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Michael J Thun

Publications and source records attributed to Michael J Thun.

At least 19 recordsLinked to original sources
PubMed2007

Glycemic load, glycemic index, and carbohydrate intake in relation to pancreatic cancer risk in a large US cohort.

BACKGROUND: Consumption of diets with high glycemic load has been hypothesized to increase pancreatic cancer risk by raising postprandial glucose levels and insulin secretion. METHODS: The authors analyzed data from the American Cancer Society Cancer Prevention Study II (CPS-II) Nutrition Cohort to examine the association between pancreatic cancer and glycemic load, glycemic index (GI), and intake of carbohydrates. Diet was assessed among 124,907 men and women who were cancer-free and non-diabetic at baseline in 1992 using a validated 68-item food frequency questionnaire (FFQ). During 9 years of follow-up, 401 incident pancreatic cancer cases were identified. Cox proportional hazards modeling was used to compute hazard rate ratios (RR) adjusted for potential confounding factors. RESULTS: We found no association between glycemic load, GI, or carbohydrate intake and risk of pancreatic cancer in this population. The hazard rate ratio (RR) was 1.01 (95% CI 0.75-1.37, trend P=0.80) for glycemic load, 0.92 (95% CI 0.68-1.24) for GI, and 1.10 (95% CI 0.80-1.51) for carbohydrate intake among men and women in the highest quintile compared to the lowest quintile of each measure. We also found no significant association between these measures and pancreatic cancer risk among individuals who show a greater susceptibility towards insulin insensitivity, such as those who are overweight or more sedentary. CONCLUSION: Overall, our data do not support the hypothesis that glycemic load or index, or carbohydrate intake are associated with a substantial increase in pancreatic cancer risk; however, a weak positive association cannot be ruled out.

Aged↗
PubMed2006

Body mass index, weight change, and risk of prostate cancer in the Cancer Prevention Study II Nutrition Cohort.

BACKGROUND: Obesity has been associated with aggressive prostate cancer. The extent of this association, which varies by stage and grade, remains unclear. The role of recent weight change had not been previously examined. METHODS: We examined body mass index (BMI) and weight change in relation to incident prostate cancer by disease stage and grade at diagnosis among 69,991 men in the Cancer Prevention Study II Nutrition Cohort. Participants provided information on height and weight in 1982, and again at enrollment in 1992. During follow-up through June 30, 2003 (excluding the first 2 years of follow-up), we documented 5,252 incident prostate cancers. Cox proportional hazards models were used to estimate rate ratios (RR) and 95% confidence intervals (95% CI). RESULTS: The association between BMI in 1992 and risk of prostate cancer differed by stage and grade at diagnosis. BMI was inversely associated with risk of nonmetastatic low-grade prostate cancer (RR, 0.84; 95% CI, 0.66-1.06), but BMI was positively associated with risk of nonmetastatic high-grade prostate cancer (RR, 1.22; 95% CI, 0.96-1.55) and risk of metastatic or fatal prostate cancer (RR, 1.54; 95% CI, 1.06-2.23). Compared with weight maintenance, men who lost >11 pounds between 1982 and 1992 were at a decreased risk of nonmetastatic high-grade prostate cancer (RR, 0.58; 95% CI, 0.42-0.79). CONCLUSION: Obesity increases the risk of more aggressive prostate cancer and may decrease either the occurrence or the likelihood of diagnosis of less-aggressive tumors. Men who lose weight may reduce their risk of prostate cancer.

Aged↗
PubMed2006

A midpoint assessment of the American Cancer Society challenge goal to halve the U.S. cancer mortality rates between the years 1990 and 2015.

