Search

Purpose Alcohol consumption is hypothesized to increase the risk of endometrial cancer by increasing circulating estrogen levels. This study sought to investigate the association between lifetime alcohol consumption and endometrial cancer risk. Methods We recruited 514 incident endometrial cancer cases and 962 frequency age-matched controls in this population-based case–control study in Alberta, Canada, from 2002 to 2006. Participants completed in-person interviews querying lifetime alcohol consumption and other relevant health and lifestyle factors. Participants reported the usual number of drinks of beer, wine, and liquor consumed; this information was compiled for each drinking pattern reported over the lifetime to estimate average lifetime exposure to alcohol. Results Lifetime average alcohol consumption was relatively low (median intake: 3.9 g/day for cases, 4.9 g/day for controls). Compared with lifetime abstainers, women consuming >2.68 and ≤8.04 g/day alcohol and >8.04 g/day alcohol on average over the lifetime showed 38 and 35 % lower risks of endometrial cancer, respectively (p trend = 0.023). In addition, average lifetime consumption of all types of alcohol was associated with decreased risks. There was no evidence for effect modification by body mass index, physical activity, menopausal status, and hormone replacement therapy use combined and effects did not differ by type of endometrial cancer (type I or II). Conclusion This study provides epidemiologic evidence for an inverse association between relatively modest lifetime average alcohol consumption (approximately 1/4 to 1/2 drink/day) and endometrial cancer risk. The direction of this relation is consistent with previous studies that examined similar levels of alcohol intake.

Purpose To determine the risk of Hodgkin lymphoma (HL) associated with exposures to multiple pesticides grouped by various classes, including carcinogenic classifications. Methods Data collected in the Cross-Canada Study of Pesticides and Health, a population-based incident case–control study in six provinces conducted between 1991 and 1994, were analyzed using unconditional logistic regression. Cases (n = 316) were identified through provincial cancer registries and hospital records. Controls (n = 1,506) were frequency-matched to cases by age (±2 years) within each province and were identified through provincial health records, telephone listings, or voter lists. The Cochran–Armitage test was used to check for trends within pesticide classes. Results Overall, there was an increase in the risk of HL among all subjects who reported use of five or more insecticides (OR 1.88, 95 % CI 0.92–3.87) and among subjects younger than 40 who reported use of two acetylcholinesterase inhibitors (OR 3.16, 95 % CI 1.02–9.29). There was an elevated odds ratio associated with reported use of three or more probably carcinogenic pesticides (OR 2.47, 95 % CI 1.06–5.75), but no increase in risk for use of possibly carcinogenic pesticides. The risk of HL from reported use of fungicides or any pesticides was greater for cases diagnosed before age 40 than for cases diagnosed at or after age 40. When analyses excluded proxy respondents, OR estimates strengthened in some circumstances. Conclusions This study found associations between HL and fungicides, insecticides, specifically acetylcholinesterase inhibitors, and pesticides previously identified as probable human carcinogens. These associations should be further evaluated, specifically in relation to age at diagnosis.

Purpose We investigated the association between serum levels of 25-hydroxyvitamin D (25-OHD) and risk of death in Norwegian cancer patients. Methods The study population was 658 patients with cancers of the breast (n = 251), colon (n = 52), lung (n = 210), and lymphoma (n = 145), obtained from JANUS, a population-based serum bank in Norway. Serum samples were collected within 90 days of cancer diagnosis and were analyzed for 25-OHD. Patients were diagnosed during 1984–2004 and were followed for death throughout 2008. We used Cox regression models to assess the relationship between serum 25-OHD and risk of death. Results Three hundred and ninety-nine patients died during follow-up, of whom 343 (86%) died from cancer. Adjusted for sex, age at diagnosis, and season of blood sampling, patients with 25-OHD levels below 46 nmol/L at diagnosis experienced shorter survival. Compared to patients in the lowest quartile of serum 25-OHD, the risk of cancer death among patients in the highest quartile was significantly reduced (HR 0.36 95% CI 0.27, 0.51). The estimated change in risk of cancer death was most pronounced between the first and the second quartile. The associations between 25-OHD levels and survival were observed for all four cancers. Conclusions Higher circulating serum levels of 25-OHD were positively associated with the survival for cancers of the breast, colon, lung, and lymphoma.

