Epidemiology of Nonsteroidal Anti-Inflammatory Drugs and Colorectal Cancer
Michael J. Thun, S. Jane Henley
Abstract
Michael J. Thun, S. Jane Henley
Abstract
The hypothesis that aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs) might protect against colorectal, and possibly other cancers, arose in the mid-1970s when higher concentrations of prostaglandins were observed in specimens from human colorectal tumors than in surrounding normal mucosa (1,2). These early observations led quickly to experimental studies assessing whether NSAIDs inhibit chemically induced colorectal cancer in rodents, and to uncontrolled clinical studies of patients with the rare hereditary condition, familial adenomatous polyposis (FAP). However, not until the 1990s did the potential efficacy and safety of NSAIDs as anticancer agents begin to be explored systematically in humans by epidemiologic studies in the general population and randomized clinical trials in high-risk groups.
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The hypothesis that aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs) might protect against colorectal, and possibly other cancers, arose in the mid-1970s when higher concentrations of prostaglandins were observed in specimens from human colorectal tumors than in surrounding normal mucosa (1,2). These early observations led quickly to experimental studies assessing whether NSAIDs inhibit chemically induced colorectal cancer in rodents, and to uncontrolled clinical studies of patients with the rare hereditary condition, familial adenomatous polyposis (FAP). However, not until the 1990s did the potential efficacy and safety of NSAIDs as anticancer agents begin to be explored systematically in humans by epidemiologic studies in the general population and randomized clinical trials in high-risk groups.
Key concepts: Aspirin, Medicine, Colorectal cancer, Nonsteroidal, Familial adenomatous polyposis, Clinical trial, Internal medicine, Epidemiology