ABSTRACT
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.
Subject(s)
Alcohol Drinking , Health Behavior , Neoplasms , Humans , Alcohol Drinking/adverse effects , Neoplasms/epidemiology , Neoplasms/etiology , RiskABSTRACT
Although short-term feeding studies demonstrated effects of grains, fiber, and gluten on gut microbiome composition, the impact of habitual intake of these dietary factors is poorly understood. We examined whether habitual intakes of whole and refined grains, fiber, and gluten are associated with gut microbiota in a cross-sectional study. This study included 779 participants from the multi-ethnic Food and Microbiome Longitudinal Investigation study. Bacterial 16SV4 rRNA gene from baseline stool was amplified and sequenced using Illumina MiSeq. Read clustering and taxonomic assignment was performed using QIIME2. Usual dietary intake was assessed by a 137-item food frequency questionnaire. Association of diet with gut microbiota was assessed with respect to overall composition and specific taxon abundances. Whole grain intake was associated with overall composition, as measured by the Jensen-Shannon divergence (multivariable-adjusted P trend for quartiles = 0.03). The highest intake quartile was associated with higher abundance of Bacteroides plebeius, Faecalibacterium prausnitzii, Blautia producta, and Erysipelotrichaceae and lower abundance of Bacteroides uniformis. These bacteria also varied by dietary fiber intake. Higher refined grain and gluten intake was associated with lower Shannon diversity (P trend < 0.05). These findings suggest that whole grain and dietary fiber are associated with overall gut microbiome structure, largely fiber-fermenting microbiota. Higher refined grain and gluten intakes may be associated with lower microbial diversity. Significance: Regular consumption of whole grains and dietary fiber was associated with greater abundance of gut bacteria that may lower risk of colorectal cancer. Further research on the association of refined grains and gluten with gut microbial composition is needed to understand their roles in health and disease.
Subject(s)
Gastrointestinal Microbiome , Humans , Gastrointestinal Microbiome/genetics , Glutens , Cross-Sectional Studies , Diet , Bacteria/genetics , Dietary Fiber/analysisABSTRACT
Nighttime light exposure may increase cancer risk by disrupting the circadian system. However, there is no well-established survey method for measuring ambient light. In the Cancer Prevention Study-3, 732 men and women answered a light survey based on seven environments. The light environment in the past year was assessed twice, one year apart, and four one-week diaries were collected between the annual surveys. A total of 170 participants wore a meter to measure photopic illuminance and circadian stimulus (CS). Illuminance and CS values were estimated for lighting environments from measured values and evaluated with a cross validation approach. The kappas for self-reported light environment comparing the two annual surveys were 0.61 on workdays and 0.49 on non-workdays. Kappas comparing the annual survey to weekly diaries were 0.71 and 0.57 for work and non-workdays, respectively. Agreement was highest for reporting of darkness (95.3%), non-residential light (86.5%), and household light (75.6%) on workdays. Measured illuminance and CS identified three peaks of light (darkness, indoor lighting, and outdoor daytime light). Estimated illuminance and CS were correlated with the measured values overall (r = 0.77 and r = 0.67, respectively) but were less correlated within each light environment (r = 0.23-0.43). The survey has good validity to assess ambient light for studies of human health.
Subject(s)
Neoplasms , Male , Humans , Female , Surveys and Questionnaires , Self Report , Darkness , LightingABSTRACT
Little is known regarding the potential relationship between clonal hematopoiesis (CH) of indeterminate potential (CHIP), which is the expansion of hematopoietic stem cells with somatic mutations, and risk of prostate cancer, the fifth leading cause of cancer death of men worldwide. We evaluated the association of age-related CHIP with overall and aggressive prostate cancer risk in two large whole-exome sequencing studies of 75 047 European ancestry men, including 7663 prostate cancer cases, 2770 of which had aggressive disease, and 3266 men carrying CHIP variants. We found that CHIP, defined by over 50 CHIP genes individually and in aggregate, was not significantly associated with overall (aggregate HR = 0.93, 95% CI = 0.76-1.13, P = 0.46) or aggressive (aggregate OR = 1.14, 95% CI = 0.92-1.41, P = 0.22) prostate cancer risk. CHIP was weakly associated with genetic risk of overall prostate cancer, measured using a polygenic risk score (OR = 1.05 per unit increase, 95% CI = 1.01-1.10, P = 0.01). CHIP was not significantly associated with carrying pathogenic/likely pathogenic/deleterious variants in DNA repair genes, which have previously been found to be associated with aggressive prostate cancer. While findings from this study suggest that CHIP is likely not a risk factor for prostate cancer, it will be important to investigate other types of CH in association with prostate cancer risk.
