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Abstract
Potentially favorable effects of wine consumption on colorectal cancer (CRC) incidence have been reported, but effects on clinical outcomes are unknown. This case-only analysis was designed to investigate outcomes among familial (n = 141) and sporadic (n = 358) CRC patients enrolled in the University of California Irvine CRC gene-environment study during 1994–1996 based on their reported frequency of wine consumption in the year prior to diagnosis. Cases were categorized as either regular or infrequent wine consumers. Univariate survival rate analyses were estimated using the Kaplan and Meier method and log-rank test. Multivariate survival analyses were performed using Cox proportionalhazards ratios (HRs). Earlier stage at presentation (P = 0.034) was noted for familial (but not sporadic) CRC cases reporting regular wine consumption. An overall survival (OS) benefit was observed for familial (but not sporadic) CRC cases that were regular (10-yr OS = 75%) versus infrequent wine consumers (10-yr OS = 47%; P = 0.002). This survival improvement for familial CRC cases remained after adjustment for age, stage, treatment, and other clinically relevant factors (HR = 0.50, 95% confidence interval = 0.25–0.99). Our findings implicate favorable effects of wine consumption on stage at presentation and survival in CRC, selectively among familial CRC cases.
∗ Dr. Anton-Culver and Dr. Holcombe contributed equally as co-senior investigators for this research.
Acknowledgments and Notes
Divisional support was received from the University of California (UC) Irvine Divisions of Hematology/Oncology and Epidemiology. The collection of cancer incidence data used in this study under subcontract No. 050N–8707–S1527 with the Public Health Institute, State of California, was supported by the California Department of Health Services as part of the statewide cancer reporting program mandated by California Health and Safety Code Sections 103875 and 103885; the National Cancer Institute's Surveillance, Epidemiology and End Results Program; and the Centers for Disease Control and Prevention National Program of Cancer Registries. The ideas and opinions expressed herein are those of the authors, and endorsement by the State of California, Department of Health Services, the National Cancer Institute, the Centers for Disease Control and Prevention, and/or the Genetic Epidemiology Research Institute of the UC Irvine is not intended nor should be inferred. This publication was supported by Public Health Service Grants 5R01CA63706 and 5R01CA67151 from the National Cancer Institute, National Institutes of Health, Department of Health and Human Services and by Grant LVS–18840 from the Lon V. Smith Foundations. Additional support for this project comes from National Institutes of Health Grant CA82450 (R. F. Holcombe). Its contents are solely the responsibility of the authors and do not necessarily represent the official views of the National Cancer Institute, National Institutes of Health, or the Lon V. Smith Foundations.
Presented in part at the AACR Colorectal Cancer: Molecular Pathways and Therapies conference, Dana Point, CA, October 21, 2005.
Notes
∗ Dr. Anton-Culver and Dr. Holcombe contributed equally as co-senior investigators for this research.
a: Abbreviations are as follows: CI, confidence interval; NOS, not otherwise specified.
a: Abbreviations are as follows: CRC, colorectal cancer; CI, confidence interval; NOS, not otherwise specified; SES, socioeconomic status.
b: By quintile rank among California residents.
c: Never or < 1 small alcoholic beverage per month.
a: Abbreviations are as follows: CRC, colorectal cancer; SES, socioeconomic status.
b: By quintile rank among California residents.
c: Never or < 1 small alcoholic beverage per month.
a: Model includes adjustment for age, gender, treatment with surgery, radiation, and chemotherapy. Abbreviations are as follows: CRC, colorectal cancer; HR, hazards ratio; SES, socioeconomic status.
