Search

To the authors' knowledge, few studies to date have examined associations between moderate to vigorous physical activity (MVPA) and sitting time with quality of life in cancer survivors compared with a cancer-free group. The current study examined differences in global mental health (GMH) and global physical health (GPH) across levels of MVPA and sitting among cancer survivors and cancer-free participants.Cancer Prevention Study II participants (59.9% of whom were female with an age of 77.8 ± 5.8 years) were grouped as: 1) survivors who were 1 to 5 years after diagnosis (3718 participants); 2) survivors who were 6 to 10 years after diagnosis (4248 participants); and 3) cancer-free participants (ie, no history of cancer; 69,860 participants). In 2009, participants completed MVPA, sitting, and Patient-Reported Outcomes Measurement Information System GMH/GPH surveys. Mean differences in GMH and GPH T scores across MVPA (none, 0 to7.5, 7.5 to15, 15 to22.5, and ≥22.5 metabolic equivalent [MET]-hours/week) and sitting (0 to3, 3 to6, and ≥6 hours/day) were assessed using multivariate generalized linear models.The mean GMH and GPH scores were statistically significantly higher in cancer-free participants compared with cancer survivor groups, although the differences were not clinically meaningful (mean difference of 0.52 for GMH and 0.88 for GPH). More MVPA was associated with higher GMH and GPH scores for all 3 groups (P for trend.001), and differences between the least and most active participants were found to be clinically meaningful (mean differences of ≥4.34 for GMH and ≥6.39 for GPH). Similarly, a lower duration of sitting was associated with higher GMH and GPH scores for all groups (P for trend.001), with clinically meaningful differences observed between the least and most sedentary participants (mean differences of ≥2.74 for GMH and ≥3.75 for GPH).The findings of the current study provide evidence of the importance of increased MVPA and decreased sitting for improved health in older adults with or without a prior cancer diagnosis.

Cadmium and lead are persistent environmental toxins that are known or probable carcinogens, based on evidence for causality for nonhematologic cancers. Associations of these metals with risk of non-Hodgkin lymphoma (NHL) and multiple myeloma (MM) are unknown but biologically plausible. To examine the associations of circulating levels of lead and cadmium exposure with risk of B-cell NHL (B-NHL) and multiple myeloma, we conducted a nested case-control study among 299 incident B-cell NHLs and 76 MM cases within the Cancer Prevention Study-II Nutrition Cohort (CPS-II NC). Each case was incidence-density matched to two eligible controls on age, race, sex and blood draw date. Conditional logistic regression was used to estimate relative risks (RR) and 95% confidence intervals (CI) for lymphoid malignancies overall and stratified by subtype. We observed a significant positive association between high erythrocyte lead concentration and risk of lymphoid malignancies overall (RR = 1.16, 95% CI: 1.02-1.33 per 17.6 μg/L (1 standard deviation [SD])) and follicular lymphoma in particular (RR = 1.80, 95% CI: 1.15-2.80 per SD). In contrast, there was no association between erythrocyte cadmium and risk of B-NHL (RR = 0.89, 95% CI: 0.75-1.06 per 0.37 μg/L [1 SD]), or any B-NHL subtypes; but a strong inverse association with MM risk (RR = 0.59, 95% CI: 0.38-0.89, per SD). Results from our study suggest a positive association between erythrocyte lead level and risk of lymphoid malignancies and a possible inverse association between cadmium and myeloma. Additional research is needed to confirm and further explore these findings.

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.

Obesity is known to be associated with primary liver cancer (PLC), but the separate effects of excess abdominal and gluteofemoral size are unclear. Thus, we examined the association between waist and hip circumference with risk of PLC overall and by histologic type-hepatocellular carcinoma (HCC) and intrahepatic cholangiocarcinoma (ICC). The Liver Cancer Pooling Project is a consortium of prospective cohort studies that include data from 1,167,244 individuals (PLC n = 2,208, HCC n = 1,154, ICC n = 335). Multivariable-adjusted hazard ratios (HRs) and 95% confidence intervals (CI) were estimated using proportional hazards regression. Waist circumference, per 5 cm increase, was associated with an 11% increased PLC risk (HR = 1.11, 95%CI: 1.09-1.14), including when adjusted for hip circumference (HR = 1.12, 95%CI: 1.08-1.17) and also when restricted to individuals in a normal body mass index (BMI) range (18.5 to

Cadmium and lead have been classified as carcinogens by the International Agency for Research on Cancer. However, their associations with breast cancer risk are unknown despite their persistence in ...

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.

