Vanderbilt Epidemiology Center and Vanderbilt Ingram Cancer Center

West End, TN, United States

Vanderbilt Epidemiology Center and Vanderbilt Ingram Cancer Center

West End, TN, United States
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Fu Z.,Vanderbilt Epidemiology Center and Vanderbilt Ingram Cancer Center | Shrubsole M.J.,Vanderbilt Epidemiology Center and Vanderbilt Ingram Cancer Center | Smalley W.E.,Vanderbilt Epidemiology Center and Vanderbilt Ingram Cancer Center | Wu H.,Vanderbilt Epidemiology Center and Vanderbilt Ingram Cancer Center | And 4 more authors.
American Journal of Epidemiology | Year: 2012

Understanding patterns of shared and type-specific etiologies for colorectal polyps may provide insights into colorectal carcinogenesis. The authors present the first systematic comparison of risk factors by colorectal polyp type in a large colonoscopy-based case-control study of 3,764 polyp-free controls and 2,543 polyp patients, including 1,444 cases with adenomas only, 662 cases with hyperplastic polyps (HPPs) only, and 437 cases with synchronous HPPs and adenomas. Surveys were completed to obtain information on usual dietary intake and other lifestyle factors. Six lifestyle factors, including cigarette smoking, obesity, no regular use of nonsteroidal anti-inflammatory drugs, high intake of red meat, low intake of fiber, and low intake of calcium, were found to be independently associated with the risk of polyps. The risk of polyps increased progressively with an increasing number of adverse lifestyle factors. Compared with participants with no or only 1 risk factor, odds ratios for those with 5 to 6 risk factors were 2.72 (95 confidence interval: 1.94, 3.79) for adenoma only, 4.12 (95 confidence interval: 2.78, 6.09) for HPPs only, and 9.03 (95 confidence interval: 5.69, 14.34) for synchronous HPPs and adenomas. This study provides strong evidence that lifestyle modification is important for the prevention of colorectal polyps, especially advanced and multiple adenomas, which are established precursors of colorectal cancer. © 2012 The Author.

Boice J.D.,National Council on Radiation Protection and Measurements | Boice J.D.,Vanderbilt Epidemiology Center and Vanderbilt Ingram Cancer Center | Cohen S.S.,EpidStat Institute | Mumma M.T.,International Epidemiology Institute | And 9 more authors.
Radiation Research | Year: 2014

Polonium-210 is a naturally occurring radioactive element that decays by emitting an alpha particle. It is in the air we breathe and also a component of tobacco smoke. Polonium-210 is used as an anti-static device in printing presses and gained widespread notoriety in 2006 after the poisoning and subsequent death of a Russian citizen in London. More is known about the lethal effects of polonium-210 at high doses than about late effects from low doses. Cancer mortality was examined among 7,270 workers at the Mound nuclear facility near Dayton, OH where polonium-210 was used (1944-1972) in combination with beryllium as a source of neutrons for triggering nuclear weapons. Other exposures included external gamma radiation and to a lesser extent plutonium-238, tritium and neutrons. Vital status and cause of death was determined through 2009. Standardized mortality ratios (SMRs) were computed for comparisons with the general population. Lifetime occupational doses from all places of employment were sought and incorporated into the analysis. Over 200,000 urine samples were analyzed to estimate radiation doses to body organs from polonium and other internally deposited radionuclides. Cox proportional hazards models were used to evaluate dose-response relationships for specific organs and tissues. Vital status was determined for 98.7% of the workers of which 3,681 had died compared with 4,073.9 expected (SMR 0.90; 95% CI 0.88-0.93). The mean dose from external radiation was 26.1 mSv (maximum 939.1 mSv) and the mean lung dose from external and internal radiation combined was 100.1 mSv (maximum 17.5 Sv). Among the 4,977 radiation workers, all cancers taken together (SMR 0.86; 95% CI 0.79-0.93), lung cancer (SMR 0.85; 95% CI 0.74-0.98), and other types of cancer were not significantly elevated. Cox regression analysis revealed a significant positive dose-response trend for esophageal cancer relative risk (RR) and 95% confidence interval at 100 mSv of 1.54 (1.15-2.07) and a negative dose-response trend for liver cancer RR (95% CI) at 100 mSv of 0.55 (0.23-1.32). For lung cancer the RR at 100 mSv was 1.00 (95% CI 0.97-1.04) and for all leukemias other than chronic lymphocytic leukemia (CLL) it was 1.04 (95% CI 0.63-1.71). There was no evidence that heart disease was associated with exposures RR at 100 mSv of 1.06 (0.95-1.18). Assuming a relative biological effectiveness factor of either 10 or 20 for polonium and plutonium alpha particle emissions had little effect on the dose-response analyses. Polonium was the largest contributor to lung dose, and a relative risk of 1.04 for lung cancer at 100 mSv could be excluded with 95% confidence. A dose related increase in cancer of the esophagus was consistent with a radiation etiology but based on small numbers. A dose-related decrease in liver cancer suggests the presence of other modifying factors of risk and adds caution to interpretations. The absence of a detectable increase in total cancer deaths and lung cancer in particular associated with occupational exposures to polonium (mean lung dose 159.8 mSv), and to plutonium to a lesser extent (mean lung dose 13.7 mSv), is noteworthy but based on small numbers. Larger combined studies of U.S. workers are needed to clarify radiation risks following prolonged exposures and radionuclide intakes. © 2014 by Radiation Research Society.