BACKGROUND: The American Cancer Society has challenged the U.S. to reduce cancer mortality rates 50% over the 25 years from 1990 to 2015. The current report is an analysis and commentary on progress toward that goal through 2002, the midpoint of the challenge period. METHODS: Cancer mortality rates were examined from 1990 through 2002, and projections to the Year 2015 were made. Cancer deaths that were prevented or deferred by the declining death rates were expressed as the difference between the observed and projected numbers of deaths and the numbers that would have been observed over that period had the 1990 death rates persisted. RESULTS: Since 1990, cancer mortality rates have been declining in the U.S. by approximately 1% per year. Trends especially have been favorable for cancers of the breast, prostate, and colorectum and for lung cancer among men. Should this rate of decline continue over the coming decade, death rates from cancer will be approximately 23% lower in the Year 2015 than they were in 1990, and approximately 1.8 million deaths from cancer will have been prevented or deferred. CONCLUSIONS: At this midpoint of the 25-year challenge period, it appears that fully reaching the goal will require substantial breakthroughs in cancer early detection and/or in cancer therapy. Between now and 2015, however, many more cancer deaths can be averted by concerted action to control tobacco and obesity, by redoubling efforts in mammography and colorectal screening, and by enacting policies to close gaps in access to cancer detection and treatment services.

Adult↗
PubMed2006

Adult weight gain and histopathologic characteristics of breast cancer among postmenopausal women.

BACKGROUND: Although the link between postmenopausal breast cancer and adiposity is well established, the association between weight gain and specific histopathologic characteristics of breast carcinoma has not been studied carefully. METHODS: Using 1200 incident invasive breast cancers among 44,161 postmenopausal women who were not taking hormone therapy in the American Cancer Society's Cancer Prevention Study II Nutrition Cohort, the authors computed age-adjusted rates and rate ratios (RR) for breast cancer by histology, stage, grade, and estrogen receptor (ER) and progesterone receptor (PR) status by categories of adult weight gain. RESULTS: Age-adjusted rates of breast cancer were highest for women who reported the most weight gain, regardless of histologic type. For weight gain >60 pounds, compared with weight gain < or =20 pounds the RR for ductal carcinoma was 1.89 (95% confidence interval [95%CI], 1.53-2.34), and the RR for lobular carcinoma was 1.54 (95%CI. 1.01-2.33). Weight gain was associated with increased risk at every tumor stage and grade. The risk for regional or distant stage was elevated significantly in every category of weight gain and was 3 times higher among women who had the greatest weight gain (RR, 3.15; 95%CI, 2.21-4.48). Weight gain was associated with increased risk of ER-positive/PR-positive tumors (P for trend <.0001) but not ER-negative/PR-negative tumors (P for trend = .09). The results essentially remained unchanged when the analysis was restricted to women who had regular screening mammograms. CONCLUSIONS: Excess adiposity is an important contributor to breast cancer risk among postmenopausal women, regardless of histologic type, and especially for tumors of advanced stage and high grade.

Age Distribution↗
PubMed2006

U.S. congressional district cancer death rates.

BACKGROUND: Geographic patterns of cancer death rates in the U.S. have customarily been presented by county or aggregated into state economic or health service areas. Herein, we present the geographic patterns of cancer death rates in the U.S. by congressional district. Many congressional districts do not follow state or county boundaries. However, counties are the smallest geographical units for which death rates are available. Thus, a method based on the hierarchical relationship of census geographic units was developed to estimate age-adjusted death rates for congressional districts using data obtained at county level. These rates may be useful in communicating to legislators and policy makers about the cancer burden and potential impact of cancer control in their jurisdictions. RESULTS: Mortality data were obtained from the National Center for Health Statistics (NCHS) for 1990-2001 for 50 states, the District of Columbia, and all counties. We computed annual average age-adjusted death rates for all cancer sites combined, the four major cancers (lung and bronchus, prostate, female breast, and colorectal cancer) and cervical cancer. Cancer death rates varied widely across congressional districts for all cancer sites combined, for the four major cancers, and for cervical cancer. When examined at the national level, broad patterns of mortality by sex, race and region were generally similar with those previously observed based on county and state economic area. CONCLUSION: We developed a method to generate cancer death rates by congressional district using county-level mortality data. Characterizing the cancer burden by congressional district may be useful in promoting cancer control and prevention programs, and persuading legislators to enact new cancer control programs and/or strengthening existing ones. The method can be applied to state legislative districts and other analyses that involve data aggregation from different geographic units.