Contemporary information on the fraction of cancers that potentially could be prevented is useful for priority setting in cancer prevention and control. Herein, the authors estimate the proportion and number of invasive cancer cases and deaths, overall (excluding nonmelanoma skin cancers) and for 26 cancer types, in adults aged 30 years and older in the United States in 2014, that were attributable to major, potentially modifiable exposures (cigarette smoking; secondhand smoke; excess body weight; alcohol intake; consumption of red and processed meat; low consumption of fruits/vegetables, dietary fiber, and dietary calcium; physical inactivity; ultraviolet radiation; and 6 cancer-associated infections). The numbers of cancer cases were obtained from the Centers for Disease Control and Prevention (CDC) and the National Cancer Institute; the numbers of deaths were obtained from the CDC; risk factor prevalence estimates were obtained from nationally representative surveys; and associated relative risks of cancer were obtained from published, large-scale pooled analyses or meta-analyses. In the United States in 2014, an estimated 42.0% of all incident cancers (659,640 of 1570,975 cancers, excluding nonmelanoma skin cancers) and 45.1% of cancer deaths (265,150 of 587,521 deaths) were attributable to evaluated risk factors. Cigarette smoking accounted for the highest proportion of cancer cases (19.0%; 298,970 cases) and deaths (28.8%; 169,180 deaths), followed by excess body weight (7.8% and 6.5%, respectively) and alcohol intake (5.6% and 4.0%, respectively). Lung cancer had the highest number of cancers (184,970 cases) and deaths (132,960 deaths) attributable to evaluated risk factors, followed by colorectal cancer (76,910 cases and 28,290 deaths). These results, however, may underestimate the overall proportion of cancers attributable to modifiable factors, because the impact of all established risk factors could not be quantified, and many likely modifiable risk factors are not yet firmly established as causal. Nevertheless, these findings underscore the vast potential for reducing cancer morbidity and mortality through broad and equitable implementation of known preventive measures. CA Cancer J Clin 2018;68:31-54. © 2017 American Cancer Society.

We assessed the association between 1,414 single nucleotide polymorphisms (SNPs) in genes involved in synthesis and metabolism of steroid hormones and insulin-like growth factor 1, and risk of breast cancer in situ (BCIS), with the aim of determining whether any of these were disease specific. This was carried out using 1,062 BCIS cases and 10,126 controls as well as 6,113 invasive breast cancer cases from the Breast and Prostate Cancer Cohort Consortium (BPC3). Three SNPs showed at least one nominally significant association in homozygous minor versus homozygous major models. ACVR2A-rs2382112 (ORhom=3.05, 95%CI=1.72-5.44, Phom=1.47 × 10-4), MAST2-rs12124649 (ORhom=1.73, 95% CI =1.18-2.54, Phom=5.24 × 10-3), and INSR-rs10500204 (ORhom=1.96, 95% CI=1.44-2.67, Phom=1.68 × 10-5) were associated with increased risk of BCIS; however, only the latter association was significant after correcting for multiple testing. Furthermore, INSR-rs10500204 was more strongly associated with the risk of BCIS than invasive disease in case-only analyses using the homozygous minor versus homozygous major model (ORhom=1.78, 95% CI=1.30-2.44, Phom=3.23 × 10-4). The SNP INSR-rs10500204 is located in an intron of the INSR gene and is likely to affect binding of the promyelocytic leukemia (PML) protein. The PML gene is known as a tumor suppressor and growth regulator in cancer. However, it is not clear on what pathway the A-allele of rs10500204 could operate to influence the binding of the protein. Hence, functional studies are warranted to investigate this further.

Circadian disruption has been linked to carcinogenesis in animal models, but the evidence in humans is inconclusive. Genetic variation in circadian rhythm genes provides a tool to investigate such associations. We examined associations of genetic variation in nine core circadian rhythm genes and six melatonin pathway genes with risk of colorectal, lung, ovarian and prostate cancers using data from the Genetic Associations and Mechanisms in Oncology (GAME-ON) network. The major results for prostate cancer were replicated in the Prostate, Lung, Colorectal and Ovarian (PLCO) cancer screening trial, and for colorectal cancer in the Genetics and Epidemiology of Colorectal Cancer Consortium (GECCO). The total number of cancer cases and controls was 15,838/18,159 for colorectal, 14,818/14,227 for prostate, 12,537/17,285 for lung and 4,369/9,123 for ovary. For each cancer site, we conducted gene-based and pathway-based analyses by applying the summary-based Adaptive Rank Truncated Product method (sARTP) on the summary association statistics for each SNP within the candidate gene regions. Aggregate genetic variation in circadian rhythm and melatonin pathways were significantly associated with the risk of prostate cancer in data combining GAME-ON and PLCO, after Bonferroni correction (Ppathway

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.