Epplein M.,Vanderbilt Epidemiology Center and Vanderbilt Ingram Cancer Center | Epplein M.,Vanderbilt University | Pawlita M.,German Cancer Research Center | Michel A.,German Cancer Research Center | And 4 more authors.
Cancer Epidemiology Biomarkers and Prevention | Year: 2013

Background: There is biologic plausibility as to why infection with Helicobacter pylori, the leading cause of gastric cancer, may also increase the risk of colorectal cancer, but the epidemiologic findings have been inconsistent. We assessed the association of H. pylori protein-specific infection and colorectal cancer risk in the prospective cohort, the Southern Community Cohort Study. Methods: Multiplex serology was used to measure antibodies to 15 H. pylori proteins in prediagnostic blood among 188 incident colorectal cancer cases and 370 controls matched by age, race, sex, and blood collection timing. Conditional logistic regression was used to calculate ORs and 95% confidence intervals (CI). Results: Overall H. pylori prevalence was not associated with colorectal cancer risk (OR, 1.03; 95% CI, 0.59-1.77). However, seropositivity to any of five specific H. pylori proteins (VacA, HP231, HP305, NapA, and HcpC) was associated with a significant 60% to 80% increase in odds of risk. These associations became even stronger when limited to colon cancer risk, particularly for the known H. pylori toxin VacA (OR, 2.24; 95% CI, 1.22-4.11), including a significant, positive dose-response association by VacA antibody levels in quartiles (P < 0.05). Associations with VacA seropositivity were especially strong for early-onset and late-stage cancers. Conclusions: The findings raise the hypothesis that individuals with high levels of antibodies to specific H. pylori proteins may be at higher risk of colon cancer. Impact: Further investigation of the H. pylori-colorectal cancer association is warranted to determine the possibility of protein-specific antibody levels as a risk biomarker. ©2013 American Association for Cancer Research.

PubMed | Epidemiology and Prevention Group, Peking Union Medical College, Seoul National University, Yonsei University and 5 more.
Type: Journal Article | Journal: International journal of epidemiology | Year: 2016

Incidence and mortality rates for gastric cancer, the fifth most commonly diagnosed and third most deadly cancer worldwide, are highest in East Asia. We sought to identify gastric cancer risk biomarkers among eight prospective studies from China, Japan and Korea.This pooled nested case-control study included 1608 incident non-cardia gastric cancer cases and 1958 matched controls. Pre-diagnostic antibody levels to 15 Helicobacter pylori proteins were assessed using multiplex serology. Conditional logistic regression models were used to calculate odds ratios (ORs) and 95% confidence intervals (CIs).Sero-positivity to 10 H. pylori antigens (Omp, CagA, VacA, HcpC, HP 0305, GroEL, NapA, HyuA, Cad, HpaA) was associated with a 1.29- to 3.26-fold increase in odds of gastric cancer. Omp and HP 0305 consistently remained associated with gastric cancer risk after mutually adjusting for all other markers. Sero-positivity to both Omp and HP 0305 was associated with an over 4-fold increase in gastric cancer incidence (OR, 4.09; 95% CI 3.26-5.13). When limited to only those who are CagA+ H. pylori+, Omp/HP 0305 sero-positivity remained strongly associated with an over 3-fold increase in the odds of gastric cancer (OR, 3.34; 95% CI 2.27-4.91). The results were highly consistent among the cohorts.We have confirmed new H. pylori biomarkers that are strongly associated with gastric cancer risk, even among those infected with the known H. pylori virulence factor CagA. These results may help to design cost-efficient prevention strategies to reduce gastric cancer incidence in East Asia.

PubMed | Vanderbilt Epidemiology Center and Vanderbilt Ingram Cancer Center, Meharry Medical College, Vanderbilt University and International Epidemiology Institute
Type: Journal Article | Journal: Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology | Year: 2014

Epidemiologic studies have shown increased risks of lung cancer among adults with low blood levels of selenium, although evidence is inconsistent. In the United States, the incidence of lung cancer is higher and mean serum selenium levels lower among Blacks than Whites, but prior studies have not assessed the selenium-lung cancer association among Blacks.From the prospective Southern Community Cohort Study, we identified 372 participants who provided blood samples and subsequently developed lung cancer. Selenoprotein P (SEPP1), the most abundant selenoprotein in plasma and a biomarker of selenium nutriture, was measured in the plasma from these individuals and from 716 matched controls.Mean SEPP1 levels were significantly (P < 0.0001) lower among Blacks than Whites. Conditional logistic regression models accounting for smoking revealed a significant trend of increasing OR of lung cancer with decreasing SEPP1 tertiles among Blacks (P = 0.0006) but not Whites (P = 0.69; Pinteraction = 0.10). The ORs and corresponding 95% confidence intervals of lung cancer risk among those with lowest versus highest tertile levels of SEPP1 were 2.4 (1.5-3.0) among Blacks and 1.1 (0.6-2.1) among Whites.Among a mostly low-income population in the southeastern United States, lower levels of SEPP1 were associated with an increasing risk of lung cancer among Blacks but not Whites.The combined findings of higher prevalence of low selenium status and higher lung cancer risk associated with low status raise the possibility that selenium deficiency may contribute to observed racial disparities in lung cancer incidence.

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