Age Distribution↗
PubMed2006

Lung cancer death rates in lifelong nonsmokers.

BACKGROUND: Few studies have directly measured the age-, sex-, and race-specific risks of lung cancer incidence and mortality among never tobacco smokers. Such data are needed to quantify the risks associated with smoking and to understand racial and sex disparities and temporal trends that are due to factors other than active smoking. METHODS: We measured age-, sex-, and race-specific rates (per 100,000 person-years at risk) of death from lung cancer among more than 940,000 adults who reported no history of smoking at enrollment in either of two large American Cancer Society Cancer Prevention Study cohorts during 1959-1972 (CPS-I) and 1982-2000 (CPS-II). We compared lung cancer death rates between men and women and between African Americans and whites and analyzed temporal trends in lung cancer death rates among never smokers across the two studies by using directly age-standardized rates as well as Poisson and Cox proportional hazards regression analyses. All statistical tests were two-sided. RESULTS: The age-standardized lung cancer death rates among never-smoking men and women in CPS-II were 17.1 and 14.7 per 100,000 person-years, respectively. Men who had never smoked had higher age-standardized lung cancer death rates than women in both studies (CPS-I: hazard ratio [HR] = 1.52, 95% confidence interval [CI] = 1.28 to 1.79; CPS-II: HR = 1.21, 95% CI = 1.09 to 1.36). The rate was higher among African American women than white women in CPS-II (HR = 1.43, CI = 1.11 to 1.85). A small temporal increase (CPS-II versus CPS-I) in lung cancer mortality was seen for white women (HR = 1.25, CI = 1.12 to 1.41) and African American women (HR = 1.22, CI = 0.64 to 2.33), but not for white men (HR = 0.89, CI = 0.74 to 1.08). Among white and African American women combined, the temporal increase was statistically significant only among those aged 70-84 years (P < .001). CONCLUSIONS: Contrary to clinical perception, the lung cancer death rate is not higher in female than in male never smokers and shows little evidence of having increased over time in the absence of smoking. Factors that affect the interpretation of lung cancer trends are discussed. Our novel finding that lung cancer mortality is higher among African American than white women never smokers should be confirmed in other studies.

Adult↗
PubMed2006

Polymorphisms in the vascular endothelial growth factor gene and breast cancer in the Cancer Prevention Study II cohort.

INTRODUCTION: Vascular endothelial growth factor (VEGF) plays a central role in promoting angiogenesis and is over-expressed in breast cancer. At least four polymorphisms in the VEGF gene have been associated with changes in VEGF expression levels: -2578C/A, -1154G/A and -634G/C are all located in the promoter region; and +936C/T is located in the 3'-untranslated region. METHOD: We examined the association between these four VEGF polymorphisms and risk for breast cancer among postmenopausal women in CPS-II (Cancer Prevention Study II) Nutrition Cohort. This cohort was established in 1992 and participants were invited to provide a blood sample between 1998 and 2001. Included in this analysis were 501 postmenopausal women who provided a blood sample and were diagnosed with breast cancer between 1992 and 2001 (cases). Control individuals were 504 cancer-free postmenopausal women matched to the cases with respect to age, race/ethnicity, and date of blood collection (controls). RESULTS: We found no association between any of the polymorphisms examined and overall breast cancer risk. However, associations were markedly different in separate analyses of invasive cancer (n = 380) and in situ cancer (n = 107). The -2578C and -1154G alleles, which are both hypothesized to increase expression of VEGF, were associated with increased risk for invasive breast cancer (odds ratio [OR] 1.46, 95% confidence interval [CI] 1.00-2.14 for -2578 CC versus AA; OR 1.64, 95% CI 1.02-2.64 for -1154 GG versus AA) but they were not associated with risk for in situ cancer. The +936C allele, which is also hypothesized to increase VEGF expression, was not clearly associated with invasive breast cancer (OR 1.21, 95% CI 0.88-1.67 for +936 CC versus TT/CT), but it was associated with reduced risk for in situ cancer (OR 0.59, 95% CI 0.37-0.93 for CC versus TT/CT). The -634 C/G polymorphism was not associated with either invasive or in situ cancer. CONCLUSION: Our findings provide limited support for the hypothesis that the -2578C and -1154G VEGF alleles are associated with increased risk for invasive but not in situ breast cancer in postmenopausal women.

