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Peter M. Glazer

Researcher at Yale University

Publications -  267
Citations -  17409

Peter M. Glazer is an academic researcher from Yale University. The author has contributed to research in topics: DNA repair & DNA. The author has an hindex of 72, co-authored 253 publications receiving 15760 citations. Previous affiliations of Peter M. Glazer include Anschutz Medical Campus & Oregon State University.

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MicroRNA silencing for cancer therapy targeted to the tumour microenvironment

TL;DR: A novel antimiR delivery platform that targets the acidic tumour microenvironment, evades systemic clearance by the liver, and facilitates cell entry via a non-endocytic pathway is introduced.
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Genetic Instability Induced by the Tumor Microenvironment

TL;DR: The results indicate that the conditions within solid tumors are mutagenic and suggest that a fundamental mechanism of tumor progression in vivo is genetic instability induced by the tumor microenvironment.
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MicroRNA Regulation of DNA Repair Gene Expression in Hypoxic Stress

TL;DR: Hypoxia-inducible miR-210 andmiR-373 play roles in modulating the expression levels of key proteins involved in the HDR and NER pathways, providing new mechanistic insight into the effect of hypoxia on DNA repair and genetic instability in cancer.
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2-Hydroxyglutarate produced by neomorphic IDH mutations suppresses homologous recombination and induces PARP inhibitor sensitivity.

TL;DR: It is reported that IDH1/2 mutations induce a homologous recombination defect that renders tumor cells exquisitely sensitive to poly(adenosine 5′-diphosphate–ribose) polymerase (PARP) inhibitors, and an unexpected link between oncometabolites, altered DNA repair, and genetic instability is uncovered.
Journal Article

Insulin-like Growth Factor-I Receptor Overexpression Mediates Cellular Radioresistance and Local Breast Cancer Recurrence after Lumpectomy and Radiation

TL;DR: Evidence is provided for the influence of IGF-ir on cellular radioresistance and response to therapy and the possibility that the radiocurability of selected tumors may be improved by pharmaceutical strategies directed toward the IGF-IR is raised.