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John I. Risinger

Researcher at Michigan State University

Publications -  96
Citations -  7529

John I. Risinger is an academic researcher from Michigan State University. The author has contributed to research in topics: Endometrial cancer & Cancer. The author has an hindex of 44, co-authored 93 publications receiving 7166 citations. Previous affiliations of John I. Risinger include University of North Carolina at Chapel Hill & National Institutes of Health.

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Journal Article

Genetic instability of microsatellites in endometrial carcinoma.

TL;DR: Microsatellite instability was observed in 17% of sporadic endometrial carcinomas and in 75% of those tumors associated with HNPCC, indicating that the H NPCC gene is also involved in heritable and somatic forms of endometrian carcinoma.
Journal Article

PTEN/MMAC1 Mutations in Endometrial Cancers

TL;DR: Data indicate that PTEN/MMAC1 is more commonly mutated than any other known gene in endometrial cancers, and may be responsible for several familial neoplastic disorders.
Journal ArticleDOI

Defective mismatch repair in extracts of colorectal and endometrial cancer cell lines exhibiting microsatellite instability.

TL;DR: In this paper, the authors compared cell-free extracts from RER+ endometrial and colorectal cancer cell lines to RER- cell lines, and found that the defect in these lines likely involves pre-incision events or the excision step, but not the incision, polymerization, or ligation steps.
Journal Article

Microsatellite Instability, Mismatch Repair Deficiency, and Genetic Defects in Human Cancer Cell Lines

TL;DR: The correlation between microsatellite instability and defective mismatch repair and the suggestion that diminuition in mismatch repair activity is a step in carcinogenesis common to several types of cancer are strengthened.
Journal Article

The role of hMLH1, hMSH3, and hMSH6 defects in cisplatin and oxaliplatin resistance : Correlation with replicative bypass of platinum-DNA adducts

TL;DR: The hypothesis that mismatch repair defects in hMutL alpha and hMutS alpha, but not in h MutS beta, contribute to increased net replicative bypass of cisplatin adducts and therefore to drug resistance by preventing futile cycles of translesion synthesis and mismatch correction is supported.