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10.1038/cr.2017.41 http://scihub22266oqcxt.onion/10.1038/cr.2017.41 C5518870!5518870!28337983     free     free     free Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cell+Res 2017 ; 27 (6): 764-83 Nephropedia Template TP {{tp|p=28337983|t=2017. Self-inflicted DNA double-strand breaks sustain tumorigenicity and stemness of cancer cells |pdf=|usr=}}{{28337983}} gab.com Text Self-inflicted DNA double-strand breaks sustain tumorigenicity and stemness of cancer cells JO: Cell Res http://www.kidney.de/pget.php?&tw=1&pmid=28337983 #FOAvip DNA double-strand breaks (DSBs) are traditionally associated with cancer through their abilities to cause chromosomal instabilities or gene mutations. Here we report a new class of self-inflicted DNA DSBs that can drive tumor growth irrespective of their effects on genomic stability. We discover a mechanism through which cancer cells cause DSBs in their own genome spontaneously independent of reactive oxygen species or replication stress. In this mechanism, low-level cytochrome c leakage from the mitochondria leads to sublethal activation of apoptotic caspases and nucleases, which causes DNA DSBs. In response to these spontaneous DNA DSBs, ATM, a key factor involved in DNA damage response, is constitutively activated. Activated ATM leads to activation of transcription factors NF-?B and STAT3, known drivers of tumor growth. Moreover, self-inflicted DNA DSB formation and ATM activation are important in sustaining the stemness of patient-derived glioma cells. In human tumor tissues, elevated levels of activated ATM correlate with poor patient survival. Self-inflicted DNA DSBs therefore are functionally important for maintaining the malignancy of cancer cells. Twit Text FOAVip Self-inflicted DNA double-strand breaks sustain tumorigenicity and stemness of cancer cells ????Cell Res http://www.kidney.de/pget.php?&tw=1&pmid=28337983 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28337983 #FOAvip English Wikipedia <ref>{{Cite pmid|28337983}}</ref> Self-inflicted DNA double-strand breaks sustain tumorigenicity and stemness of cancer cells #MMPMID28337983 Liu X; Li F; Huang Q; Zhang Z; Zhou L; Deng Y; Zhou M; Fleenor DE; Wang H; Kastan MB; Li CY Cell Res 2017[Jun]; 27 (6): 764-83 PMID28337983show ga DNA double-strand breaks (DSBs) are traditionally associated with cancer through their abilities to cause chromosomal instabilities or gene mutations. Here we report a new class of self-inflicted DNA DSBs that can drive tumor growth irrespective of their effects on genomic stability. We discover a mechanism through which cancer cells cause DSBs in their own genome spontaneously independent of reactive oxygen species or replication stress. In this mechanism, low-level cytochrome c leakage from the mitochondria leads to sublethal activation of apoptotic caspases and nucleases, which causes DNA DSBs. In response to these spontaneous DNA DSBs, ATM, a key factor involved in DNA damage response, is constitutively activated. Activated ATM leads to activation of transcription factors NF-?B and STAT3, known drivers of tumor growth. Moreover, self-inflicted DNA DSB formation and ATM activation are important in sustaining the stemness of patient-derived glioma cells. In human tumor tissues, elevated levels of activated ATM correlate with poor patient survival. Self-inflicted DNA DSBs therefore are functionally important for maintaining the malignancy of cancer cells. äSelf-inflicted DNA double-strand breaks sustain tumorigenicity and ste(epmc).pdf DeepDyve Pubget Overpricing