63 to 0.90; ≥9 kg lost: HR = 0.68, 95% CI = 0.50 to 0.93). Women who lost at least 9 kg and gained back some (but not all) of it were also at a lower risk of breast cancer. Other patterns of weight loss and gain over the two intervals had a similar risk of breast cancer to women with stable weight., Conclusions: These results suggest that sustained weight loss, even modest amounts, is associated with lower breast cancer risk for women aged 50 years and older. Breast cancer prevention may be a strong weight-loss motivator for the two-thirds of American women who are overweight or obese., (© The Author(s) 2019. Published by Oxford University Press. All rights reserved. For permissions, please email: journals.permissions@oup.com.)

Introduction: Muscle-strengthening activity (MSA) has beneficial effects on hypertension, glucose homeostasis, and other health conditions; however, its association with mortality is not as well understood., Methods: We analyzed data from the Cancer Prevention Study-II Nutrition Cohort (data collection 1982-2014), a prospective US cohort that consisted of 72,462 men and women who were free of major chronic diseases; 18,034 of the cohort died during 13 years of follow-up (2001-2014). We used Cox proportional hazards modeling, controlling for various potential confounding factors, to calculate hazard ratios (HRs) and 95% confidence intervals (CIs) for MSA (none, >0 to <1 h/wk, 1 to <2 h/wk, and ≥2 h/wk) in relation to mortality risk, independent of and in combination with aerobic physical activity., Results: The association between MSA and mortality appeared to be nonlinear (quadratic trend P value, <.001). After multivariable adjustment and comparison with no MSA, engaging in less than 2 hours per week of MSA was associated with lowered all-cause mortality (>0 to <1 h/wk: HR = 0.88, 95% CI, 0.82-0.94; 1 to <2 h/wk: HR = 0.90, 95% CI, 0.84-0.97), but engaging in 2 or more hours per week was not associated with reduced risk (HR = 1.01; 95% CI, 0.92-1.09). Associations were similar but not significant for cancer mortality. Engaging in >0 to <1 hr/wk of MSA was associated with a 19% lower risk (HR = 0.81; 95% CI, 0.71-0.92) of cardiovascular disease mortality, but more time spent in MSA was not associated with reduced risk (quadratic trend P value =.005). Associations did not vary by amount of moderate-to-vigorous aerobic physical activity., Conclusion: Engaging in ≥2 hours per week of MSA was associated with lower all-cause mortality, independent of aerobic activity. Reasons for the lack of association with higher amounts of MSA are unclear. Our findings support recommending muscle-strengthening activities for overall health.

Purpose: Evidence supports a role of whole grains in colorectal cancer (CRC) prevention, but the association between gluten intake and CRC risk in healthy populations is unclear. We examined the association of grain and gluten intake with risk of CRC overall and by subsite among Cancer Prevention Study-II Nutrition Cohort participants., Methods: In 1999, 50,118 men and 62,031 women completed food frequency questionnaires assessing grain intake. Gluten intake was estimated using the protein content of grain products. Multivariable-adjusted hazards ratio (HR) and 95% confidence interval (CI) of CRC risk were estimated using Cox proportional hazards regression., Results: During follow-up through 2013, 1742 verified CRC cases occurred. For the highest vs. lowest quintiles of whole grain intake, HRs (95% CIs) of CRC risk were 0.77 (0.61-0.97; P trend = 0.03) among men and 1.10 (95% CI 0.88-1.36; P trend = 0.14) among women (P interaction by sex = 0.01). Men in the highest vs. lowest quintile of whole grain intake had a 43% lower risk of rectal cancer (HR = 0.57, 95% CI 0.35-0.93, P trend = 0.04). Gluten intake was not associated with CRC risk overall (HR = 1.10, 95% CI 0.93-1.32, P trend = 0.10), but was associated with risk of proximal colon cancer among men and women, combined (HR = 1.37, 95% CI 1.07-1.75, quintile 5 vs. 1, P trend = 0.001) and separately. Refined grains and grain-based sweets were not associated with CRC risk., Conclusions: We found that higher whole grain intake was associated with lower CRC risk among older US men, but not women. The positive association of gluten intake with the risk of proximal colon cancer deserves further study.

