Medical Hypotheses
Volume 52, Issue 1 , Pages 27-30, January 1999

Chronic inflammation and cancer: potential role of Bcl-2 gene family members as regulators of cellular antioxidant status

  • T.O. Frommel

      Affiliations

    • Section of Medical Oncology, Rush Presbyterian–St Luke's Medical Center, 1725W Harrison Street, Chicago, IL, 60612–3824, U.S.A. Division of Digestive Diseases and Nutrition, Loyola University Medical Center, Maywood, IL, U.S.A.
    • Rush Presbyterian–St Luke's Medical Center, 1725W Harrison Street, Chicago, IL, 60612–3824, U.S.A. Department of Medicine, Division of Digestive Diseases and Nutrition, Loyola University Medical Center, Maywood, IL, U.S.A.
    • ,
  • E.J. Zarling

      Affiliations

    • Rush Presbyterian–St Luke's Medical Center, 1725W Harrison Street, Chicago, IL, 60612–3824, U.S.A. Department of Medicine, Division of Digestive Diseases and Nutrition, Loyola University Medical Center, Maywood, IL, U.S.A.

Received 8 August 1997; accepted 9 September 1997.

Abstract 

The incidence of cancer is increased in all gastrointestinal (GI) tissues as a result of chronic inflammation. These cancers may develop in cells that are selected for resistance to inflammatory products by virtue of overexpressing the antioxidant protein Bcl-2 or other Bcl-2 gene family members that have antioxidant activity. Unfortunately, Bcl-2 also functions as an anti-apoptotic. Bcl-2 overexpression can increase cellular lifetime and increase the likelihood that other cancer-related mutations will accumulate in individual cells. Thus, Bcl-2 expression is cytoprotective, but its expression also increases the risk of cancer incidence. This is perhaps more evident in the GI tract, which is exposed to more potential mutagens relative to other tissues.

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PII: S0306-9877(97)90621-6

doi:10.1054/mehy.1997.0621

Medical Hypotheses
Volume 52, Issue 1 , Pages 27-30, January 1999

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