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C. Rahj Robinson

Researcher at Johns Hopkins University

Publications -  6
Citations -  2423

C. Rahj Robinson is an academic researcher from Johns Hopkins University. The author has contributed to research in topics: Familial adenomatous polyposis & Adenomatous polyposis coli. The author has an hindex of 6, co-authored 6 publications receiving 2395 citations.

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Treatment of Colonic and Rectal Adenomas with Sulindac in Familial Adenomatous Polyposis

TL;DR: Sulindac reduces the number and size of colorectal adenomas in patients with familial adenomatous polyposis, but its effect is incomplete, and it is unlikely to replace colectomy as primary therapy.
Journal Article

Molecular Detection of Genetic Alterations in the Serum of Colorectal Cancer Patients

TL;DR: The frequent detection of p53 mutation in the serum of patients with early stage tumors suggests a possible use of this approach for clinical prognosis and cancer monitoring of colorectal cancer patients.
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Phenotypic and genotypic characteristics of aberrant crypt foci in human colorectal mucosa.

TL;DR: The findings suggest that "aberrant crypt focus" is a generic term analogous to "polyp" and requires further histopathologic, phenotypic, or genotypic classification into dysplastic and heteroplastic types.
Journal Article

Size-dependent Increase in Prostanoid Levels in Adenomas of Patients with Familial Adenomatous Polyposis

TL;DR: A role for prostanoids in progression of colorectalPolyposis in familial adenomatosis polyposis patients patients is suggested, and the relative levels of three prostanoid were elevated in adenomas compared to normal-appearing mucosa from the same patients, andThe resulting ratios were correlated with the size of the adenoma.
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Prostaglandin levels in human colorectal mucosa: Effects of sulindac in patients with familial adenomatous polyposis

TL;DR: Sulindac treatment, at drug doses shown to regress colorectal adenomas in FAP patients, has heterogeneous effects on the level of major prostaglandins in their rectal mucosa and may not prevent coloreCTal cancer due to uncoupling ofprostaglandin levels and carcinogenesis.