Background: Height and weight are commonly used metrics in epidemiologic studies to calculate body mass index. Large cohort studies generally assess height and weight by self-report rather than by measurement. The aim of this study was to assess the validity of self-reported height and weight in the Cancer Prevention Study-3 (CPS-3), a large, nationwide cohort recruited by the American Cancer Society between 2006-2013., Methods: In a subset of CPS-3 participants (n = 2,643), weight and height were assessed at the same time via self-report and in-person measurement. BMI was calculated and classified underweight (<18.5 kg/m2), normal (18.5-<25 kg/m2), overweight (25-<30 kg/m2), or obese (≥30 kg/m2). Self-reported and measured height, weight, and BMI were compared using mean differences and Bland-Altman plots and examined by sex, race/ethnicity, education, marital status, age group, and BMI category., Results: Men and women slightly overreported height and underreported weight. BMI calculated from self-reported data was lower than for measured data for men and women. In analyses stratified by race/ethnicity, age, education, and marital status, older women and women with less than a college degree overreported height. Approximately 13% of men and 7% of women were misclassified into a lower self-reported BMI category, with misclassification of BMI being greatest in obese men and women., Conclusions: Overall, height, weight, and BMI were well-reported, and this study further suggests that BMI computed from self-reported weight and height is a valid measure in men and women across different socio-demographic groups., Competing Interests: The authors have declared that no competing interests exist.

Purpose: To determine whether recommended amounts of leisure-time physical activity (ie, 7.5-15 metabolic equivalent task [MET] hours/week) are associated with lower cancer risk, describe the shape of the dose-response relationship, and explore associations with moderate- and vigorous-intensity physical activity., Methods: Data from 9 prospective cohorts with self-reported leisure-time physical activity and follow-up for cancer incidence were pooled. Multivariable Cox regression was used to estimate adjusted hazard ratios (HRs) and 95% CIs of the relationships between physical activity with incidence of 15 types of cancer. Dose-response relationships were modeled with restricted cubic spline functions that compared 7.5, 15.0, 22.5, and 30.0 MET hours/week to no leisure-time physical activity, and statistically significant associations were determined using tests for trend ( P < .05) and 95% CIs (< 1.0)., Results: A total of 755,459 participants (median age, 62 years [range, 32-91 years]; 53% female) were followed for 10.1 years, and 50,620 incident cancers accrued. Engagement in recommended amounts of activity (7.5-15 MET hours/week) was associated with a statistically significant lower risk of 7 of the 15 cancer types studied, including colon (8%-14% lower risk in men), breast (6%-10% lower risk), endometrial (10%-18% lower risk), kidney (11%-17% lower risk), myeloma (14%-19% lower risk), liver (18%-27% lower risk), and non-Hodgkin lymphoma (11%-18% lower risk in women). The dose response was linear in shape for half of the associations and nonlinear for the others. Results for moderate- and vigorous-intensity leisure-time physical activity were mixed. Adjustment for body mass index eliminated the association with endometrial cancer but had limited effect on other cancer types., Conclusion: Health care providers, fitness professionals, and public health practitioners should encourage adults to adopt and maintain physical activity at recommended levels to lower risks of multiple cancers.

Benzene is considered a carcinogen, mostly based on evidence of causality for myeloid leukemia from high levels of exposure in occupational studies. We used United States Environmental Protection Agency National Ambient Toxics Assessment (NATA) estimates of low-level ambient benzene to examine potential associations for the general public between benzene exposure and risk of hematologic cancers. Exposure was estimated by linking participants' residential address to the NATA benzene estimates for that census tract. Among 115,996 American Cancer Society Cancer Prevention Study-II Nutrition cohort participants (52,554 men, 63,442 women), 2,595 were diagnosed with incident hematologic cancer between 1997 and 2013. Extended Cox regression modeling was used to estimate hazard ratios (HR) and 95% confidence intervals (CI). Among all participants, ambient benzene was positively associated with myelodysplastic syndromes (HR = 1.16, 95% CI: 1.01-1.33 per μg/m 3 ) and T-cell lymphoma (HR = 1.29, 95% CI: 1.08-1.53 per μg/m 3 ). Among men, ambient benzene was also positively associated with any hematologic malignancy (HR = 1.07, 95% CI: 1.01-1.15 per μg/m 3 ) and follicular lymphoma (HR = 1.28, 95% CI: 1.09-1.50 per μg/m 3 ). No significant associations were observed for women only, but associations were suggestive for MDS and T-cell lymphoma. It is possible that the NATA ambient benzene estimates are a better proxy for benzene exposure for men than women in this cohort. The results of this study support an association between ambient benzene and risk of hematologic malignancies, particularly MDS, T-cell lymphoma and follicular lymphoma. More research in large scale or pooled studies is needed to further explore these associations., (© 2019 UICC.)