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

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/m2 (HRpooled = 1·36, 95% CI: 1·12-1·59) and BMI ≥30 kg/m2 (HRpooled = 1·43, 95% CI: 1·18-1·69) were associated with higher risk of myeloid leukaemia overall, compared to a BMI

The prevalence of excess body weight and the associated cancer burden have been rising over the past several decades globally. Between 1975 and 2016, the prevalence of excess body weight in adults-defined as a body mass index (BMI) ≥ 25 kg/m2 -increased from nearly 21% in men and 24% in women to approximately 40% in both sexes. Notably, the prevalence of obesity (BMI ≥ 30 kg/m2 ) quadrupled in men, from 3% to 12%, and more than doubled in women, from 7% to 16%. This change, combined with population growth, resulted in a more than 6-fold increase in the number of obese adults, from 100 to 671 million. The largest absolute increase in obesity occurred among men and boys in high-income Western countries and among women and girls in Central Asia, the Middle East, and North Africa. The simultaneous rise in excess body weight in almost all countries is thought to be driven largely by changes in the global food system, which promotes energy-dense, nutrient-poor foods, alongside reduced opportunities for physical activity. In 2012, excess body weight accounted for approximately 3.9% of all cancers (544,300 cases) with proportion varying from less than 1% in low-income countries to 7% or 8% in some high-income Western countries and in Middle Eastern and Northern African countries. The attributable burden by sex was higher for women (368,500 cases) than for men (175,800 cases). Given the pandemic proportion of excess body weight in high-income countries and the increasing prevalence in low- and middle-income countries, the global cancer burden attributable to this condition is likely to increase in the future. There is emerging consensus on opportunities for obesity control through the multisectoral coordinated implementation of core policy actions to promote an environment conducive to a healthy diet and active living. The rapid increase in both the prevalence of excess body weight and the associated cancer burden highlights the need for a rejuvenated focus on identifying, implementing, and evaluating interventions to prevent and control excess body weight.

Ovarian cancer risk factors differ by histotype; however, within subtype, there is substantial variability in outcomes. We hypothesized that risk factor profiles may influence tumor aggressiveness, defined by time between diagnosis and death, independent of histology. Among 1.3 million women from 21 prospective cohorts, 4,584 invasive epithelial ovarian cancers were identified and classified as highly aggressive (death in

Objectives Whether endogenous sex hormones play a role in cardiovascular disease (CVD) risk in men is unclear. Few studies have examined associations of sex hormones with atherosclerosis measured by coronary artery calcium score (CACS) and carotid intima-media thickness (cIMT). We evaluated the association of testosterone (T) and other sex hormones with CACS and cIMT. Methods Using the large multi-ethnic cohort of 3164 men without known CVD in the Multi-Ethnic Study of Atherosclerosis (MESA), cross-sectional associations of tertiles of endogenous sex hormones with CACS and cIMT were analysed. Results In regard to CAC, there was a significant negative trend (P-trend = 0·02) for CACS>0 over tertiles of free T (FT) with RRs (95% CI) for the lowest to highest tertiles. There was also a marginally significant positive trend (P-trend = 0·06) for CACS>0 over tertiles of sex hormone-binding globulin (SHBG) with RRs for the lowest to highest tertiles. There were no significant associations with CACS >0 for tertiles of TT (Total T), bioavailable T (BT), oestradiol (E2) and dehydroepiandrosterone (DHEA). There was significantly higher log CACS after adjustment for CVD risk factors for lower TT levels, compared to higher levels, using 9·54 and 10·4 nmol/l as cut-off points. In regard to cIMT, there was a significant positive trend (P = 0·003) in mean cIMT over the tertiles of BT, but not for TT, FT, E2, DHEA and SHBG. There was significantly lower cIMT after adjustment for CVD risk factors for lower TT levels compared to higher levels. Conclusion In a population of male subjects with no known CVD, lower FT is associated with higher RR of CACS>0 and lower TT is associated with higher log CACS. Lower BT and TT are associated with lower cIMT. While these findings support the positive correlation between low T and coronary atherosclerosis, the opposite findings on cIMT warrant further evaluation.

The survival of breast cancer patients is largely influenced by tumor characteristics, such as TNM stage, tumor grade and hormone receptor status. However, there is growing evidence that inherited ...

BACKGROUND. ABO blood group has been associated with risk of cancers of the pancreas, stomach, ovary, kidney, and skin, but has not been evaluated in relation to risk of aggressive prostate cancer. ...