Subject(s)
Clonal Hematopoiesis , Prostatic Neoplasms , Male , Humans , Hematopoiesis/genetics , Risk Factors , Hematopoietic Stem Cells , Prostatic Neoplasms/genetics , MutationABSTRACT
BACKGROUND: Epidemiologic studies suggest that coffee consumption may be inversely associated with risk of endometrial cancer (EC), the most common gynecological malignancy in developed countries. Furthermore, coffee consumption may lower circulating concentrations of estrogen and insulin, hormones implicated in endometrial carcinogenesis. Antioxidants and other chemopreventive compounds in coffee may have anticarcinogenic effects. Based on available meta-analyses, the World Cancer Research Fund (WCRF) concluded that consumption of coffee probably protects against EC. OBJECTIVES: Our main aim was to examine the association between coffee consumption and EC risk by combining individual-level data in a pooled analysis. We also sought to evaluate potential effect modification by other risk factors for EC. METHODS: We combined individual-level data from 19 epidemiologic studies (6 cohort, 13 case-control) of 12,159 EC cases and 27,479 controls from the Epidemiology of Endometrial Cancer Consortium (E2C2). Logistic regression was used to calculate ORs and their corresponding 95% CIs. All models were adjusted for potential confounders including age, race, BMI, smoking status, diabetes status, study design, and study site. RESULTS: Coffee drinkers had a lower risk of EC than non-coffee drinkers (multiadjusted OR: 0.87; 95% CI: 0.79, 0.95). There was a dose-response relation between higher coffee consumption and lower risk of EC: compared with non-coffee drinkers, the adjusted pooled ORs for those who drank 1, 2-3, and >4 cups/d were 0.90 (95% CI: 0.82, 1.00), 0.86 (95% CI: 0.78, 0.95), and 0.76 (95% CI: 0.66, 0.87), respectively (P-trend < 0.001). The inverse association between coffee consumption and EC risk was stronger in participants with BMI > 25 kg/m2. CONCLUSIONS: The results of the largest analysis to date pooling individual-level data further support the potentially beneficial health effects of coffee consumption in relation to EC, especially among females with higher BMI.
Subject(s)
Endometrial Neoplasms , Female , Humans , Risk Factors , Endometrial Neoplasms/epidemiology , Endometrial Neoplasms/etiology , Endometrial Neoplasms/prevention & control , Logistic Models , Case-Control Studies , Data CollectionABSTRACT
INTRODUCTION: Geriatric assessment evaluates multiple domains of health that, together, are superior to using chronologic age for predicting outcomes, such as hospitalization and mortality among patients with cancer. Most studies have not included comparison groups of individuals without cancer and assessed domains around the time of initial cancer diagnosis. Further, the potential for brief, self-reported measures to capture deficits that similarly predict mortality has not been well examined. This study compared age-related health deficit prevalence between older, long-term cancer survivors and individuals without a cancer history, and estimated associations between deficits and mortality risk among survivors. MATERIALS AND METHODS: Analyses included participants in the Cancer Prevention Study (CPS)-II Nutrition Cohort who were cancer-free at enrollment in 1992/1993 and completed the Patient Reported Outcome Measurement Information System® (PROMIS®) global health questionnaire in 2011. Age-related deficits in five domains (comorbidities, functional status, mental health, malnutrition/weight loss, and social support) were self-reported. Cancer information was self-reported and confirmed via medical records or state cancer registries. Vital status through 2016 and cause of death was ascertained by linkage with the National Death Index. RESULTS: Analyses included 9979 participants (median age = 80) diagnosed with invasive cancer 5-20 years prior to completing the 2011 survey and 63,578 participants without a cancer history (median age = 79). Overall deficits in the five domains were similar among long-term cancer survivors and controls. However, survivors of specific cancer types - non-Hodgkin lymphoma (NHL), lung, and kidney cancer - were more likely to report deficits in mental health and functional status than the control group. Among all survivors, each domain was independently associated with all-cause mortality, particularly functional status (hazard ratio [HR] = 2.02; 95% confidence interval [CI]: 1.80-2.27) and mental health (HR = 1.84; 95% CI: 1.65-2.04). Mortality risk increased with the number of deficits. DISCUSSION: These results suggest that, several years after treatment, NHL, lung, and kidney cancer survivors are still more likely to experience age-related deficits compared to other similarly-aged individuals. Furthermore, results show that shorter, self-reported physical and mental health assessments, such as the PROMIS® global health questions, are predictive of mortality among older, long-term cancer survivors and, therefore, may be useful in clinical and research settings.
