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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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Ornithine decarboxylase as a therapeutic target for endometrial cancer

TL;DR: The study indicates that some endometrial cancers appear particularly sensitive to DFMO and that the polyamine pathway in endometrioid cancers in general and specifically those most likely to suffer adverse clinical outcomes could be targeted for effective treatment, chemoprevention or chemOPrevention of recurrence.
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Cellular resistance and hypermutability in mismatch repair-deficient human cancer cell lines following treatment with methyl methanesulfonate

TL;DR: The findings suggest that cytotoxic response and mutagenic response at the hypoxanthine-guanine phosphoribosyl transferase (HPRT) locus to the S(N)2 alkylating agent methyl methanesultfonate (MMS) is mediated through MMR, and that resistance to such damage in MMR-defective cells correlates with an increase in genomic mutations.
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Characterization of distinct human endometrial carcinoma cell lines deficient in mismatch repair that originated from a single tumor.

TL;DR: A critical role for hPMS2 in human MMR is supported, while the role of the hMSH2/hMSH3 heterodimer in the repair of base:base mismatches is defined, supported by observing the reduction in base substitution mutation rate at HPRT in HEC-1-B cells.
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Gene Expression in Uterine Leiomyoma from Tumors Likely to Be Growing (from Black Women over 35) and Tumors Likely to Be Non-Growing (from White Women over 35)

TL;DR: This is the first study to compare two groups of tumors that are likely to have different growth rates in order to reveal molecular signals likely to be influential in tumor growth.