Circadian disruption has been linked to carcinogenesis in animal models, but the evidence in humans is inconclusive. Genetic variation in circadian rhythm genes provides a tool to investigate such associations. We examined associations of genetic variation in nine core circadian rhythm genes and six melatonin pathway genes with risk of colorectal, lung, ovarian and prostate cancers using data from the Genetic Associations and Mechanisms in Oncology (GAME-ON) network. The major results for prostate cancer were replicated in the Prostate, Lung, Colorectal and Ovarian (PLCO) cancer screening trial, and for colorectal cancer in the Genetics and Epidemiology of Colorectal Cancer Consortium (GECCO). The total number of cancer cases and controls was 15,838/18,159 for colorectal, 14,818/14,227 for prostate, 12,537/17,285 for lung and 4,369/9,123 for ovary. For each cancer site, we conducted gene-based and pathway-based analyses by applying the summary-based Adaptive Rank Truncated Product method (sARTP) on the summary association statistics for each SNP within the candidate gene regions. Aggregate genetic variation in circadian rhythm and melatonin pathways were significantly associated with the risk of prostate cancer in data combining GAME-ON and PLCO, after Bonferroni correction (p pathway < 0.00625). The two most significant genes were NPAS2 (p gene =0.0062) and AANAT (p gene =0.00078); the latter being significant after Bonferroni correction. For colorectal cancer, we observed a suggestive association with the circadian rhythm pathway in GAME-ON (p pathway =0.021); this association was not confirmed in GECCO (p pathway =0.76) or the combined data (p pathway =0.17). No significant association was observed for ovarian and lung cancer. These findings support a potential role for circadian rhythm and melatonin pathways in prostate carcinogenesis. Further functional studies are needed to better understand the underlying biologic mechanisms.

Intrauterine devices (IUDs) long-acting and reversible contraceptives induce a number of immunological and biochemical changes in the uterine environment that could affect endometrial cancer (EC) risk. We addressed this relationship through a pooled analysis of data collected in the Epidemiology of Endometrial Cancer Consortium. We combined individual-level data from 4 cohort and 14 case-control studies in total 8801 EC cases and 15357 controls. Using multivariable logistic regression we estimated pooled odds ratios (pooled-ORs) and 95% confidence intervals (CIs) for EC risk associated with ever use type of device ages at first and last use duration of use and time since last use stratified by study and adjusted for confounders. Ever use of IUDs was inversely related to EC risk (pooled-OR = 0.81 95% CI = 0.74-0.90). Compared with never use reduced risk of EC was observed for inert IUDs (pooled-OR = 0.69 95% CI = 0.58-0.82) older age at first use (>/= 35 years pooled-OR = 0.53 95% CI = 0.43-0.67) older age at last use (>/= 45 years pooled-OR = 0.60 95% CI = 0.50-0.72) longer duration of use (>/= 10 years pooled-OR = 0.61 95% CI = 0.52-0.71) and recent use (within 1 year of study entry pooled-OR = 0.39 95% CI = 0.30-0.49). Future studies are needed to assess the respective roles of detection biases and biologic effects related to foreign body responses in the endometrium heavier bleeding (and increased clearance of carcinogenic cells) and localized hormonal changes. (c) 2014 UICC.

Genome-wide association studies have identified more than 80 risk variants for prostate cancer, mainly in European or Asian populations. The generalizability of these variants in other racial/ethnic populations needs to be understood before the loci can be used widely in risk modeling. In our study, we examined 82 previously reported risk variants in 4,853 prostate cancer cases and 4,678 controls of African ancestry. We performed association testing for each variant using logistic regression adjusted for age, study and global ancestry. Of the 82 known risk variants, 68 (83%) had effects that were directionally consistent in their association with prostate cancer risk and 30 (37%) were significantly associated with risk at p < 0.05, with the most statistically significant variants being rs116041037 (p = 3.7 × 10(-26) ) and rs6983561 (p = 1.1 × 10(-16) ) at 8q24, as well as rs7210100 (p = 5.4 × 10(-8) ) at 17q21. By exploring each locus in search of better markers, the number of variants that captured risk in men of African ancestry (p < 0.05) increased from 30 (37%) to 44 (54%). An aggregate score comprised of these 44 markers was strongly associated with prostate cancer risk [per-allele odds ratio (OR) = 1.12, p = 7.3 × 10(-98) ]. In summary, the consistent directions of effects for the vast majority of variants in men of African ancestry indicate common functional alleles that are shared across populations. Further exploration of these susceptibility loci is needed to identify the underlying biologically relevant variants to improve prostate cancer risk modeling in populations of African ancestry.

Epstein-Barr virus (EBV) causes rare, malignant lymphomas. The role of EBV in other non-Hodgkin lymphomas (NHLs) remains unclear, but mildly reduced immune function could lead to reactivation of EBV and subsequent NHL. We examined the association between prospectively-collected plasma EBV antibodies and NHL risk in the Cancer Prevention Study-II (CPS-II) Nutrition Cohort and conducted a meta-analysis of our and published results. The CPS-II study included 225 NHL cases and 2:1 matched controls. No associations were observed between EBV serostatus or antibody levels and risk of NHL overall. However, when including only the three most common types of NHL (diffuse large B-cell lymphoma, follicular lymphoma, chronic lymphocytic leukemia/small lymphocytic lymphoma), high compared to low early antigen (EA-D) diffuse and BZLF1-encoded replication activator antibodies were associated with approximately 60% higher risk of NHL. Odds ratios (ORs) for EBV nuclear antigen-1 and viral capsid antigen (VCA)-p18 were elevated but not statistically significant. In the meta-analysis, both EA (summary OR = 1.52, 95% confidence interval (CI): 1.16–2.00) and VCA (summary OR = 1.20, 95% CI: 1.00–1.44) were positively associated with NHL risk. These results suggest EBV may be associated with a wider spectrum of NHL subtypes, but further study is needed to confirm and fully understand these associations.