Breast Neoplasms↗
PubMed2006

Folate nutrition and prostate cancer incidence in a large cohort of US men.

Folate has important roles in DNA synthesis, repair, and methylation and is inversely associated with the risk of some cancers. The authors examined this association among 65,836 men in the American Cancer Society Cancer Prevention Study II Nutrition Cohort. During 9 years of follow-up, 5,158 men were diagnosed with prostate cancer. Folate intakes were estimated from the questionnaire administered at enrollment in 1992-1993, and Cox proportional hazards models were used to calculate hazard rate ratios adjusted for potential confounders. Neither dietary nor total folate intake was associated with prostate cancer overall. However, higher folate levels were associated with a nonsignificant decreased risk of advanced prostate cancer (multivariate rate ratio=0.78, 95% confidence interval: 0.53, 1.15 for the highest vs. lowest quintiles of dietary folate and rate ratio=0.79, 95% confidence interval: 0.54, 1.17 for the highest vs. lowest quintile of total folate). The association was similar for quintiles 2-5, suggesting that only a small increase in folate intake was needed to alter the risk of advanced prostate cancer. Because the statistical power of the analysis with advanced prostate cancer was limited by the low number of cases, further study is needed to establish this association.

Aged↗
PubMed2006

Recreational physical activity and sedentary behavior in relation to ovarian cancer risk in a large cohort of US women.

Factors that influence circulating sex hormones, such as physical activity, have been proposed to influence ovarian cancer risk; however, results from previous epidemiologic studies have been inconsistent. The authors examined the association among physical activity, sedentary behavior, and ovarian cancer risk in the American Cancer Society Cancer Prevention Study II Nutrition Cohort, a prospective study of cancer incidence and mortality, using information obtained at baseline in 1992. From 1992 to 2001, 314 incident ovarian cancer cases were identified among 59,695 postmenopausal women who were cancer free at enrollment. Cox proportional hazards modeling was used to compute hazard rate ratios while adjusting for potential confounders. No overall association was observed between measures of past physical activity or with recreational physical activity at baseline and risk of ovarian cancer in this study (for the highest category of physical activity compared with none: hazard rate ratio = 0.73, 95% confidence interval: 0.40, 1.34). However, a prolonged duration of sedentary behavior was associated with an increased risk (for > or = 6 vs. < 3 hours per day: hazard rate ratio = 1.55, 95% confidence interval: 1.08, 2.22; p(trend) = 0.01). Results from this study suggest that high levels of sedentary behavior may increase the risk of ovarian cancer, but they do not support a major impact of light and moderate physical activity on ovarian cancer risk.

Aged↗
PubMed2006

Haplotype analysis of the HSD17B1 gene and risk of breast cancer: a comprehensive approach to multicenter analyses of prospective cohort studies.