Subject(s)
Cancer Survivors , Neoplasms , Aged , Aged, 80 and over , Cohort Studies , Humans , Neoplasms/therapy , Proportional Hazards Models , SurvivorsABSTRACT
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.
Subject(s)
Cancer Survivors , Neoplasms , American Cancer Society , Diet , Exercise , Humans , Neoplasms/therapy , Survivors , United States/epidemiologyABSTRACT
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.
Subject(s)
Prostatic Neoplasms , Biomarkers , Cohort Studies , Glucose , Homeostasis , Humans , Inflammation/complications , Male , Prospective Studies , Prostatic Neoplasms/pathology , Risk FactorsABSTRACT
A rare African ancestry-specific germline deletion variant in HOXB13 (X285K, rs77179853) was recently reported in Martinican men with early-onset prostate cancer. Given the role of HOXB13 germline variation in prostate cancer, we investigated the association between HOXB13 X285K and prostate cancer risk in a large sample of 22 361 African ancestry men, including 11 688 prostate cancer cases. The risk allele was present only in men of West African ancestry, with an allele frequency in men that ranged from 0.40% in Ghana and 0.31% in Nigeria to 0% in Uganda and South Africa, with a range of frequencies in men with admixed African ancestry from North America and Europe (0-0.26%). HOXB13 X285K was associated with 2.4-fold increased odds of prostate cancer (95% confidence interval [CI] = 1.5-3.9, p = 2 × 10-4), with greater risk observed for more aggressive and advanced disease (Gleason ≥8: odds ratio [OR] = 4.7, 95% CI = 2.3-9.5, p = 2 × 10-5; stage T3/T4: OR = 4.5, 95% CI = 2.0-10.0, p = 2 × 10-4; metastatic disease: OR = 5.1, 95% CI = 1.9-13.7, p = 0.001). We estimated that the allele arose in West Africa 1500-4600 yr ago. Further analysis is needed to understand how the HOXB13 X285K variant impacts the HOXB13 protein and function in the prostate. Understanding who carries this mutation may inform prostate cancer screening in men of West African ancestry. PATIENT SUMMARY: A rare African ancestry-specific germline deletion in HOXB13, found only in men of West African ancestry, was reported to be associated with an increased risk of overall and advanced prostate cancer. Understanding who carries this mutation may help inform screening for prostate cancer in men of West African ancestry.
Subject(s)
Early Detection of Cancer , Prostatic Neoplasms , Case-Control Studies , Genetic Predisposition to Disease , Germ Cells/pathology , Germ-Line Mutation , Homeodomain Proteins/genetics , Humans , Male , Prostate-Specific Antigen/genetics , Prostatic Neoplasms/genetics , Prostatic Neoplasms/pathologyABSTRACT
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.
