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• W2157788359 abstract "// Genglin Jin 1 , Christopher J. Pirozzi 1 , Lee H. Chen 1 , Giselle Y. Lopez 1 , Christopher G. Duncan 1 , Jie Feng 1 , Ivan Spasojevic 2 , Darell D. Bigner 1 , Yiping He 1 , and Hai Yan 1 1 The Preston Robert Tisch Brain Tumor Center, The Pediatric Brain Tumor Foundation Institute, and The Department of Pathology, 2 The Clinical Pharmacology Laboratory, Duke Cancer Institute and Department of Medicine/Oncology , Duke University Medical Center, Durham, North Carolina, USA Correspondence: Hai Yan, email: // Keywords : IDH1, cell survival Received : July 27, 2012, Accepted : August 04, 2012, Published : August 09, 2012 Abstract Frequent somatic hotspot mutations in isocitrate dehydrogenase 1 (IDH1) have been identified in gliomas, acute myeloid leukemias, chondrosarcomas, and other cancers, providing a likely avenue for targeted cancer therapy. However, whether mutant IDH1 protein is required for maintaining IDH1 mutated tumor cell growth remains unknown. Here, using a genetically engineered inducible system, we report that selective suppression of endogenous mutant IDH1 expression in HT1080, a fibrosarcoma cell line with a native IDH1 R132C heterozygous mutation, significantly inhibits cell proliferation and decreases clonogenic potential. Our findings offer insights into changes that may contribute to the inhibition of cell proliferation and offer a strong preclinical rationale for utilizing mutant IDH1 as a valid therapeutic target." @default.
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• W2157788359 date "2012-08-09" @default.
• W2157788359 modified "2023-10-16" @default.
• W2157788359 title "Mutant IDH1 is required for IDH1 mutated tumor cell growth" @default.
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• W2157788359 doi "https://doi.org/10.18632/oncotarget.577" @default.
• W2157788359 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3478455" @default.
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