Objective To identify factors that mediate or moderate the effects of exercise on postmenopausal sex hormone concentrations. Methods Postmenopausal women were randomized to 12 months of aerobic exercise for 200 min/week (n = 160) or to a control group (n = 160). Intention-to-treat analyses were performed using general linear models with sex hormone concentrations at 6 and 12 months as the outcome. Mediation by adiposity and insulin was investigated by examining changes in effect estimates after adjustment for changes in these factors over 12 months. Moderation was studied as the interaction between group assignment and eight baseline characteristics. Results Intervention effects on sex hormone–binding globulin (SHBG) and estradiol changes were attenuated with adjustment for change in overall body fat, while there was less attenuation adjusting for intra-abdominal fat change. Intervention effects on SHBG levels were unaffected by adjustment for insulin change. Significant interactions were identified between treatment and physical fitness (for SHBG and testosterone) and age (for testosterone), implying subgroup differences in intervention effect. Conclusions Our data suggest that overall fat loss partially mediated exercise-induced changes in estradiol and SHBG concentrations. No previous RCT in postmenopausal women has studied moderators of exercise-induced sex hormone changes; therefore, future studies are needed to corroborate our results.

Objective Finasteride reduces prostate cancer risk by blocking the conversion of testosterone to dihydrotestosterone. However, whether finasteride affects estrogens levels or change in estrogens affects prostate cancer risk is unknown. Methods These questions were investigated in a case–control study nested within the prostate cancer prevention trial (PCPT) with 1,798 biopsy-proven prostate cancer cases and 1,798 matched controls. Results Among men on placebo, no relationship of serum estrogens with risk of prostate cancer was found. Among those on finasteride, those in the highest quartile of baseline estrogen levels had a moderately increased risk of Gleason score

Background We examine whether the lung cancer risk due to smoking has increased over time. Methods Lung cancer risk equations based on prospective mortality data collected from 1960 to 1972 were applied to 5-year birth-cohort-specific estimates of smoking behaviors among white males to estimate lung cancer mortality rates for U.S. white males from 1960 to 2000. These estimated rates were compared to U.S. white male mortality rates for the same birth cohorts. Results Observed birth-cohort-specific U.S. lung cancer mortality rates are substantially higher than those expected from changes in smoking behaviors, and the proportional difference increases with advancing calendar year. This trend persisted even when the duration term was increased in the risk equation. However, adjusting for changes in cigarette design over time by adding a term for the duration of smoking after 1972 resulted in the predicted rates closely approximating the observed U.S. mortality rates. Conclusion Lung cancer risk estimates observed during the 1960s under predict current lung cancer mortality rates in U.S. white males. Adjustment for the duration of smoking after 1972 results in estimates that reasonably approximate the observed U.S. lung cancer mortality, suggesting that lung cancer risks from smoking are increasing in the United States coincident with changes in cigarette design.

Background: We investigated the association between hypertension, antihypertensive (AH) medication use, and breast cancer in a large prospective study, the California Teachers Study (CTS). Methods: Information on history of hypertension and lifetime regular use of AH medications was collected from 114,549 women in 1995-1996. Among them, 4,151 invasive breast cancers were diagnosed between 1995 and 2006. Additional information on AH use was collected from 73,742 women in 2000-2001, and 1,714 of these women were subsequently diagnosed with breast cancer. Cox proportional hazards regression was used to estimate relative risks (RR) and 95% confidence intervals (CI) for breast cancer. Results: Use of AH medication for ≥5 years, when compared with no use, was associated with a modest increased risk of invasive breast cancer (RR = 1.18, 95%CI 1.02-1.36). This increased risk appeared to be confined to estrogen receptor (ER)-positive tumors (RR = 1.21, 95%CI 1.03-1.43) and pre-/peri-menopausal women (RR = 1.58, 95%CI 1.11-2.25). Conclusions: Increased risk of invasive breast cancer was observed for long-term (≥5 years) AH use, and this appeared to be confined to ER + breast cancer and younger women. © 2010 The Author(s).

