Sulindac causes regression of rectal polyps in familial adenomatous polyposis.
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Summary
Sulindac is effective in inducing the regression of rectal polyps in familial adenomatous polyposis and an immunohistochemical study of the cellular proliferation index was not able to show a sulindac-induced modification of the Ki 67 index.
- Type
- article
- Published
- 1991-09-01
- Cited by
- 766
- References
- 24
- Access
- Open access
- OpenAlex
- https://openalex.org/W1783022590
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:40270164
Keywords
Sulindac, Familial adenomatous polyposis, Rectal Polyp, Medicine, Gastroenterology
References
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- The Surgical Management of Multiple Polyposis
- Postcolectomy regression of adenomatous polyps of the rectum.
- Cell cycle analysis of a cell proliferation-associated human nuclear antigen defined by the monoclonal antibody Ki-67.
- Inhibition of development of methylnitrosourea-induced rat colon tumors by indomethacin treatment.
- Inhibition by prostaglandin synthesis inhibitors of the induction of epidermal ornithine decarboxylase activity, the accumulation of prostaglandins, and tumor promotion caused by 12-O-tetradecanoylphorbol-13-acetate.
- Production of a mouse monoclonal antibody reactive with a human nuclear antigen associated with cell proliferation
- Regression of head and neck carcinoma with a prostaglandin-synthesis inhibitor.
- The disposition of sulindac
- STUDIES ON THE ABSORPTION, DISTRIBUTION AND EXCRETION OF INDOMETHACIN IN VARIOUS SPECIES
- Inhibition of development of methylnitrosourea-induced rat colonic tumors by peroral administration of indomethacin.
- Nd:YAG laser photocoagulation in colorectal adenoma. Evaluation of its safety, usefulness, and efficacy.
- [Rectal micropolyps after total colectomy in familial polyposis. Efficacy of sulindac].
Cited by
- The adenoma‐adenocarcinoma sequence in the large bowel: Variations on a theme
- Mucosal prostanoid receptors and synthesis in familial adenomatous polyposis
- Sulindac in familial adenomatous polyposis.
- NSAID use and decreased risk of gastrointestinal cancers.
- Non‐steroidal anti‐inflammatory drugs with different cyclooxygenase inhibitory profiles that prevent aberrant crypt foci formation but vary in acute gastrotoxicity in a rat model 1
- Association of Enhanced Cyclooxygenase-2 Expression With Possible Local Immunosuppression in Human Colorectal Carcinomas
- Model of estimated rates of colorectal cancer from polyp growth by year of surveillance
- Induction of cyclooxygenase-2 and invasiveness by transforming growth factor-β1 in immortalized mouse colonocytes expressing oncogenic ras
- Increased cyclooxygenase-2 expression in large flat colorectal tumors (laterally spreading tumors)
- Daily soluble aspirin and prevention of colorectal adenoma recurrence: one-year results of the APACC trial.
- Expression of cyclooxygenase-2 in human esophageal squamous cell carcinomas.
- C-reactive protein and the risk of incident colorectal cancer.
- Oral contraceptives and polyp regression in familial adenomatous polyposis.
- Effect of aspirin on the Wnt/β-catenin pathway is mediated via protein phosphatase 2A
- The effects of selected drugs and dietary compounds on proliferation and apoptosis in colorectal carcinoma
- Growth regulation of Gardner's syndrome colorectal cancer cells by NSAIDs.
- Colon cancer: polyps, prevention, and politics.
- Use of nitrous oxide and oxygen for conscious sedation to manage pain and anxiety.
- Sulindac sulfone induced regression of rectal polyps in patients with familial adenomatous polyposis.
- Cyclo-oxygenase 2 inhibitors: emerging roles in the gut
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