4.5 Article

Associations of Tobaccoand Alcohol Use with Risk of Neuroendocrine Tumors of the Small Intestine in Utah

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CANCER EPIDEMIOLOGY BIOMARKERS & PREVENTION
卷 28, 期 12, 页码 1998-2004

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AMER ASSOC CANCER RESEARCH
DOI: 10.1158/1055-9965.EPI-19-0465

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资金

  1. National Institutes of Health (NIH) National Cancer Institute [R21 CA205796]
  2. Cancer Center Support Grant [P30 CA42014]
  3. National Cancer Institute's SEER Program [HHSN261201800016I]
  4. U.S. Center for Disease Control and Prevention's National Program of Cancer Registries [NU58DP0063200]
  5. National Center for Research Resources grant, Sharing Statewide Health Data for Genetic Research [R01 RR021746]
  6. Utah State Department of Health
  7. University of Utah
  8. Huntsman Cancer Foundation
  9. NIH Clinical and Translational Science Award [UL1TR002538, 5UL1TR001067-05, 8UL1TR000105, UL1RR025764]
  10. Pedigree and Population Resource

向作者/读者索取更多资源

Background: Incidence of small-intestine neuroendocrine tumors (SINT) has been increasing in the United States over the past 40 years, with higher incidence in Utah than elsewhere. As information about how these tumors arise is limited, elucidating lifestyle factors associated with SINT in a statewide cohort could potentially identify those at risk to help mitigate their effects. Methods: Cases of SINT with a carcinoid histology (8240 or 8241) diagnosed in Utah from 1996 to 2014 with no prior history of cancer within 5 years (n = 433) were matched to population controls (1:10 ratio). Tobacco and alcohol exposures before case diagnosis were identified from International Classification of Diseases codes in state-wide medical records and from self-reported data captured at patient encounters beginning in 1996. Multivariate logistic regression was used to estimate risk of SINT associated with tobacco and alcohol in cases compared with controls. Results: An increased risk of SINT was observed in tobacco- exposed individuals compared with unexposed [OR, 1.44; 95% confidence interval (CI), 1.11-1.86; P = 0.006]. Those who were exposed to alcohol exhibited an increased risk of SINT (OR, 1.62; 95% CI, 1.05-2.49; P = 0.03). Conclusions: This study supports tobacco and alcohol use as risk factors for SINT, independent of family history. However, low rates of smoking and alcohol use in Utah coupled with higher rates of SINT suggest other factors may contribute to development of these tumors. Impact: Although tobacco and alcohol modestly contribute to risk, our study suggests in addition to greater detection of tumors, other as-of-yet undefined exposures may drive rising SINT incidence.

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