Subject(s)
Alcoholic Beverages/adverse effects , Neoplasms/chemically induced , Neoplasms/epidemiology , Harm Reduction , Health Behavior , Humans , Risk FactorsABSTRACT
Self-reported type 2 diabetes mellitus (T2DM) is a risk factor for many cancers, suggesting its pathology relates to carcinogenesis. We conducted a case-cohort study to examine associations of hemoglobin A1c (HbA1c) and c-peptide with cancers associated with self-reported T2DM. This study was drawn from a prospective cohort of 32,383 women and men who provided blood specimens at baseline: c-peptide and HbA1c were assessed in 3,000 randomly selected participants who were cancer-free-at-baseline and an additional 2,281 participants who were cancer-free-at-baseline and subsequently diagnosed with incident colorectal, liver, pancreatic, female breast, endometrial, ovarian, bladder, or kidney cancers. Weighted-Cox regression models estimated hazards ratios (HRs) and 95% confidence intervals (CI), adjusted for covariates. C-peptide was associated with higher risk of liver cancer (per standard deviation (SD) HR: 1.80; 95%CI: 1.32-2.46). HbA1c was associated with higher risk of pancreatic cancer (per SD HR: 1.21 95%CI 1.05-1.40) and with some suggestion of higher risks for all-cancers-of-interest (per SD HR: 1.05; 95%CI: 0.99-1.11) and colorectal (per SD HR: 1.09; 95%CI: 0.98-1.20), ovarian (per SD HR: 1.18; 95%CI 0.96-1.45) and bladder (per SD HR: 1.08; 95%CI 0.96-1.21) cancers. Compared to no self-reported T2DM and HbA1c <6.5% (reference group), self-reported T2DM and HbA1c <6.5% (i.e., T2DM in good glycemic control) was not associated with risk of colorectal cancer, whereas it was associated with higher risks of all-cancers-of-interest combined (HR: 1.28; 95%CI: 1.01-1.62), especially for breast and endometrial cancers. Additional large, prospective studies are needed to further explore the roles of hyperglycemia, hyperinsulinemia, and related metabolic traits with T2DM-associated cancers to better understand the mechanisms underlying the self-reported T2DM-cancer association and to identify persons at higher cancer risk.
Subject(s)
Colorectal Neoplasms , Diabetes Mellitus, Type 2 , Liver Neoplasms , Female , Humans , Male , C-Peptide , Cohort Studies , Colorectal Neoplasms/diagnosis , Diabetes Mellitus, Type 2/epidemiology , Glycated Hemoglobin , Liver Neoplasms/complications , Hemoglobin AABSTRACT
AIM: Recessive genetic variation is thought to play a role in non-Hodgkin lymphoma (NHL) etiology. Runs of homozygosity (ROH), defined based on long, continuous segments of homozygous SNPs, can be used to estimate both measured and unmeasured recessive genetic variation. We sought to examine genome-wide homozygosity and NHL risk. METHODS: We used data from eight genome-wide association studies of four common NHL subtypes: 3061 chronic lymphocytic leukemia (CLL), 3814 diffuse large B-cell lymphoma (DLBCL), 2784 follicular lymphoma (FL), and 808 marginal zone lymphoma (MZL) cases, as well as 9374 controls. We examined the effect of homozygous variation on risk by: (1) estimating the fraction of the autosome containing runs of homozygosity (FROH); (2) calculating an inbreeding coefficient derived from the correlation among uniting gametes (F3); and (3) examining specific autosomal regions containing ROH. For each, we calculated beta coefficients and standard errors using logistic regression and combined estimates across studies using random-effects meta-analysis. RESULTS: We discovered positive associations between FROH and CLL (ß = 21.1, SE = 4.41, P = 1.6 × 10-6) and FL (ß = 11.4, SE = 5.82, P = 0.02) but not DLBCL (P = 1.0) or MZL (P = 0.91). For F3, we observed an association with CLL (ß = 27.5, SE = 6.51, P = 2.4 × 10-5). We did not find evidence of associations with specific ROH, suggesting that the associations observed with FROH and F3 for CLL and FL risk were not driven by a single region of homozygosity. CONCLUSION: Our findings support the role of recessive genetic variation in the etiology of CLL and FL; additional research is needed to identify the specific loci associated with NHL risk.