The 17beta-hydroxysteroid dehydrogenase 1 gene (HSD17B1) encodes 17HSD1, which catalyzes the final step of estradiol biosynthesis. Despite the important role of HSD17B1 in hormone metabolism, few epidemiologic studies of HSD17B1 and breast cancer have been conducted. This study includes 5,370 breast cancer cases and 7,480 matched controls from five large cohorts in the Breast and Prostate Cancer Cohort Consortium. We characterized variation in HSD17B1 by resequencing and dense genotyping a multiethnic sample and identified haplotype-tagging single nucleotide polymorphisms (htSNP) that capture common variation within a 33.3-kb region around HSD17B1. Four htSNPs, including the previously studied SNP rs605059 (S312G), were genotyped to tag five common haplotypes in all cases and controls. Conditional logistic regression was used to estimate odds ratios (OR) for disease. We found no evidence of association between common HSD17B1 haplotypes or htSNPs and overall risk of breast cancer. The OR for each haplotype relative to the most common haplotype ranged from 0.98 to 1.07 (omnibus test for association: X2 = 3.77, P = 0.58, 5 degrees of freedom). When cases were subdivided by estrogen receptor (ER) status, two common haplotypes were associated with ER-negative tumors (test for trend, Ps = 0.0009 and 0.0076; n = 353 cases). HSD17B1 variants that are common in Caucasians are not associated with overall risk of breast cancer; however, there was an association among the subset of ER-negative tumors. Although the probability that these ER-negative findings are false-positive results is high, these findings were consistent across each cohort examined and warrant further study.

17-Hydroxysteroid Dehydrogenases↗
PubMed2006

Cholesterol-lowering drugs and colorectal cancer incidence in a large United States cohort.

3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors, commonly known as statins, account for most cholesterol-lowering drug use in the United States. A recent large case-control study reported that use of statins for more than 5 years was associated with a 47% reduction in risk of colorectal cancer. No other large studies have examined this association. We examined the association between use of cholesterol-lowering drugs and colorectal cancer incidence among 132,136 men and women in the Cancer Prevention Study II Nutrition Cohort. We identified 815 incident cases of colorectal cancer among study participants during follow-up from the date of completion of a study questionnaire in 1997 through August 31, 2001. Current use of cholesterol-lowering drugs was not associated with colorectal cancer incidence (multivariable adjusted rate ratio [RR] = 1.03, 95% confidence interval [CI] = 0.85 to 1.26). Current use of cholesterol-lowering drugs for 5 years or more was also not associated with colorectal cancer incidence (multivariable adjusted RR = 1.09, 95% CI = 0.83 to 1.43). Our results do not support the hypothesis that statin use strongly reduces risk of colorectal cancer. However, we cannot rule out a small reduction in risk or an effect associated with only specific types or doses of statins.

Adult↗
PubMed2006

Pesticide exposure and risk for Parkinson's disease.

OBJECTIVE: Chronic, low-dose exposure to pesticides is suspected to increase the risk for Parkinson's disease (PD), but data are inconclusive. METHODS: We prospectively examined whether individuals exposed to pesticides have higher risk for PD than those not exposed. The study population comprised participants in the Cancer Prevention Study II Nutrition Cohort, a longitudinal investigation of US men and women initiated in 1992 by the American Cancer Society. Follow-up surveys were conducted in 1997, 1999, and 2001. The 143,325 individuals who returned the 2001 survey and did not have a diagnosis or symptoms of PD at baseline (1992) were included in the analyses. RESULTS: Exposure to pesticides was reported by 7,864 participants (5.7%), including 1,956 farmers, ranchers, or fishermen. Individuals exposed to pesticides had a 70% higher incidence of PD than those not exposed (adjusted relative risk, 1.7; 95% confidence interval, 1.2-2.3; p = 0.002). The relative risk for pesticide exposure was similar in farmers and nonfarmers. No relation was found between risk for PD and exposure to asbestos, chemical/acids/solvents, coal or stone dust, or eight other occupational exposures. INTERPRETATION: These data support the hypothesis that exposure to pesticides may increase risk for PD. Future studies should seek to identify the specific chemicals responsible for this association.

Aged↗
PubMed2006

Meat consumption among Black and White men and risk of prostate cancer in the Cancer Prevention Study II Nutrition Cohort.

