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10.18632/oncotarget.14153 http://scihub22266oqcxt.onion/10.18632/oncotarget.14153 C5352396!5352396!28030809     free     free     free Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Oncotarget 2017 ; 8 (5): 8226-38 Nephropedia Template TP {{tp|p=28030809|t=2017. Genomic regulation of invasion by STAT3 in triple negative breast cancer |pdf=|usr=}}{{28030809}} gab.com Text Genomic regulation of invasion by STAT3 in triple negative breast cancer JO: Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=28030809 #FOAvip Breast cancer is a heterogeneous disease comprised of four molecular subtypes defined by whether the tumor-originating cells are luminal or basal epithelial cells. Breast cancers arising from the luminal mammary duct often express estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth receptor 2 (HER2). Tumors expressing ER and/or PR are treated with anti-hormonal therapies, while tumors overexpressing HER2 are targeted with monoclonal antibodies. Immunohistochemical detection of ER, PR, and HER2 receptors/proteins is a critical step in breast cancer diagnosis and guided treatment. Breast tumors that do not express these proteins are known as ?triple negative breast cancer? (TNBC) and are typically basal-like. TNBCs are the most aggressive subtype, with the highest mortality rates and no targeted therapy, so there is a pressing need to identify important TNBC tumor regulators. The signal transducer and activator of transcription 3 (STAT3) transcription factor has been previously implicated as a constitutively active oncogene in TNBC. However, its direct regulatory gene targets and tumorigenic properties have not been well characterized. By integrating RNA-seq and ChIP-seq data from 2 TNBC tumors and 5 cell lines, we discovered novel gene signatures directly regulated by STAT3 that were enriched for processes involving inflammation, immunity, and invasion in TNBC. Functional analysis revealed that STAT3 has a key role regulating invasion and metastasis, a characteristic often associated with TNBC. Our findings suggest therapies targeting STAT3 may be important for preventing TNBC metastasis. Twit Text FOAVip Genomic regulation of invasion by STAT3 in triple negative breast cancer ????Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=28030809 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28030809 #FOAvip English Wikipedia <ref>{{Cite pmid|28030809}}</ref> Genomic regulation of invasion by STAT3 in triple negative breast cancer #MMPMID28030809 McDaniel JM; Varley KE; Gertz J; Savic DS; Roberts BS; Bailey SK; Shevde LA; Ramaker RC; Lasseigne BN; Kirby MK; Newberry KM; Christopher Partridge E.; Jones AL; Boone B; Levy SE; Oliver PG; Sexton KC; Grizzle WE; Forero A; Buchsbaum DJ; Cooper SJ; Myers RM Oncotarget 2017[Jan]; 8 (5): 8226-38 PMID28030809show ga Breast cancer is a heterogeneous disease comprised of four molecular subtypes defined by whether the tumor-originating cells are luminal or basal epithelial cells. Breast cancers arising from the luminal mammary duct often express estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth receptor 2 (HER2). Tumors expressing ER and/or PR are treated with anti-hormonal therapies, while tumors overexpressing HER2 are targeted with monoclonal antibodies. Immunohistochemical detection of ER, PR, and HER2 receptors/proteins is a critical step in breast cancer diagnosis and guided treatment. Breast tumors that do not express these proteins are known as ?triple negative breast cancer? (TNBC) and are typically basal-like. TNBCs are the most aggressive subtype, with the highest mortality rates and no targeted therapy, so there is a pressing need to identify important TNBC tumor regulators. The signal transducer and activator of transcription 3 (STAT3) transcription factor has been previously implicated as a constitutively active oncogene in TNBC. However, its direct regulatory gene targets and tumorigenic properties have not been well characterized. By integrating RNA-seq and ChIP-seq data from 2 TNBC tumors and 5 cell lines, we discovered novel gene signatures directly regulated by STAT3 that were enriched for processes involving inflammation, immunity, and invasion in TNBC. Functional analysis revealed that STAT3 has a key role regulating invasion and metastasis, a characteristic often associated with TNBC. Our findings suggest therapies targeting STAT3 may be important for preventing TNBC metastasis. äGenomic regulation of invasion by STAT3 in triple negative breast canc(epmc).pdf DeepDyve Pubget Overpricing