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10.1158/0008-5472.CAN-09-1102 http://scihub22266oqcxt.onion/10.1158/0008-5472.CAN-09-1102 C4572892!4572892!20028869     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=20028869&cmd=llinks): Failed to open stream: HTTP request failed! 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Elimination of Human Lung Cancer Stem Cells through Targeting of the Stem Cell Factor?c-kit Autocrine Signaling Loop |pdf=|usr=}}{{20028869}} gab.com Text Elimination of Human Lung Cancer Stem Cells through Targeting of the Stem Cell Factor c-kit Autocrine Signaling Loop JO: Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=20028869 #FOAvip Cancer stem cells (CSC) are thought to be responsible for tumor initiation and tumor regeneration after chemotherapy. Previously, we showed that chemotherapy of non?small cell lung cancer (NSCLC) cells lines can select for outgrowth of highly tumorigenic and metastatic CSCs. The high malignancy of lung CSCs was associated with an efficient cytokine network. In this study, we provide evidence that blocking stem cell factor (SCF)?c-kit signaling is sufficient to inhibit CSC proliferation and survival promoted by chemotherapy. CSCs were isolated from NSCLC cell lines as tumor spheres under CSC-selective conditions and their stem properties were confirmed. In contrast to other tumor cells, CSCs expressed c-kit receptors and produced SCF. Proliferation of CSCs was inhibited by SCF-neutralizing antibodies or by imatinib (Gleevec), an inhibitor of c-kit. Although cisplatin treatment eliminated the majority of tumor cells, it did not eliminate CSCs, whereas imatinib or anti-SCF antibody destroyed CSCs. Significantly, combining cisplatin with imatinib or anti-SCF antibody prevented the growth of both tumor cell subpopulations. Our findings reveal an important role for the SCF?c-kit signaling axis in self-renewal and proliferation of lung CSCs, and they suggest that SCF?c-kit signaling blockade could improve the antitumor efficacy of chemotherapy of human NSCLC. Twit Text FOAVip Elimination of Human Lung Cancer Stem Cells through Targeting of the Stem Cell Factor c-kit Autocrine Signaling Loop ????Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=20028869 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=20028869 #FOAvip English Wikipedia <ref>{{Cite pmid|20028869}}</ref> Elimination of Human Lung Cancer Stem Cells through Targeting of the Stem Cell Factor?c-kit Autocrine Signaling Loop #MMPMID20028869 Levina V; Marrangoni A; Wang T; Parikh S; Su Y; Herberman R; Lokshin A; Gorelik E Cancer Res 2010[Jan]; 70 (1): 338-46 PMID20028869show ga Cancer stem cells (CSC) are thought to be responsible for tumor initiation and tumor regeneration after chemotherapy. Previously, we showed that chemotherapy of non?small cell lung cancer (NSCLC) cells lines can select for outgrowth of highly tumorigenic and metastatic CSCs. The high malignancy of lung CSCs was associated with an efficient cytokine network. In this study, we provide evidence that blocking stem cell factor (SCF)?c-kit signaling is sufficient to inhibit CSC proliferation and survival promoted by chemotherapy. CSCs were isolated from NSCLC cell lines as tumor spheres under CSC-selective conditions and their stem properties were confirmed. In contrast to other tumor cells, CSCs expressed c-kit receptors and produced SCF. Proliferation of CSCs was inhibited by SCF-neutralizing antibodies or by imatinib (Gleevec), an inhibitor of c-kit. Although cisplatin treatment eliminated the majority of tumor cells, it did not eliminate CSCs, whereas imatinib or anti-SCF antibody destroyed CSCs. Significantly, combining cisplatin with imatinib or anti-SCF antibody prevented the growth of both tumor cell subpopulations. Our findings reveal an important role for the SCF?c-kit signaling axis in self-renewal and proliferation of lung CSCs, and they suggest that SCF?c-kit signaling blockade could improve the antitumor efficacy of chemotherapy of human NSCLC. äElimination of Human Lung Cancer Stem Cells through Targeting of the S(epmc).pdf DeepDyve Pubget Overpricing