ABSTRACT
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.
Subject(s)
National Cancer Institute (U.S.)/organization & administration , Strategic Planning , Humans , Organizational Objectives , Surveys and Questionnaires , United StatesABSTRACT
BACKGROUND: It is not known whether modifiable lifestyle factors that predict survival after invasive breast cancer differ by subtype. METHODS: We analyzed data for 121,435 women diagnosed with breast cancer from 67 studies in the Breast Cancer Association Consortium with 16,890 deaths (8,554 breast cancer specific) over 10 years. Cox regression was used to estimate associations between risk factors and 10-year all-cause mortality and breast cancer-specific mortality overall, by estrogen receptor (ER) status, and by intrinsic-like subtype. RESULTS: There was no evidence of heterogeneous associations between risk factors and mortality by subtype (P adj > 0.30). The strongest associations were between all-cause mortality and BMI ≥30 versus 18.5-25 kg/m2 [HR (95% confidence interval (CI), 1.19 (1.06-1.34)]; current versus never smoking [1.37 (1.27-1.47)], high versus low physical activity [0.43 (0.21-0.86)], age ≥30 years versus <20 years at first pregnancy [0.79 (0.72-0.86)]; >0-<5 years versus ≥10 years since last full-term birth [1.31 (1.11-1.55)]; ever versus never use of oral contraceptives [0.91 (0.87-0.96)]; ever versus never use of menopausal hormone therapy, including current estrogen-progestin therapy [0.61 (0.54-0.69)]. Similar associations with breast cancer mortality were weaker; for example, 1.11 (1.02-1.21) for current versus never smoking. CONCLUSIONS: We confirm associations between modifiable lifestyle factors and 10-year all-cause mortality. There was no strong evidence that associations differed by ER status or intrinsic-like subtype. IMPACT: Given the large dataset and lack of evidence that associations between modifiable risk factors and 10-year mortality differed by subtype, these associations could be cautiously used in prognostication models to inform patient-centered care.
Subject(s)
Breast Neoplasms/mortality , Breast Neoplasms/pathology , Life Style , Adult , Aged , Cause of Death , Female , Humans , Middle Aged , Neoplasm Invasiveness/pathology , Neoplasm Staging , Prospective Studies , Risk Factors , Survival AnalysisABSTRACT
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.
Subject(s)
Alcohol Drinking/adverse effects , Neoplasms/epidemiology , Neoplasms/mortality , Adult , Aged , Aged, 80 and over , Alcohol Drinking/epidemiology , Behavioral Risk Factor Surveillance System , Female , Humans , Incidence , Male , Middle Aged , Risk Factors , United States/epidemiologyABSTRACT
BACKGROUND: Population-based estimates of the risk of breast cancer associated with germline pathogenic variants in cancer-predisposition genes are critically needed for risk assessment and management in women with inherited pathogenic variants. METHODS: In a population-based case-control study, we performed sequencing using a custom multigene amplicon-based panel to identify germline pathogenic variants in 28 cancer-predisposition genes among 32,247 women with breast cancer (case patients) and 32,544 unaffected women (controls) from population-based studies in the Cancer Risk Estimates Related to Susceptibility (CARRIERS) consortium. Associations between pathogenic variants in each gene and the risk of breast cancer were assessed. RESULTS: Pathogenic variants in 12 established breast cancer-predisposition genes were detected in 5.03% of case patients and in 1.63% of controls. Pathogenic variants in BRCA1 and BRCA2 were associated with a high risk of breast cancer, with odds ratios of 7.62 (95% confidence interval [CI], 5.33 to 11.27) and 5.23 (95% CI, 4.09 to 6.77), respectively. Pathogenic variants in PALB2 were associated with a moderate risk (odds ratio, 3.83; 95% CI, 2.68 to 5.63). Pathogenic variants in BARD1, RAD51C, and RAD51D were associated with increased risks of estrogen receptor-negative breast cancer and triple-negative breast cancer, whereas pathogenic variants in ATM, CDH1, and CHEK2 were associated with an increased risk of estrogen receptor-positive breast cancer. Pathogenic variants in 16 candidate breast cancer-predisposition genes, including the c.657_661del5 founder pathogenic variant in NBN, were not associated with an increased risk of breast cancer. CONCLUSIONS: This study provides estimates of the prevalence and risk of breast cancer associated with pathogenic variants in known breast cancer-predisposition genes in the U.S. population. These estimates can inform cancer testing and screening and improve clinical management strategies for women in the general population with inherited pathogenic variants in these genes. (Funded by the National Institutes of Health and the Breast Cancer Research Foundation.).