It has been hypothesized that a high intake of dairy protein may increase prostate cancer risk by increasing the production of insulin-like growth factor 1 (IGF-1). Several single nucleotide polymo ...

Addictive behaviors, such as cigarette smoking and coffee drinking, have been associated with a reduced risk of Parkinson's disease (PD). Whether alcohol consumption is also associated with PD risk is less certain. We prospectively followed 132,403 participants in the Cancer Prevention Study II Nutrition Cohort from 1992 to 2005. Alcohol intake was assessed at baseline. Incident cases of PD (n = 605; 389 male and 216 female) were confirmed by treating physicians and medical record review. Relative risks (RRs) were estimated using proportional hazards models, adjusting for age, smoking, and other risk factors. Alcohol consumption was not significantly associated with PD risk. After adjustment for age, smoking, and other risk factors, the RR comparing men consuming 30 or more grams of alcohol per day (highest category) to nondrinker men was 1.29 (95% confidence interval [CI]: 0.90, 1.86; P trend: 0.40), and the RR comparing women consuming 15 or more grams of alcohol (highest category) per day to nondrinker women was 0.77 (95% CI: 0.41, 1.45; P trend: 0.87). Consumption of beer, wine, or liquor was also not associated with PD risk. The results of this large, prospective study do not support an association between alcohol intake and risk of PD.

Results of studies that examined the relationship between physical activity and non-Hodgkin lymphoid neoplasms (NHL) are inconsistent, and only one study to date examined time spent sitting in relation to NHL. We examined recreational physical activity and leisure-time sitting in relation to risk of NHL in the American Cancer Society Cancer Prevention Study II Nutrition Cohort. Between 1992 and 2007, 2,002 incident cases were identified among 146,850 participants who were cancer-free at enrollment. Cox proportional hazards regression was used to compute hazard ratios (HR) and 95% confidence intervals (CI) while adjusting for potential confounders. Women who sat for at least 6 hr/day were at 28% higher risk of NHL compared to women who sat for fewer than 3 hr/day. In analyses of specific subtypes, sitting time was associated with risk of multiple myeloma only (6+ vs. 3 hr/day sitting: HR = 2.40, 95% CI: 1.45-3.97). Women who engaged in any recreational physical activity had a nonsignificant 20%-30% lower risk of NHL (p-trend = 0.05) compared to women who reported no recreational physical activity. Neither leisure-time sitting nor recreational physical activity was associated with risk of NHL or major NHL subtype in men. There was no evidence of statistical interaction between physical activity and sitting time, or between body mass index and physical activity or sitting time. Further research is needed to confirm an association between sitting time and multiple myeloma and explore a possible association between physical activity and NHL.

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.

Although the value of cervical cancer screening is widely acknowledged, the effectiveness of an organized cervical cancer screening program in Korea has never been evaluated. We investigated the associations of the frequency of cervical cancer screening with cervical cancer incidence using data from a large prospective cohort study. In this analysis, 253,472 women without a hysterectomy or previous cancer diagnosis were included. Follow-up was between 1995 and 2002. Frequency of Pap smear testing was determined by searching the National Health Examination Database. Using the Korean Central Cancer Registry, 248 cases of invasive cervical cancer and 346 cases of carcinoma in situ (CIS) of the cervix were identified. Subjects screened 2 or more times showed a 71% (corrected reduction 60%) and a 66% (corrected reduction 53%) reduced risk of invasive cervical cancer and CIS of the cervix, respectively, as compared with unscreened subjects [relative risk (RR) = 0.29; 95% confidence interval (CI) = 0.20-0.45; RR = 0.34; 95% CI = 0.25-0.46, respectively]. Women with a normal or benign pap smear had a statistically significantly lower risk of invasive cervical cancer and CIS of cervix compared with those never screened. In age-stratified analyses, there was a significant reduction in cervical cancer incidence among women aged 30 and over who were screened 2 or more times compared with women never screened. The results of this prospective cohort study show that regular screening of cervical cancer reduces invasive cervical cancer incidence and CIS of the cervix among Korean women.

