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10.1111/cas.13312 http://scihub22266oqcxt.onion/10.1111/cas.13312 C5581511!5581511!28865172     free     free     free Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cancer+Sci 2017 ; 108 (9): 1726-31 Nephropedia Template TP {{tp|p=28865172|t=2017. Intersection of retinoblastoma tumor suppressor function, stem cells, metabolism, and inflammation |pdf=|usr=}}{{28865172}} gab.com Text Intersection of retinoblastoma tumor suppressor function, stem cells, metabolism, and inflammation JO: Cancer Sci http://www.kidney.de/pget.php?&tw=1&pmid=28865172 #FOAvip The Retinoblastoma (RB) tumor suppressor regulates G1/S transition during cell cycle progression by modulating the activity of E2F transcription factors. The RB pathway plays a central role in the suppression of most cancers, and RB mutation was initially discovered by virtue of its role in tumor initiation. However, as cancer genome sequencing has evolved to profile more advanced and treatment?resistant cancers, it has become increasingly clear that, in the majority of cancers, somatic RB inactivation occurs during tumor progression. Furthermore, despite the presence of deregulation of cell cycle control due to an INK4A deletion, additional CCND amplification and/or other mutations in the RB pathway, mutation or deletion of the RB gene is often observed during cancer progression. Of note, RB inactivation during cancer progression not only facilitates G1/S transition but also enhances some characteristics of malignancy, including altered drug sensitivity and a return to the undifferentiated state. Recently, we reported that RB inactivation enhances pro?inflammatory signaling through stimulation of the interleukin?6/STAT3 pathway, which directly promotes various malignant features of cancer cells. In this review, we highlight the consequences of RB inactivation during cancer progression, and discuss the biological and pathological significance of the interaction between RB and pro?inflammatory signaling. Twit Text FOAVip Intersection of retinoblastoma tumor suppressor function, stem cells, metabolism, and inflammation ????Cancer Sci http://www.kidney.de/pget.php?&tw=1&pmid=28865172 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28865172 #FOAvip English Wikipedia <ref>{{Cite pmid|28865172}}</ref> Intersection of retinoblastoma tumor suppressor function, stem cells, metabolism, and inflammation #MMPMID28865172 Kitajima S; Takahashi C Cancer Sci 2017[Sep]; 108 (9): 1726-31 PMID28865172show ga The Retinoblastoma (RB) tumor suppressor regulates G1/S transition during cell cycle progression by modulating the activity of E2F transcription factors. The RB pathway plays a central role in the suppression of most cancers, and RB mutation was initially discovered by virtue of its role in tumor initiation. However, as cancer genome sequencing has evolved to profile more advanced and treatment?resistant cancers, it has become increasingly clear that, in the majority of cancers, somatic RB inactivation occurs during tumor progression. Furthermore, despite the presence of deregulation of cell cycle control due to an INK4A deletion, additional CCND amplification and/or other mutations in the RB pathway, mutation or deletion of the RB gene is often observed during cancer progression. Of note, RB inactivation during cancer progression not only facilitates G1/S transition but also enhances some characteristics of malignancy, including altered drug sensitivity and a return to the undifferentiated state. Recently, we reported that RB inactivation enhances pro?inflammatory signaling through stimulation of the interleukin?6/STAT3 pathway, which directly promotes various malignant features of cancer cells. In this review, we highlight the consequences of RB inactivation during cancer progression, and discuss the biological and pathological significance of the interaction between RB and pro?inflammatory signaling. äIntersection of retinoblastoma tumor suppressor function, stem cells, (epmc).pdf DeepDyve Pubget Overpricing