Subject(s)
Breast Neoplasms/genetics , Genetic Predisposition to Disease/genetics , Genetic Variation , Adult , Aged , Aged, 80 and over , Case-Control Studies , Female , Humans , Middle Aged , Mutation , Odds Ratio , Risk , Sequence Analysis, DNA , Young AdultABSTRACT
Prostate cancer is a highly heritable disease with large disparities in incidence rates across ancestry populations. We conducted a multiancestry meta-analysis of prostate cancer genome-wide association studies (107,247 cases and 127,006 controls) and identified 86 new genetic risk variants independently associated with prostate cancer risk, bringing the total to 269 known risk variants. The top genetic risk score (GRS) decile was associated with odds ratios that ranged from 5.06 (95% confidence interval (CI), 4.84-5.29) for men of European ancestry to 3.74 (95% CI, 3.36-4.17) for men of African ancestry. Men of African ancestry were estimated to have a mean GRS that was 2.18-times higher (95% CI, 2.14-2.22), and men of East Asian ancestry 0.73-times lower (95% CI, 0.71-0.76), than men of European ancestry. These findings support the role of germline variation contributing to population differences in prostate cancer risk, with the GRS offering an approach for personalized risk prediction.
Subject(s)
Genetic Loci , Genetic Predisposition to Disease , Genome-Wide Association Study , Prostatic Neoplasms/genetics , Racial Groups/genetics , Humans , Male , Middle Aged , Molecular Sequence Annotation , Neoplasm Invasiveness , Odds Ratio , Prostatic Neoplasms/diagnosis , Risk FactorsABSTRACT
BACKGROUND: Identifying risk factors for women at high risk of symptom-detected breast cancers that were missed by screening would enable targeting of enhanced screening regimens. To this end, we examined associations of breast cancer risk factors by mode of detection in screened women from the Cancer Prevention Study (CPS)-II Nutrition Cohort. METHODS: Among 77,206 women followed for a median of 14.8 years, 2711 screen-detected and 1281 symptom-detected breast cancer cases were diagnosed. Multivariable-adjusted associations were estimated using joint Cox proportional hazards regression models with person-time calculated contingent on screening. RESULTS: Factors associated with higher risks of symptom-detected and screen-detected breast cancer included current combined hormone therapy (HT) use (HR 2.07, 95% CI 1.72-2.48 and 1.45, 1.27-1.65, respectively) and history of benign breast disease (1.85, 1.64-2.08 and 1.43, 1.31-1.55, respectively). Current estrogen-only HT use was associated with symptom-detected (1.40, 1.15-1.71) but not screen-detected (0.95, 0.83-1.09) breast cancer. Higher risk of screen-detected but not symptom-detected breast cancer was observed for obese vs. normal body mass index (1.22, 1.01-1.48 and 0.76, 0.56-1.01, respectively), per 3 h/day sitting time (1.10, 1.04-1.16 and 0.97, 0.89-1.06, respectively), and ≥ 2 drinks per day vs. nondrinker (1.40, 1.16-1.69 and 1.27, 0.97-1.66, respectively). CONCLUSIONS: Differences in risk factors for symptom-detected vs. screen-detected breast cancer were observed and most notably, use of combined and estrogen-only HT and a history of benign breast disease were associated with increased risk of symptomatic detected breast cancer. IMPACT: If confirmed, these data suggest that such women may benefit from more intensive screening to facilitate early detection.