Elevation of ST height in the absence of coronary artery disease was first described in 1936 by Shipley and Hallaran1. This phenomenon has been referred to as “unusual RT segment deviation”, “normal RST elevation variant”, “Benign Early Repolarization” and finally “Early Repolarization” 2,3. Although non-ischemic ST elevation had been thought to be “benign”, patients with Brugada Syndrome who have right bundle branch block and ST elevation in the right precordial leads are at increased risk for sudden death4. In addition, polymorphisms in genes coding for ion channels appear to differ across ethnic groups; some of these polymorphisms might lead to ST elevations associated with sudden death5. Finally, ethnic differences in the incidence of sudden death have been described and could be related to ethnic differences in repolarization properties 6,7. Thus, a better understanding of population and ethnic distribution of ST height could provide information as to whether ST elevation is a marker of arrhythmic risk. Although initially described in non-Hispanic whites, ST elevation appears to be present in all ethnic groups. In one study, early repolarization had 0.9% overall prevalence; the incidence is 1.8% and 0.2 % respectively in men and women8. We are aware of only two studies that examined racial/ethnic differences in ST height or repolarization. Using data from the Atherosclerosis Risk in Communities Study, Vitelli et al9 found that ST height in leads V2 to V5 was statistically significantly higher in African Americans compared to Caucasians. In a population-based study conducted by Klatsky et al 8, the incidence of early repolarization, as determined by blinded cardiologists’ reading, was assessed. In that study, which contained predominantly African Americans and Caucasians and a limited number of Asians (less than 10%), the incidence of early repolarization was 1.5% in African American’s, 0.6% in Caucasians and 1.6% in Asians. To date, there are no studies comparing ST height among African Americans, Asians, Hispanics and non-Hispanic white men and women. The Multi-ethnic Study of Atherosclerosis is a longitudinal study of the health of older men and women from each of the four ethnic groups with measurements of lifestyle, anthropometric and coronary heart disease risk factors, and ST height measured at baseline. A comparison of ST height across ethnic groups is of particular interest because of the ethnic differences in inherited arrhythmia syndromes and in sudden death unassociated with the known syndromes noted above.

Background and Objectives Surgical resection is the only curative treatment for pancreatic cancer. The aim of this project was to compare risk and prognostic factors between pancreatic cancer patients treated with and without surgery. Methods Data from 32,318 cases collected from 1988 to 2002 in the Surveillance Epidemiology and End Results program were used to evaluate the odds of having surgery for pancreatic adenocarcinoma. Multivariate logistic regression was used to estimate odds ratios and 95% confidence intervals for the associations of demographic and tumor characteristics with surgical treatment. Results Overall, men were less likely to have surgery than women (OR = 0.90, 95% CI 0.83, 0.98). Compared to married patients, surgery was significantly less likely among those who were divorced/separated (OR = 0.78, 95% CI 0.68, 0.89) or widowed (OR = 0.76, 95% CI 0.67, 0.85). Black patients were less likely to receive surgery than white patients (OR = 0.79, 95% CI 0.70, 0.91). Patients diagnosed in 1997–2002 were more likely to have surgery then those diagnosed in 1988–1996. Geographic differences also exist in the frequency of surgical treatment reported by different registries. Conclusions There are differences in sociodemographic characteristics between surgically and non-surgically treated pancreatic cancers that are not entirely attributable to age, primary site, or stage at diagnosis. J. Surg. Oncol. 2008;97:578–582. © 2008 Wiley-Liss, Inc.

Summary Several chemicals have been associated with risk of non-Hodgkin’s lymphoma (NHL), many of which are substrates for N-acetyltransferase (NAT) and glutathione S-transferase (GST) enzymes. We investigated the association between polymorphisms in genes coding for these enzymes and NHL risk in a population-based study (389 cases and 535 controls). NAT1 slow genotype was associated with a slightly increased risk in women [odds ratios (OR) ¼ 1AE4; 95% confidence interval (CI) ¼ 0AE9–2AE3], but not in men. NAT2 slow genotype was not associated with risk in either sex. The two slow genotypes of NAT1 and NAT2 combined were associated with a minor increase of risk in women (OR ¼ 1AE4; 0AE8–2AE4). There was no association with the GSTM1 or GSTT1 null genotype in either sex, irrespective of histological subtypes. Individuals with GSTP1 Val homozygotes had non-significant excessive risk of marginal zone lymphoma (OR ¼ 1AE8; 0AE6–5AE1) and ‘other’ Bcell NHLs (OR ¼ 1AE6; 0AE7–3AE6), but lower risk of diffuse large B-cell lymphoma (OR ¼ 0AE2; 0AE1–0AE96). Risk did not elevate with an increasing number of high-risk GST alleles in either sex. In summary, although NAT1, NAT2, GSTM1, GSTT1 ,o rGSTP1 polymorphisms do not appear to be associated with NHL risk overall, there might be gender-specific and subtypespecific associations that require confirmation.