There is insufficient evidence linking excess body weight to risk of myeloid malignancies. We investigated this association using data from the Cancer Prevention Study-II (CPS-II), and a meta-analysis of published cohort studies. Among 152 090 CPS-II participants, 387 acute myeloid leukaemias (AML), 100 chronic myeloid leukaemias (CML) and 170 MDS were identified over 21 years of follow-up. In CPS-II, body mass index (BMI) was weakly associated with risk of CML (hazard ratio [HR] = 1·04, 95% confidence interval [CI]: 0·99-1·09 per 1 unit increase in BMI), AML (HR = 1·01, 95% CI: 0·98-1·03) and MDS (HR = 1·03, 95% CI: 0·99-1·07). After controlling for other anthropometric factors, no clear association was observed for height, BMI at age 18 years or weight change. In the meta-analysis (n = 7117 myeloid leukaemias), BMI 25-29·9 kg/m 2 (HR pooled  = 1·36, 95% CI: 1·12-1·59) and BMI ≥30 kg/m 2 (HR pooled  = 1·43, 95% CI: 1·18-1·69) were associated with higher risk of myeloid leukaemia overall, compared to a BMI <25 kg/m 2 . Likewise, BMI ≥25 kg/m 2 was positively associated with both AML and CML risk individually in the meta-analysis. These results underscore the need for large studies to detect associations with rare cancers, and show a modest, but positive association between excess body weight and myeloid malignancy risk., (© 2019 British Society for Haematology and John Wiley & Sons Ltd.)

Introduction: Excess sitting is a risk factor for early mortality. This may be resulting, at least in part, from the displacement of physical activity with sedentary behaviors. The purpose of this observational study was to examine the mortality risk reductions associated with replacing 30minutes/day sitting for an equivalent duration of light or moderate to vigorous physical activity (MVPA)., Methods: Participants included 37,924 men and 54,617 women in the Cancer Prevention Study-II Nutrition Cohort, of which 14,415 men and 13,358 women died during follow-up (1999-2014). An isotemporal substitution approach to the Cox proportional hazards regression model was used to estimate adjusted hazard ratios and 95% CIs for mortality associated with the substitution of 30minutes/day self-reported sitting for light physical activity or MVPA. Analyses were conducted in 2018., Results: Among the least active participants (≤17minutes/day MVPA), the replacement of 30minutes/day sitting with light physical activity was associated with a 14% mortality risk reduction (hazard ratio=0.86, 95% CI=0.81, 0.89) and replacement with MVPA was associated with a 45% mortality risk reduction (hazard ratio=0.55, 95% CI=0.47, 0.62). Similar associations were seen among moderately active participants (light physical activity replacement, hazard ratio=0.94, 95% CI=0.91, 0.97; MVPA replacement, hazard ratio=0.83, 95% CI=0.76, 0.88). However, for the most active (MVPA >38 minutes/day), substitution of sitting time with light physical activity or MVPA was not associated with a reduction in mortality risk (hazard ratio=1.00, 95% CI=0.97, 1.03, and hazard ratio=0.99, 95% CI=0.95, 1.02, respectively)., Conclusions: These findings suggest that the replacement of modest amounts of sitting time with even light physical activity may have the potential to reduce the risk of premature death among less active adults., (Copyright © 2019 American Journal of Preventive Medicine. All rights reserved.)