Previous epidemiologic studies have suggested that intake of red meat may be associated with increased risk of prostate cancer. Few studies, however, have examined these associations by race. We examined intake of red meat, processed meat, and poultry in relation to incident prostate cancer among Black and White men in the Cancer Prevention Study II Nutrition Cohort. Participants in the study completed a detailed questionnaire on diet, medical history, and lifestyle in 1992 to 1993. After excluding men with a history of cancer and incomplete dietary information, 692 Black and 64,856 White men were included in the cohort. During follow-up through August 31, 2001, we documented 85 and 5,028 cases of incident prostate cancer among Black and White men, respectively. Cox proportional hazards models were used to estimate rate ratios (RR) and 95% confidence intervals (95% CI). No measure of meat consumption was associated with risk of prostate cancer among White men. Among Black men, total red meat intake (processed plus unprocessed red meat) was associated with higher risk of prostate cancer (RR, 2.0; 95% CI, 1.0-4.2 for highest versus lowest quartile; P(trend) = 0.05); this increase in risk was mainly due to risk associated with consumption of cooked processed meats (sausages, bacon, and hot dogs; RR, 2.7; 95% CI, 1.3-5.3 for highest versus lowest quartile; P(trend) = 0.008). This study suggests that high consumption of cooked processed meats may contribute to prostate cancer risk among Black men in the United States.

Adult↗
PubMed2006

Association of polymorphisms in the paraoxonase 1 gene with breast cancer incidence in the CPS-II Nutrition Cohort.

Paraoxonase 1 (PON1) plays an important role in the high-density lipoprotein-mediated prevention of low-density lipoprotein oxidation and the metabolism of lipid-soluble radicals. In this study, we investigated the association of two common, nonsynonymous polymorphisms in the PON1 gene (Q192R and L55M) with breast cancer risk in postmenopausal women through a nested case-control study within the American Cancer Society Cancer Prevention Study II Nutrition Cohort. Using conditional logistic regression of genotyping results from 502 cases and 502 cancer-free controls matched on age, race/ethnicity, and date of blood draw, we found that the L55M single nucleotide polymorphism (SNP) was associated with an increased risk of breast cancer [odds ratio (OR), 1.58; 95% confidence interval (95% CI), 1.05-2.37 for MM]. No association was found for the Q192R SNP. The L55M association with breast cancer was modified by nonsteroidal anti-inflammatory drug (NSAID) use. The association was limited to women who took NSAIDs and was somewhat stronger among women who reported regular (> or = 15 times per month) NSAID use (OR, 3.24; 95% CI, 1.17-9.00) than in those who reported any NSAID use (OR, 2.46; 95% CI, 1.39-4.36). These results suggest that genetic variation in PON1, particularly at the L55M SNP, may be associated with increased risk of breast cancer in postmenopausal women. Furthermore, NSAID use seems to modify this risk.

Aged↗
PubMed2006

Interpreting cancer trends.

The interpretation of cancer incidence trends is complicated by short-term random variation, artifactual fluctuations introduced by screening, changes in diagnosis or disease classification, completeness of reporting, and by the multiplicity of factors that may affect risk for specific cancer sites. We analyzed trends in 56 different cancer sites and subsites in the U.S. SEER registries in the period 1975-2002 using join-point analysis. The increase in cancer incidence for all sites combined that became evident with the inception of the SEER registries in the mid-1970s has abated since the early 1990s. Among the 15 most common cancer sites in men, sites with increasing incidence rates during the most recent time period include melanoma of the skin and cancers of the prostate, kidney and renal pelvis (kidney), and esophagus. Among women, incidence rates are increasing for leukemia, non-Hodgkin's lymphoma, melanoma, and cancers of the breast, thyroid, urinary bladder, and kidney. Incidence rates for all childhood cancers combined increased 0.6% per year from 1975 to 2002. Cancer mortality rates have decreased in the United States since 1991 in both men and in women; site-specific death rates have decreased in the most recent time period for 12 of the top 15 cancer sites in men and 9 of the top 15 cancer sites in women. Similar trends in cancer incidence and mortality have been reported in other industrialized countries. Possible reasons for these trends are discussed.

Child, Preschool↗