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10.1073/pnas.1610921114

http://scihub22266oqcxt.onion/10.1073/pnas.1610921114
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C5187672!5187672!27930300
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suck abstract from ncbi


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pmid27930300      Proc+Natl+Acad+Sci+U+S+A 2016 ; 113 (51): E8247-56
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  • An NAD+-dependent transcriptional program governs self-renewal and radiation resistance in glioblastoma #MMPMID27930300
  • Gujar AD; Le S; Mao DD; Dadey DYA; Turski A; Sasaki Y; Aum D; Luo J; Dahiya S; Yuan L; Rich KM; Milbrandt J; Hallahan DE; Yano H; Tran DD; Kim AH
  • Proc Natl Acad Sci U S A 2016[Dec]; 113 (51): E8247-56 PMID27930300show ga
  • Glioblastoma, the most common primary malignant brain tumor in adults, remains challenging despite multimodality therapy, necessitating the discovery of new therapies. Nicotinamide adenine dinucleotide (NAD+) plays a pivotal role in cancer cell metabolism, but how NAD+ impacts functional signaling events in glioblastoma is not well understood. We provide clinical evidence that high expression of NAMPT, the rate-limiting step in NAD+ biosynthesis, in glioblastoma tumors is associated with poor overall survival in patients, and demonstrate NAMPT and NAD+ are required for the maintenance of patient-derived glioblastoma stem-like cells (GSCs). Moreover, we delineate a NAD+-dependent transcriptional program that governs GSC self-renewal and dictates the radiation resistance of these cells. These findings identify potential new therapeutic avenues for the treatment of glioblastoma.
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