Importance: Excess body weight (EBW) is an established cause of cancer. Despite variations in the prevalence of EBW among US states, there is little information on the EBW-related cancer burden by state; this information would be useful for setting priorities for cancer-control initiatives., Objective: To calculate the population attributable fraction (PAF) of incident cancer cases attributable to EBW among adults 30 years or older in 2011 to 2015 in all 50 states and the District of Columbia., Design, Setting, and Participants: State-level, self-reported body mass index (BMI [calculated as weight in kilograms divided by height in meters squared]) data from the Behavioral Risk Factor Surveillance System were adjusted by sex, age, race/ethnicity, and education using objectively measured BMI values from the National Health and Nutrition Examination Survey. Age- and sex-specific cancer incidence data by state were obtained from the US Cancer Statistics database. All analyses were performed between February 15, 2018, and July 17, 2018., Main Outcomes and Measures: Sex-, age-, and state-specific adjusted prevalence estimates for 4 high BMI categories and corresponding relative risks from large-scale pooled analyses or meta-analyses were used to compute the PAFs for each US state for esophageal adenocarcinoma, multiple myeloma, and cancers of the gastric cardia, colorectum, liver, gallbladder, pancreas, female breast, corpus uteri, ovary, kidney and renal pelvis, and thyroid., Results: Each year, an estimated 37 670 cancer cases in men (4.7% of all cancer cases excluding nonmelanoma skin cancers) and 74 690 cancer cases in women (9.6%) 30 years or older in the United States were attributable to EBW from 2011 to 2015. In both men and women, there was at least a 1.5-fold difference in the proportions of cancers attributable to EBW between states with the highest and lowest PAFs. Among men, the PAF ranged from 3.9% (95% CI, 3.6%-4.3%) in Montana to 6.0% (95% CI, 5.6%-6.4%) in Texas. The PAF for women was approximately twice as high as for men, ranging from 7.1% (95% CI, 6.7%-7.6%) in Hawaii to 11.4% (95% CI, 10.7%-12.2%) in the District of Columbia. The largest PAFs were found mostly in southern and midwestern states, as well as Alaska and the District of Columbia., Conclusions and Relevance: The proportion of cancers attributable to EBW varies among states, but EBW accounts for at least 1 in 17 of all incident cancers in each state. Broad implementation of known community- and individual-level interventions is needed to reduce access to and marketing of unhealthy foods (eg, through a tax on sugary drinks) and to promote and increase access to healthy foods and physical activity, as well as preventive care.

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. Cancer Epidemiol Biomarkers Prev; 27(11); 1307-19. ©2018 AACR., (©2018 American Association for Cancer Research.)

Purpose: Many cohort studies in the United States link with the National Death Index to detect deaths. Although linkage with National Death Index is relatively sensitive, some participant deaths will be missed. These participants continue to contribute person-time to the data set after their death, resulting in bias, which we refer to as ghost-time bias. We sought to evaluate the influence of ghost-time bias on mortality relative risk (RR) estimates., Methods: Simulations were performed to determine the magnitude of ghost-time bias under a variety of plausible conditions., Results: Our simulations demonstrate that ghost-time bias can be substantial, particularly among the elderly, where it can reverse the direction of the RR. For example, we conducted a simulation of a cohort of men beginning follow-up at age of 70 years, assuming 5% missed deaths and a true RR of 2.0. In this simulation, observed RRs were 1.89 during the year the cohort was aged 85 years, 1.60 during the year the cohort was aged 90 years, and 0.61 during the year the cohort was aged 95 years. We also provide results from actual cohort data that are consistent with ghost-time bias., Conclusions: Ghost-time bias may meaningfully affect mortality RR estimates under conditions that can plausibly occur in aging cohorts., (Copyright © 2018 Elsevier Inc. All rights reserved.)

Background: Dysbiosis of the oral microbiome can lead to local oral disease and potentially to cancers of the head, neck, and digestive tract. However, little is known regarding exogenous factors contributing to such microbial imbalance., Results: We examined the impact of alcohol consumption on the oral microbiome in a cross-sectional study of 1044 US adults. Bacterial 16S rRNA genes from oral wash samples were amplified, sequenced, and assigned to bacterial taxa. We tested the association of alcohol drinking level (non-drinker, moderate drinker, or heavy drinker) and type (liquor, beer, or wine) with overall microbial composition and individual taxon abundance. The diversity of oral microbiota and overall bacterial profiles differed between heavy drinkers and non-drinkers (α-diversity richness p = 0.0059 and β-diversity unweighted UniFrac p = 0.0036), and abundance of commensal order Lactobacillales tends to be decreased with higher alcohol consumption (fold changes = 0.89 and 0.94 for heavy and moderate drinkers, p trend = 0.005 [q = 0.064]). Additionally, certain genera were enriched in subjects with higher alcohol consumption, including Actinomyces, Leptotrichia, Cardiobacterium, and Neisseria; some of these genera contain oral pathogens, while Neisseria can synthesize the human carcinogen acetaldehyde from ethanol. Wine drinkers may differ from non-drinkers in microbial diversity and profiles (α-diversity richness p = 0.048 and β-diversity unweighted UniFrac p = 0.059) after controlling for drinking amount, while liquor and beer drinkers did not. All significant differences between drinkers and non-drinkers remained after exclusion of current smokers., Conclusions: Our results, from a large human study of alcohol consumption and the oral microbiome, indicate that alcohol consumption, and heavy drinking in particular, may influence the oral microbiome composition. These findings may have implications for better understanding the potential role that oral bacteria play in alcohol-related diseases.