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10.1158/2326-6066.CIR-13-0158 http://scihub22266oqcxt.onion/10.1158/2326-6066.CIR-13-0158 C4264658!4264658 !24958280     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\24958280 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Cancer+Immunol+Res 2014 ; 2 (9 ): 878-89 Nephropedia Template TP {{tp|p=24958280 |t=2014. CALGB 150905 (Alliance): rituximab broadens the antilymphoma response by activating unlicensed NK cells |pdf=|usr=}}{{24958280 }} gab.com Text CALGB 150905 (Alliance): rituximab broadens the antilymphoma response by activating unlicensed NK cells JO: Cancer Immunol Res http://www.kidney.de/pget.php?&tw=1&pmid=24958280 #FOAvip Natural killer (NK) cells contribute to clinical responses in patients treated with rituximab, but the rules determining NK-cell responsiveness to mAb therapies are poorly defined. A deeper understanding of the mechanisms responsible for antibody-dependent cellular cytotoxicity (ADCC) could yield useful biomarkers for predicting clinical responses in patients. Unlicensed NK cells, defined as NK cells lacking expression of an inhibitory KIR for self-HLA class I ligands, are hyporesponsive in steady state, but are potent effectors in inflammatory conditions. We hypothesized that antitumor antibodies such as rituximab can overcome NK-cell dependence on licensing, making unlicensed NK cells important for clinical responses. Here, we examined the influences of variations in KIR and HLA class I alleles on in vitro responses to rituximab. We tested the clinical significance in a cohort of patients with follicular lymphoma treated with rituximab-containing mAb combinations, and show that rituximab triggers responses from all NK-cell populations regardless of licensing. Neither IL2 nor accessory cells are required for activating unlicensed NK cells, but both can augment rituximab-mediated ADCC. Moreover, in 101 patients with follicular lymphoma treated with rituximab-containing mAb combinations, a "missing ligand" genotype (predictive of unlicensed NK cells) is associated with a higher rate of progression-free survival. Our data suggest that the clinical efficacy of rituximab may be driven, in part, by its ability to broaden the NK-cell repertoire to include previously hyporesponsive, unlicensed NK cells. A "missing ligand" KIR and HLA class I genotype may be predictive of this benefit and useful for personalizing treatment decisions in lymphomas and other tumors. Twit Text FOAVip CALGB 150905 (Alliance): rituximab broadens the antilymphoma response by activating unlicensed NK cells ????Cancer Immunol Res http://www.kidney.de/pget.php?&tw=1&pmid=24958280 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24958280 #FOAvip English Wikipedia <ref>{{Cite pmid|24958280 }}</ref> CALGB 150905 (Alliance): rituximab broadens the antilymphoma response by activating unlicensed NK cells #MMPMID24958280 Du J ; Lopez-Verges S ; Pitcher BN ; Johnson J ; Jung SH ; Zhou L ; Hsu K ; Czuczman MS ; Cheson B ; Kaplan L ; Lanier LL ; Venstrom JM Cancer Immunol Res 2014[Sep]; 2 (9 ): 878-89 PMID24958280 show ga Natural killer (NK) cells contribute to clinical responses in patients treated with rituximab, but the rules determining NK-cell responsiveness to mAb therapies are poorly defined. A deeper understanding of the mechanisms responsible for antibody-dependent cellular cytotoxicity (ADCC) could yield useful biomarkers for predicting clinical responses in patients. Unlicensed NK cells, defined as NK cells lacking expression of an inhibitory KIR for self-HLA class I ligands, are hyporesponsive in steady state, but are potent effectors in inflammatory conditions. We hypothesized that antitumor antibodies such as rituximab can overcome NK-cell dependence on licensing, making unlicensed NK cells important for clinical responses. Here, we examined the influences of variations in KIR and HLA class I alleles on in vitro responses to rituximab. We tested the clinical significance in a cohort of patients with follicular lymphoma treated with rituximab-containing mAb combinations, and show that rituximab triggers responses from all NK-cell populations regardless of licensing. Neither IL2 nor accessory cells are required for activating unlicensed NK cells, but both can augment rituximab-mediated ADCC. Moreover, in 101 patients with follicular lymphoma treated with rituximab-containing mAb combinations, a "missing ligand" genotype (predictive of unlicensed NK cells) is associated with a higher rate of progression-free survival. Our data suggest that the clinical efficacy of rituximab may be driven, in part, by its ability to broaden the NK-cell repertoire to include previously hyporesponsive, unlicensed NK cells. A "missing ligand" KIR and HLA class I genotype may be predictive of this benefit and useful for personalizing treatment decisions in lymphomas and other tumors. |Adult [MESH] |Aged [MESH] |Aged, 80 and over [MESH] |Antibodies, Monoclonal, Murine-Derived/*therapeutic use [MESH] |Antibodies, Neoplasm/*therapeutic use [MESH] |Antibody-Dependent Cell Cytotoxicity [MESH] |Antigens, CD20/metabolism [MESH] |Antineoplastic Agents/*therapeutic use [MESH] |Cell Line, Tumor [MESH] |Disease-Free Survival [MESH] |Female [MESH] |Humans [MESH] |Killer Cells, Natural/*immunology [MESH] |Lymphocyte Activation [MESH] |Lymphoma/*drug therapy [MESH] |Male [MESH] |Middle Aged [MESH] |Receptors, KIR/immunology [MESH] |Rituximab [MESH]CALGB 150905 (Alliance): rituximab broadens the antilymphoma response (epmc).pdf DeepDyve Pubget Overpricing