Objective Very few studies have simultaneously examined incidence of the leading cancers in relation to socioeconomic status (SES) and race/ethnicity in populations including Hispanics and Asians. This study aims to describe SES disparity in cancer incidence within each of four major racial/ethnic groups (non-Hispanic white, black, Hispanic, and Asian/Pacific Islander) for five major cancer sites, including female breast cancer, colorectal cancer, cervical cancer, lung cancer, and prostate cancer. Methods Invasive cancers of the five major sites diagnosed from 1998 to 2002 (n = 376,158) in California were included in the study. Composite area-based SES measures were used to quantify SES level and to calculate cancer incidence rates stratified by SES. Relative index of inequality (RII) was generated to measure SES gradient of cancer incidence within each racial/ethnic group. Results Significant variations were detected in SES disparities across the racial/ethnic groups for all five major cancer sites. Female breast cancer and prostate cancer incidence increased with increased SES in all groups, with the trend strongest among Hispanics. Incidence of cervical cancer increased with decreased SES, with the largest gradient among non-Hispanic white women. Lung cancer incidence increased with decreased SES with the exception of Hispanic men and women, for whom SES gradient was in the opposite direction. For colorectal cancer, higher incidence was associated with lower SES in non-Hispanic whites but with higher SES in Hispanics and Asian/Pacific Islander women. Conclusions Examining SES disparity stratified by race/ethnicity enhances our understanding of the complex relationships between cancer incidence, SES, and race/ethnicity.

OBJECTIVE: Although the effect of fruit and vegetables on the risk of bladder cancer has been widely studied, little is known about their micronutrient components. Our aim was to investigate associations between minerals and vitamins and bladder cancer. METHODS: A case-control study was conducted in New Hampshire, USA. Dietary data were collected from 322 cases and 239 controls using a 121-item food frequency questionnaire. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated using logistic regression adjusting for sex, age, smoking characteristics, and energy intake. RESULTS: The ORs (95% CI) for highest quartile versus lowest quartile for total intake of vitamin E was 0.66 (0.36-1.20; p trend = 0.09) and 0.49 (0.21-1.17; p trend = 0.13) for dietary phosphorus. The odds of bladder cancer for heavy smokers with the highest total intake of vitamin E, carotenoids, and niacin were 0.58 (0.34-0.99), 0.62 (0.36-1.09), and 0.66 (0.39-1.14), respectively. Higher total intakes of carotenoids, vitamin D, thiamin, niacin, and vitamin E were inversely related to bladder cancer risk among older individuals. CONCLUSION: Our findings suggest further investigation of the effect of vitamin E, carotenoids, vitamin D, thiamin, and niacin on bladder cancer risk may be warranted. Future studies should focus on high risk groups such as heavy smokers and older individuals.

Contains fulltext : 88547.pdf (Publisher’s version ) (Closed access) OBJECTIVE: To examine the association between fruit and vegetable consumption and risk of different histological subtypes of lung cancer among participants of the European Prospective Investigation into Cancer and Nutrition study. METHODS: Multivariable Cox proportional hazard models were used to analyze the data. A calibration study in a subsample was used to reduce dietary measurement errors. RESULTS: During a mean follow-up of 8.7 years, 1,830 incident cases of lung cancer (574 adenocarcinoma, 286 small cell, 137 large cell, 363 squamous cell, 470 other histologies) were identified. In line with our previous conclusions, we found that after calibration a 100 g/day increase in fruit and vegetables consumption was associated with a reduced lung cancer risk (HR 0.94; 95% CI 0.89-0.99). This was also seen among current smokers (HR 0.93; 95% CI 0.90-0.97). Risks of squamous cell carcinomas in current smokers were reduced for an increase of 100 g/day of fruit and vegetables combined (HR 0.85; 95% CI 0.76-0.94), while no clear effects were seen for the other histological subtypes. CONCLUSION: We observed inverse associations between the consumption of vegetables and fruits and risk of lung cancer without a clear effect on specific histological subtypes of lung cancer. In current smokers, consumption of vegetables and fruits may reduce lung cancer risk, in particular the risk of squamous cell carcinomas. 01 maart 2010