Despite evidence supporting the involvement of the IGF system in the development of breast and other cancers, the major determinants of interindividual variability in circulatory IGF-I levels are not well understood. Previous research has pointed to important genetic influences as well as dietary effects through marked calorie or protein restriction. We conducted a randomized trial to determine the effects of 2 dietary patterns on serum IGF-1, IGFBP1 and IGFBP3 in free-living premenopausal women: phase 1, an isocaloric low-fat, high-fiber (LFHF) vs. usual diet, and phase 2, a soy supplement either with or without isoflavones (soy+IF vs. soy-IF). Participants completed 12 menstrual cycles on phase 1 and then were randomly assigned to a soy supplement for 3 cycles while maintaining the phase 1 diet. Before and after each phase, 154 women provided serum. We found no difference in the change in IGF-I, BP1 or BP3 in the LFHF group compared to the usual diet group. In phase 2, there were no differences in any IGF protein between the soy+IF and the soy-IF groups or any evidence of interaction between isoflavone exposure and the background diet. However, there was a small but statistically significant decrease (2.3%) in BP3 and an increase in the IGF-I:BP3 molar ratio among all 153 subjects following either soy supplement. These changes were correlated with changes in intake of calcium, total vegetable protein and soy. The results are compatible with previous data suggesting that increases in dietary calcium, protein and soy, in particular, could increase circulating levels of bioavailable IGF-I.

BACKGROUND Reduction of cumulative exposure to endogenous ovarian steroid hormones is a postulated method for reducing the risk of carcinoma of the breast and other malignancies. Although there are data from trials evaluating the effect of low-fat and high-fiber diets on sex hormone levels in premenopausal women, to the authors' knowledge none of these trials has combined a relatively large number of participants, follow-up of > 2–3 months, parallel controls receiving a usual diet, and careful timing of blood sampling within the menstrual cycle. METHODS A total of 213 healthy women, ages 20–40 years, were randomly assigned to follow their usual diet or to adopt an isocaloric diet with goals of 20% calories as fat, total fiber of 25 g/day, and at least 8 fruit or vegetable servings per day. Serum levels of total estradiol (E2), sex hormone-binding globulin (SHBG), non-SHBG-bound estradiol (NSBE2), SHBG, and progesterone were evaluated during a menstrual cycle at baseline, and at 4 cycles (C4) and 12 cycles (C12) after the start of the intervention. Serum was collected during each test cycle 7–9 days after the detection of an luteinizing hormone peak in the urine. One hundred eighty-nine women provided serum at C4 and 176 women at C12. RESULTS Serum E2 decreased by an average of 7.5% or 7.8 pg/mL (95% confidence interval [95% CI], −16.0–0.04) at C12 in the intervention group, versus a decrease of 0.9% or 0.9 pg/mL (95% CI, −9.5–7.7) in the control group (the P value for the difference between the treatment groups was 0.25). Results for NSBE2 were very similar to those for total estradiol. There were no material effects found to result from intervention with regard to SHBG or progesterone. The results did not differ by baseline age, body mass index, or baseline hormone level above or below the median, and were not likely to be affected by weight change, which amounted to a mean loss of only 0.23 kg in the diet group versus a gain of 0.17 kg in the control group. The decrease in serum E2 associated with intervention was not greater when subjects were stratified by self-reported adherence to the dietary goals. CONCLUSIONS The results of the current study suggest that the effects of this isocaloric low-fat, high-fiber diet pattern on circulating ovarian steroids were modest or nonexistent. However, the observed 7.5% reduction in estradiol could have biologic significance if it persisted over many years. Moreover, underestimation of the true dietary effect could have occurred because of incomplete adherence to assigned diets. Weight loss and weight control through midlife could be a more effective and feasible approach to dietary intervention in reducing the risk of breast carcinoma. Cancer 2003. © 2003 American Cancer Society.

Results of epidemiologic studies suggest an inverse association between breast cancer risk and physical activity; this is one of the few modifiable breast cancer risk factors identified to date. However, only 2 previous studies assessed the association between physical activity and the extent of mammographically-detected fibroglandular breast density, a marker of breast cancer risk. Moreover, there has been no study of physical inactivity and percent breast density, nor a study of this relationship in Hispanic women, who are less physically active than non-Hispanic whites. In the Chicago Breast Health Project, we collected information on sociodemographic, reproductive, medical and lifestyle factors and percent breast density, assessed quantitatively using full-field digital mammography, from 294 Hispanic women. In our study, we examined the independent associations of hours per day of physical inactivity with percent breast density using multivariate linear regression analysis adjusting for age, education, body mass index, parity, menopausal status, use of hormone replacement therapy and smoking status. Overall, the mean percent breast density was low (i.e., 17.7%) and ranged from 1.9% to 54.6%. There was no difference in percent breast density for women who reported 1.5-3.0 hr of physical inactivity per day compared to women who reported 0-1 hr per day (beta = -0.08, p = 0.95), but percent density was marginally significantly higher for women who were reported at least 3.5 hr per day of physical inactivity (beta = 3.18, p = 0.056). Results were similar, albeit less statistically significant, in analyses of pre/perimenopausal and postmenopausal women separately. These results support the need for further research investigating the effect of physical activity on breast cancer risk.

