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10.1158/1541-7786.MCR-13-0490-T http://scihub22266oqcxt.onion/10.1158/1541-7786.MCR-13-0490-T C4201973!4201973 !25053806     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 243.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 243.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 243.2 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\25053806 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Mol+Cancer+Res 2014 ; 12 (10 ): 1470-9 Nephropedia Template TP {{tp|p=25053806 |t=2014. Differential requirement for Src family tyrosine kinases in the initiation, progression, and metastasis of prostate cancer |pdf=|usr=}}{{25053806 }} gab.com Text Differential requirement for Src family tyrosine kinases in the initiation, progression, and metastasis of prostate cancer JO: Mol Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=25053806 #FOAvip Prostate cancer (CaP) recurrence after androgen ablation therapy remains a significant cause of mortality in aging men. Malignant progression and metastasis are typically driven by genetic and epigenetic changes controlled by the androgen receptor (AR). However, evidence suggests that activated nonreceptor tyrosine kinases, including those of the Src family kinases (SFK), directly phosphorylate AR, thereby activating its transcriptional activity in the absence of serum androgen levels. To ascertain whether CaP progression and metastasis require SFK members, an autochthonous transgenic adenocarcinoma (AD) of the mouse prostate (TRAMP) model was crossed into Src-, Lyn- or Fyn-null backgrounds. Primary-site CaP formation was dependent on Src, to a lesser extent, Lyn, but not Fyn. Only Src(-) (/) (-);TRAMP prostate tumors were marked by reactive stroma. SFK deficiency did not affect progression to neuroendocrine (NE) disease, although there were fewer new cancer cases initiating after 34 weeks in the SFK(-/-);TRAMP mice compared with TRAMP controls. Of note, 15% to 21% of older (>33 weeks) Lyn- or Fyn-null TRAMP mice lacking primary-site tumors suffered from aggressive metastatic AD growths, compared with 3% of TRAMP mice. Taken with the data that TRAMP mice lacking Src or Lyn exhibited fewer macroscopic metastases compared with Fyn(-) (/) (-);TRAMP and TRAMP controls, this suggests that SFK can either promote or suppress specific parameters of metastatic growth, possibly depending on cross-talk with primary tumors. These data identify critical, yet potentially opposing roles played by various SFKs in the initiation and metastatic potential of CaP using the TRAMP model. IMPLICATIONS: Genetically defined mouse models indicate a critical role for Src tyrosine kinase in CaP initiation and metastatic progression. Twit Text FOAVip Differential requirement for Src family tyrosine kinases in the initiation, progression, and metastasis of prostate cancer ????Mol Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=25053806 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25053806 #FOAvip English Wikipedia <ref>{{Cite pmid|25053806 }}</ref> Differential requirement for Src family tyrosine kinases in the initiation, progression, and metastasis of prostate cancer #MMPMID25053806 Gelman IH ; Peresie J ; Eng KH ; Foster BA Mol Cancer Res 2014[Oct]; 12 (10 ): 1470-9 PMID25053806 show ga Prostate cancer (CaP) recurrence after androgen ablation therapy remains a significant cause of mortality in aging men. Malignant progression and metastasis are typically driven by genetic and epigenetic changes controlled by the androgen receptor (AR). However, evidence suggests that activated nonreceptor tyrosine kinases, including those of the Src family kinases (SFK), directly phosphorylate AR, thereby activating its transcriptional activity in the absence of serum androgen levels. To ascertain whether CaP progression and metastasis require SFK members, an autochthonous transgenic adenocarcinoma (AD) of the mouse prostate (TRAMP) model was crossed into Src-, Lyn- or Fyn-null backgrounds. Primary-site CaP formation was dependent on Src, to a lesser extent, Lyn, but not Fyn. Only Src(-) (/) (-);TRAMP prostate tumors were marked by reactive stroma. SFK deficiency did not affect progression to neuroendocrine (NE) disease, although there were fewer new cancer cases initiating after 34 weeks in the SFK(-/-);TRAMP mice compared with TRAMP controls. Of note, 15% to 21% of older (>33 weeks) Lyn- or Fyn-null TRAMP mice lacking primary-site tumors suffered from aggressive metastatic AD growths, compared with 3% of TRAMP mice. Taken with the data that TRAMP mice lacking Src or Lyn exhibited fewer macroscopic metastases compared with Fyn(-) (/) (-);TRAMP and TRAMP controls, this suggests that SFK can either promote or suppress specific parameters of metastatic growth, possibly depending on cross-talk with primary tumors. These data identify critical, yet potentially opposing roles played by various SFKs in the initiation and metastatic potential of CaP using the TRAMP model. IMPLICATIONS: Genetically defined mouse models indicate a critical role for Src tyrosine kinase in CaP initiation and metastatic progression. |*Disease Progression [MESH] |Adenocarcinoma/pathology [MESH] |Animals [MESH] |Carcinogenesis/*pathology [MESH] |Cell Death [MESH] |Cell Proliferation [MESH] |Disease Models, Animal [MESH] |Lung Neoplasms/*secondary [MESH] |Male [MESH] |Mice, Transgenic [MESH] |Neuroendocrine Tumors/enzymology/pathology [MESH] |Prostatic Neoplasms/*enzymology/*pathology [MESH]Differential requirement for Src family tyrosine kinases in the initia(epmc).pdf DeepDyve Pubget Overpricing