Background Human papilloma virus (HPV) prevalence studies performed in different regions and population groups across Canada would inform public health decisions regarding implementation of anti-HPV vaccines. Methods A total of 8,700 liquid-based specimens from 8,660 women aged 13–86 from throughout British Columbia were collected. DNA was isolated from 4,980 of these samples and assessed for HPV prevalence and type distribution. HPV was detected by PCR analysis using tagged GP5+/6+ consensus primers to amplify the L1 region of HPV; typing was done by bi-directional sequencing of PCR products. Results Overall HPV prevalence was 16.8% (age adjusted 15.5%). Prevalence of high-risk HPV was 13.9, and 10.7% of samples contained HPV16. HPV prevalence was highest in the youngest group of women (

Background Epidemiologic research into cancer and subsequent decision making to reduce the cancer burden in the population are dependent on the quality of available data. The more reliable the data, the more confident we can be that the decisions made would have the desired effect in the population. The North American Association of Central Cancer Registries (NAACCR) certifies population-based cancer registries, ensuring uniformity of data quality. An important assessment of registry quality is provided by the index of completeness of cancer case ascertainment. NAACCR currently computes this index assuming that the ratio of cancer incidence rates to cancer mortality rates is constant across geographic areas within cancer site, gender, and race groups. NAACCR does not incorporate the variability of this index into the certification process. Methods We propose an improved method for calculating this index based on a statistical model developed at the National Cancer Institute to predict expected incidence using demographic and lifestyle data. We calculate the variance of our index using statistical approximation. Results We use the incidence model to predict the number of new incident cases in each registry area, based on all available registry data. Then we adjust the registry-specific expected numbers for reporting delay and data corrections. The proposed completeness index is the ratio of the observed number to the adjusted prediction for each registry. We calculate the variance of the new index and propose a simple method of incorporating this variability into the certification process. Conclusions Better modeling reduces the number of registries with unrealistically high completeness indices. We provide a fuller picture of registry performance by incorporating variability into the certification process.

Objectives We report cancer incidence, mortality, and stage distributions among Asians and Pacific Islanders (API) residing in the U.S. and note health disparities, using the cancer experience of the non-Hispanic white population as the referent group. New databases added to publicly available SEER*Stat software will enable public health researchers to further investigate cancer patterns among API groups. Methods Cancer diagnoses among API groups occurring from 1 January 1998 to 31 December 2002 were included from 14 Surveillance, Epidemiology, and End Results (SEER) Program state and regional population-based cancer registries covering 54% of the U.S. API population. Cancer deaths were included from the seven states that report death information for detailed API groups and which cover over 68% of the total U.S. API population. Using detailed racial/ethnic population data from the 2000 decennial census, we produced incidence rates centered on the census year for Asian Indians/Pakistanis, Chinese, Filipinos, Guamanians, Native Hawaiians, Japanese, Kampucheans, Koreans, Laotians, Samoans, Tongans, and Vietnamese. State vital records offices do not report API deaths separately for Kampucheans, Laotians, Pakistanis, and Tongans, so mortality rates were analyzed only for the remaining API groups. Results Overall cancer incidence rates for the API groups tended be lower than overall rates for non-Hispanic whites, with the exception of Native Hawaiian women (All cancers rate = 488.5 per 100,000 vs. 448.5 for non-Hispanic white women). Among the API groups, overall cancer incidence and death rates were highest for Native Hawaiian and Samoan men and women due to high rates for cancers of the prostate, lung, and colorectum among Native Hawaiian men; cancers of the prostate, lung, liver, and stomach among Samoan men; and cancers of the breast and lung among Native Hawaiian and Samoan women. Incidence and death rates for cancers of the liver, stomach, and nasopharynx were notably high in several of the API groups and exceeded rates generally seen for non-Hispanic white men and women. Incidence rates were lowest among Asian Indian/Pakistani and Guamanian men and women and Kampuchean women. Asian Indian and Guamanian men and women also had the lowest cancer death rates. Selected API groups had less favorable distributions of stage at diagnosis for certain cancers than non-Hispanic whites. Conclusions Possible disparities in cancer incidence or mortality between specific API groups in our study and non-Hispanic whites (referent group) were identified for several cancers. Unfavorable patterns of stage at diagnosis for cancers of the colon and rectum, breast, cervix uteri, and prostate suggest a need for cancer control interventions in selected groups. The observed variation in cancer patterns among API groups indicates the importance of monitoring these groups separately, as these patterns may provide etiologic clues that could be investigated by analytic epidemiological studies.