BACKGROUND Although axillary lymph node metastasis is one of the most important prognostic determinants of breast carcinoma prognoses, the reasons why tumors vary in their capability to produce for axillary metastases remain unclear. METHODS The authors used data from the nationwide Patient Care Evaluation (PCE) survey of the American College of Surgeons to evaluate the correlations between patient/tumor characteristics and lymph node status, and to explore the use of these factors, which are all known prior to axillary dissection, in predicting lymph node status. The PCE data set contained 18,025 breast carcinoma cases diagnosed in 1990 after exclusion of women older than 79 years or with fewer than 6 lymph nodes examined. RESULTS In a multivariate logistic regression model, larger tumor size, young age, African American or Hispanic race, outer half tumor location, poor or moderate differentiation, aneuploidy, and infiltrating ductal histology were independently associated with a higher likelihood of one or more positive lymph nodes. Contrary to expectation, cases negative for estrogen receptor (ER) and progesterone receptor (PR) had a lower risk of positive lymph nodes when adjusted for other factors (odds ratio = 0.82; 95% confidence interval: 0.74–0.91) compared with cases positive for both receptors. This model accurately predicted lymph node status in 2 validation data sets (a 50% random sample of 1990 PCE data and 1992 data from the National Cancer Data Base), but was less accurate in a third, older data set (1983 PCE data). However, the percentage of cases (1990 validation set) with predicted probabilities less than 0.05 or greater than 0.95 were only 4.6% and

BACKGROUND It has been postulated that different biologic characteristics of a tumor might account for at least a portion of the disparity in breast cancer survival for patients across racial and ethnic groups. The hormone receptor status of breast tumors is one characteristic with prognostic significance. Results of several studies indicate a higher proportion of estrogen receptor negative (ER-) breast tumors among black or Hispanic women compared with non-Hispanic whites. We investigated whether the association between race and ethnicity and the joint combination of ER and progesterone receptor (PR) status was independent of age and other tumor characteristics at diagnosis. METHODS Relevant data were obtained from 13,239 breast cancer cases identified as part of the 1990 Patient Care Evaluation Study of Breast Cancer. RESULTS In univariate analysis, the proportions of ER+PR+, ER+PR−, ER−PR+, and ER−PR− tumors among non-Hispanic whites were 59%, 15%, 6%, and 20%, respectively; among Hispanics the proportions were 58%, 12%, 8%, and 22%, respectively; and among blacks the proportions were 44%, 14%, 7%, and 35%, respectively. After controlling for age, tumor size, and histology, using polychotomous logistic regression, there was no difference in hormone-receptor status between Hispanic and non-Hispanic white women. However, ER−PR− tumors were more likely to occur in blacks than in non-Hispanic whites (odds ratio = 1.8, 95% confidence interval = 1.6, 2.1) CONCLUSIONS The results of this study corroborate differences in hormone-receptor status between non-Hispanic white and black women, but not between Hispanics. Future studies of breast cancer should examine differences in epidemiologic risk factors between blacks and whites stratified on ER/PR status. Cancer 1996; 77:1465-71.

Chromatographic, peptide mapping and mass spectrometric analysis were used to examine hemoglobin (Hb) from heavy drinkers and abstainers for alcohol consumption-related modifications. Heavy drinker and abstainer hemoglobin samples contained similar amounts of glycosylated Hb and significantly different (p < 0.05) amounts of "fast" hemoglobin. The presence of higher amounts of "fast" Hb in heavy drinker relative to abstainer samples suggested the presence of alcohol-consumption related modifications. To further examine Hb for modifications, tryptic peptides of the "fast" hemoglobin HbA1c were isolated and analyzed by plasma desorption mass spectrometry (PDMS). [14C]acetaldehyde (AcH)-Hb was synthesized in vivo for use as a standard. Specific peptides were chosen based on co-migration with radiolabeled peptides from a tryptic digest of the [14C]acetaldehyde-Hb. The masses obtained by PDMS for two heavy drinker peptides were identical to two radiolabeled peptides; the two pairs of peptides co-migrated on HPLC. A comparison of the observed mass for the peptides with the theoretical masses for acetaldehyde-modified Hb peptides suggested that the peptides were AcH-modified alpha and beta chain N-termini of Hb. The modified peptides were found in five of six heavy drinker samples. This is the first description of site-specific AcH-Hb adducts occurring in vivo. The routine detection of such adducts has potential for characterizing usual alcohol intake.