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10.1158/0008-5472.CAN-10-4225 http://scihub22266oqcxt.onion/10.1158/0008-5472.CAN-10-4225 C3156382/?report=reader!3156382!21697282     free     free     free Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 251.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cancer+Res 2011 ; 71 (16): 5488-99 Nephropedia Template TP {{tp|p=21697282|t=2011. Api6/AIM/Sp?/CD5L Overexpression in Alveolar Type II Epithelial Cells Induces Spontaneous Lung Adenocarcinoma |pdf=|usr=}}{{21697282}} gab.com Text Api6/AIM/Sp /CD5L Overexpression in Alveolar Type II Epithelial Cells Induces Spontaneous Lung Adenocarcinoma JO: Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=21697282 #FOAvip Chronic inflammation is an important contributor to the development of lung cancers, one of the most common malignancies worldwide, but the underlying molecular mechanisms of inflammation that specifically cue cancer risk remain poorly understood. Apoptosis inhibitor 6 (Api6, AIM, Spalpha, CD5L) is a downstream target gene of neutral lipids and peroxisome proliferator-activated receptor gamma (PPARgamma) in lung alveolar type II (AT II) epithelial cells. An association between increased expression of Api6 in certain settings of pathogenic lung inflammation in mice prompted us to hypothesize a possible role in cancer. Here we report that Api6 promotes malignant transformation by limiting lung epithelial cell apoptosis and promoting immune escape. The specific function of Api6 in AT II cells was determined using a doxycycline-inducible Api6 mouse model. Api6 overexpression inhibited apoptosis and activated oncogenic signaling in AT II lung epithelial cells, inducing emphysema and adenocarcinoma. Additionally, Api6 overexpression in AT II cells increased the concentrations of pro-inflammatory cytokines/chemokines in bronchoalveolar lavage fluid and serum, promoting expansion of myeloid derived suppressor cells (MDSCs) in lung and blood but not in bone marrow or spleen. Lung MDSCs suppressed T cell proliferation and activity in vitro and reduced levels of T cells in vivo following doxycycline treatment to activate Api6. Together, our findings establish that Api6 promotes lung tumorigenesis by blocking a mechanism of epithelial apoptosis that would normally support immunosurveillance. Twit Text FOAVip Api6/AIM/Sp /CD5L Overexpression in Alveolar Type II Epithelial Cells Induces Spontaneous Lung Adenocarcinoma ????Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=21697282 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=21697282 #FOAvip English Wikipedia <ref>{{Cite pmid|21697282}}</ref> Api6/AIM/Sp?/CD5L Overexpression in Alveolar Type II Epithelial Cells Induces Spontaneous Lung Adenocarcinoma #MMPMID21697282 Li Y; Qu P; Wu L; Li B; Du H; Yan C Cancer Res 2011[Aug]; 71 (16): 5488-99 PMID21697282show ga Chronic inflammation is an important contributor to the development of lung cancers, one of the most common malignancies worldwide, but the underlying molecular mechanisms of inflammation that specifically cue cancer risk remain poorly understood. Apoptosis inhibitor 6 (Api6, AIM, Spalpha, CD5L) is a downstream target gene of neutral lipids and peroxisome proliferator-activated receptor gamma (PPARgamma) in lung alveolar type II (AT II) epithelial cells. An association between increased expression of Api6 in certain settings of pathogenic lung inflammation in mice prompted us to hypothesize a possible role in cancer. Here we report that Api6 promotes malignant transformation by limiting lung epithelial cell apoptosis and promoting immune escape. The specific function of Api6 in AT II cells was determined using a doxycycline-inducible Api6 mouse model. Api6 overexpression inhibited apoptosis and activated oncogenic signaling in AT II lung epithelial cells, inducing emphysema and adenocarcinoma. Additionally, Api6 overexpression in AT II cells increased the concentrations of pro-inflammatory cytokines/chemokines in bronchoalveolar lavage fluid and serum, promoting expansion of myeloid derived suppressor cells (MDSCs) in lung and blood but not in bone marrow or spleen. Lung MDSCs suppressed T cell proliferation and activity in vitro and reduced levels of T cells in vivo following doxycycline treatment to activate Api6. Together, our findings establish that Api6 promotes lung tumorigenesis by blocking a mechanism of epithelial apoptosis that would normally support immunosurveillance. äApi6/AIM/Sp?/CD5L Overexpression in Alveolar Type II Epithelial Cells (epmc).pdf DeepDyve Pubget Overpricing