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10.1186/s12864-018-4828-1 http://scihub22266oqcxt.onion/10.1186/s12864-018-4828-1 C5987572!5987572!29866045     free     free     free Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       BMC+Genomics 2018 ; 19 (ä): ä Nephropedia Template TP {{tp|p=29866045|t=2018. Landscape of transcriptional deregulation in lung cancer |pdf=|usr=}}{{29866045}} gab.com Text Landscape of transcriptional deregulation in lung cancer JO: BMC Genomics http://www.kidney.de/pget.php?&tw=1&pmid=29866045 #FOAvip Background: Lung cancer is a very heterogeneous disease that can be pathologically classified into different subtypes including small-cell lung carcinoma (SCLC), lung adenocarcinoma (LUAD), lung squamous cell carcinoma (LUSC) and large-cell carcinoma (LCC). Although much progress has been made towards the oncogenic mechanism of each subtype, transcriptional circuits mediating the upstream signaling pathways and downstream functional consequences remain to be systematically studied. Results: Here we trained a one-class support vector machine (OC-SVM) model to establish a general transcription factor (TF) regulatory network containing 325 TFs and 18724 target genes. We then applied this network to lung cancer subtypes and identified those deregulated TFs and downstream targets. We found that the TP63/SOX2/DMRT3 module was specific to LUSC, corresponding to squamous epithelial differentiation and/or survival. Moreover, the LEF1/MSC module was specifically activated in LUAD and likely to confer epithelial-to-mesenchymal transition, known important for cancer malignant progression and metastasis. The proneural factor, ASCL1, was specifically up-regulated in SCLC which is known to have a neuroendocrine phenotype. Also, ID2 was differentially regulated between SCLC and LUSC, with its up-regulation in SCLC linking to energy supply for fast mitosis and its down-regulation in LUSC linking to the attenuation of immune response. We further described the landscape of TF regulation among the three major subtypes of lung cancer, highlighting their functional commonalities and specificities. Conclusions: Our approach uncovered the landscape of transcriptional deregulation in lung cancer, and provided a useful resource of TF regulatory network for future studies. Electronic supplementary material: The online version of this article (10.1186/s12864-018-4828-1) contains supplementary material, which is available to authorized users. Twit Text FOAVip Landscape of transcriptional deregulation in lung cancer ????BMC Genomics http://www.kidney.de/pget.php?&tw=1&pmid=29866045 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29866045 #FOAvip English Wikipedia <ref>{{Cite pmid|29866045}}</ref> Landscape of transcriptional deregulation in lung cancer #MMPMID29866045 Zhang S; Li M; Ji H; Fang Z BMC Genomics 2018[]; 19 (ä): ä PMID29866045show ga Background: Lung cancer is a very heterogeneous disease that can be pathologically classified into different subtypes including small-cell lung carcinoma (SCLC), lung adenocarcinoma (LUAD), lung squamous cell carcinoma (LUSC) and large-cell carcinoma (LCC). Although much progress has been made towards the oncogenic mechanism of each subtype, transcriptional circuits mediating the upstream signaling pathways and downstream functional consequences remain to be systematically studied. Results: Here we trained a one-class support vector machine (OC-SVM) model to establish a general transcription factor (TF) regulatory network containing 325 TFs and 18724 target genes. We then applied this network to lung cancer subtypes and identified those deregulated TFs and downstream targets. We found that the TP63/SOX2/DMRT3 module was specific to LUSC, corresponding to squamous epithelial differentiation and/or survival. Moreover, the LEF1/MSC module was specifically activated in LUAD and likely to confer epithelial-to-mesenchymal transition, known important for cancer malignant progression and metastasis. The proneural factor, ASCL1, was specifically up-regulated in SCLC which is known to have a neuroendocrine phenotype. Also, ID2 was differentially regulated between SCLC and LUSC, with its up-regulation in SCLC linking to energy supply for fast mitosis and its down-regulation in LUSC linking to the attenuation of immune response. We further described the landscape of TF regulation among the three major subtypes of lung cancer, highlighting their functional commonalities and specificities. Conclusions: Our approach uncovered the landscape of transcriptional deregulation in lung cancer, and provided a useful resource of TF regulatory network for future studies. Electronic supplementary material: The online version of this article (10.1186/s12864-018-4828-1) contains supplementary material, which is available to authorized users. äLandscape of transcriptional deregulation in lung cancer (epmc).pdf DeepDyve Pubget Overpricing