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Association of Manganese Superoxide Dismutase Expression With Progression of Carcinogenesis in Barrett Esophagus—Invited Critique
John W. Harmon, MD;
Pramod Bonde, MD;
Chiming Wei, MD, PhD
Arch Surg. 2005;140:1209.
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Gastroesophageal reflux disease appears to cause cancer through an inflammatory pathway driven by oxygen free radicals.1 We have recently found extensive oxidative DNA damage in an experimental animal model of gastroesophageal reflux disease–induced esophageal cancer.2 It is reasonable to think that SOD could modulate the degree of inflammation and would be important in this type of carcinogenesis.
Superoxide dismutase has at least 2 important potential clinical roles in cancer. First, inadequate levels of SOD can accelerate oxidative inflammatory processes and carcinogenesis. Second, it can be expressed at high levels in tumors and make them nonresponders to radiotherapy.
This report by Hermann et al showed most importantly that MnSOD levels were lower in Barrett metaplasia but also in cancer. This suggests a role for SOD in promoting carcinogenesis but not in causing resistance to radiotherapeutic treatment.
The reader should be . . . [Full Text of this Article]
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RELATED ARTICLE
Association of Manganese Superoxide Dismutase Expression With Progression of Carcinogenesis in Barrett Esophagus
Bruce Hermann, Yan Li, Mukunda B. Ray, John M. Wo, and Robert C. G. Martin, II
Arch Surg. 2005;140(12):1204-1209.
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