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10.1158/1541-7786.MCR-15-0307 http://scihub22266oqcxt.onion/10.1158/1541-7786.MCR-15-0307 C4794404!4794404!26631572     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Mol+Cancer+Res 2016 ; 14 (3): 287-95 Nephropedia Template TP {{tp|p=26631572|t=2016. Cancer-associated Fibroblasts Induce a Collagen Cross-link Switch in Tumor Stroma |pdf=|usr=}}{{26631572}} gab.com Text Cancer-associated Fibroblasts Induce a Collagen Cross-link Switch in Tumor Stroma JO: Mol Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=26631572 #FOAvip Intratumoral collagen cross-links heighten stromal stiffness and stimulate tumor cell invasion, but it is unclear how collagen cross-linking is regulated in epithelial tumors. To address this question, we used KrasLA1 mice, which develop lung adenocarcinomas from somatic activation of a KrasG12D allele. The lung tumors in KrasLA1 mice were highly fibrotic and contained cancer-associated fibroblasts (CAFs) that produced collagen and generated stiffness in collagen gels. In xenograft tumors generated by injection of wild-type mice with lung adenocarcinoma cells alone or in combination with CAFs, the total concentration of collagen cross-links was the same in tumors generated with or without CAFs, but co-injected tumors had higher hydroxylysine aldehyde-derived collagen cross-links (HLCCs) and lower lysine-aldehyde-derived collagen cross-links (LCCs). Therefore, we postulated that an LCC-to-HLCC switch induced by CAFs promotes the migratory and invasive properties of lung adenocarcinoma cells. To test this hypothesis, we created co-culture models in which CAFs are positioned interstitially or peripherally in tumor cell aggregates, mimicking distinct spatial orientations of CAFs in human lung cancer. In both contexts, CAFs enhanced the invasive properties of tumor cells in 3-dimensional (3D) collagen gels. Tumor cell aggregates that attached to CAF networks on a Matrigel surface dissociated and migrated on the networks. Lysyl hydroxylase 2 (PLOD2/LH2), which drives HLCC formation, was expressed in CAFs, and LH2 depletion abrogated the ability of CAFs to promote tumor cell invasion and migration. Twit Text FOAVip Cancer-associated Fibroblasts Induce a Collagen Cross-link Switch in Tumor Stroma ????Mol Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=26631572 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26631572 #FOAvip English Wikipedia <ref>{{Cite pmid|26631572}}</ref> Cancer-associated Fibroblasts Induce a Collagen Cross-link Switch in Tumor Stroma #MMPMID26631572 Pankova D; Chen Y; Terajima M; Schliekelman MJ; Baird BN; Fahrenholtz M; Sun L; Gill BJ; Vadakkan TJ; Kim MP; Ahn YH; Roybal JD; Liu X; Parra Cuentas ER; Rodriguez J; Wistuba II; Creighton CJ; Gibbons DL; Hicks JM; Dickinson ME; West JL; Grande-Allen KJ; Hanash SM; Yamauchi M; Kurie JM Mol Cancer Res 2016[Mar]; 14 (3): 287-95 PMID26631572show ga Intratumoral collagen cross-links heighten stromal stiffness and stimulate tumor cell invasion, but it is unclear how collagen cross-linking is regulated in epithelial tumors. To address this question, we used KrasLA1 mice, which develop lung adenocarcinomas from somatic activation of a KrasG12D allele. The lung tumors in KrasLA1 mice were highly fibrotic and contained cancer-associated fibroblasts (CAFs) that produced collagen and generated stiffness in collagen gels. In xenograft tumors generated by injection of wild-type mice with lung adenocarcinoma cells alone or in combination with CAFs, the total concentration of collagen cross-links was the same in tumors generated with or without CAFs, but co-injected tumors had higher hydroxylysine aldehyde-derived collagen cross-links (HLCCs) and lower lysine-aldehyde-derived collagen cross-links (LCCs). Therefore, we postulated that an LCC-to-HLCC switch induced by CAFs promotes the migratory and invasive properties of lung adenocarcinoma cells. To test this hypothesis, we created co-culture models in which CAFs are positioned interstitially or peripherally in tumor cell aggregates, mimicking distinct spatial orientations of CAFs in human lung cancer. In both contexts, CAFs enhanced the invasive properties of tumor cells in 3-dimensional (3D) collagen gels. Tumor cell aggregates that attached to CAF networks on a Matrigel surface dissociated and migrated on the networks. Lysyl hydroxylase 2 (PLOD2/LH2), which drives HLCC formation, was expressed in CAFs, and LH2 depletion abrogated the ability of CAFs to promote tumor cell invasion and migration. äCancer-associated Fibroblasts Induce a Collagen Cross-link Switch in T(epmc).pdf DeepDyve Pubget Overpricing