Use my Search Websuite to scan PubMed, PMCentral, Journal Hosts and Journal Archives, FullText. Kick-your-searchterm to multiple Engines kick-your-query now !>

A dictionary by aggregated review articles of nephrology, medicine and the life sciences Your one-stop-run pathway from word to the immediate pdf of peer-reviewed on-topic knowledge.

10.1093/jnci/djx059 http://scihub22266oqcxt.onion/10.1093/jnci/djx059 C5436301!5436301 !28521333     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28521333 &cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\28521333 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       J+Natl+Cancer+Inst 2017 ; 109 (11 ): ä Nephropedia Template TP {{tp|p=28521333 |t=2017. Drugging the Cancers Addicted to DNA Repair |pdf=|usr=}}{{28521333 }} gab.com Text Drugging the Cancers Addicted to DNA Repair JO: J Natl Cancer Inst http://www.kidney.de/pget.php?&tw=1&pmid=28521333 #FOAvip Defects in DNA repair can result in oncogenic genomic instability. Cancers occurring from DNA repair defects were once thought to be limited to rare inherited mutations (such as BRCA1 or 2). It now appears that a clinically significant fraction of cancers have acquired DNA repair defects. DNA repair pathways operate in related networks, and cancers arising from loss of one DNA repair component typically become addicted to other repair pathways to survive and proliferate. Drug inhibition of the rescue repair pathway prevents the repair-deficient cancer cell from replicating, causing apoptosis (termed synthetic lethality). However, the selective pressure of inhibiting the rescue repair pathway can generate further mutations that confer resistance to the synthetic lethal drugs. Many such drugs currently in clinical use inhibit PARP1, a repair component to which cancers arising from inherited BRCA1 or 2 mutations become addicted. It is now clear that drugs inducing synthetic lethality may also be therapeutic in cancers with acquired DNA repair defects, which would markedly broaden their applicability beyond treatment of cancers with inherited DNA repair defects. Here we review how each DNA repair pathway can be attacked therapeutically and evaluate DNA repair components as potential drug targets to induce synthetic lethality. Clinical use of drugs targeting DNA repair will markedly increase when functional and genetic loss of repair components are consistently identified. In addition, future therapies will exploit artificial synthetic lethality, where complementary DNA repair pathways are targeted simultaneously in cancers without DNA repair defects. Twit Text FOAVip Drugging the Cancers Addicted to DNA Repair ????J Natl Cancer Inst http://www.kidney.de/pget.php?&tw=1&pmid=28521333 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28521333 #FOAvip English Wikipedia <ref>{{Cite pmid|28521333 }}</ref> Drugging the Cancers Addicted to DNA Repair #MMPMID28521333 Nickoloff JA ; Jones D ; Lee SH ; Williamson EA ; Hromas R J Natl Cancer Inst 2017[Nov]; 109 (11 ): ä PMID28521333 show ga Defects in DNA repair can result in oncogenic genomic instability. Cancers occurring from DNA repair defects were once thought to be limited to rare inherited mutations (such as BRCA1 or 2). It now appears that a clinically significant fraction of cancers have acquired DNA repair defects. DNA repair pathways operate in related networks, and cancers arising from loss of one DNA repair component typically become addicted to other repair pathways to survive and proliferate. Drug inhibition of the rescue repair pathway prevents the repair-deficient cancer cell from replicating, causing apoptosis (termed synthetic lethality). However, the selective pressure of inhibiting the rescue repair pathway can generate further mutations that confer resistance to the synthetic lethal drugs. Many such drugs currently in clinical use inhibit PARP1, a repair component to which cancers arising from inherited BRCA1 or 2 mutations become addicted. It is now clear that drugs inducing synthetic lethality may also be therapeutic in cancers with acquired DNA repair defects, which would markedly broaden their applicability beyond treatment of cancers with inherited DNA repair defects. Here we review how each DNA repair pathway can be attacked therapeutically and evaluate DNA repair components as potential drug targets to induce synthetic lethality. Clinical use of drugs targeting DNA repair will markedly increase when functional and genetic loss of repair components are consistently identified. In addition, future therapies will exploit artificial synthetic lethality, where complementary DNA repair pathways are targeted simultaneously in cancers without DNA repair defects. |Antineoplastic Agents/*therapeutic use [MESH] |DNA End-Joining Repair/drug effects [MESH] |DNA Mismatch Repair/drug effects [MESH] |DNA Repair/*drug effects [MESH] |Genes, BRCA1 [MESH] |Genes, BRCA2 [MESH] |Homologous Recombination/drug effects [MESH] |Humans [MESH] |Molecular Targeted Therapy [MESH] |Neoplasms/*genetics [MESH] |Poly(ADP-ribose) Polymerase Inhibitors/*therapeutic use [MESH]Drugging the Cancers Addicted to DNA Repair (epmc).pdf DeepDyve Pubget Overpricing