LEADER 03262nam  2200421z- 450 
001 9910136797603321
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035   $a(CKB)3710000000631146
035   $a(oapen)https://directory.doabooks.org/handle/20.500.12854/61176
035   $a(EXLCZ)993710000000631146
100   $a20202102d2015      |y             0
101 0 $aeng
135   $aurmn|---annan
181   $ctxt$2rdacontent
182   $cc$2rdamedia
183   $acr$2rdacarrier
200 10$aTranscriptional Regulation in Cancers and Metabolic Diseases
210   $cFrontiers Media SA$d2015
215   $a1 electronic resource (98 p.)
225 1 $aFrontiers Research Topics
311   $a2-88919-712-3 
330   $aThe transcription factor (TF) mediated regulation of gene expression is a process fundamental to all biological and physiological processes. Genetic changes and epigenetic modifications of TFs affect target gene expression during the formation of malignant cells. Extensive work has been done on the critical TFs in various disease models. Despite the success of numerous TF-targeted therapies, there remain significant hurdles understanding the mechanisms, transcriptional targets and networks of physiologic pathways that govern TF action. This effort is now beginning to produce exciting new avenues of research. A clinically relevant topic for genetic change of TF is the mutant isoforms of p53, the most famous tumor suppressor. The p53 mutations either results in loss of function, or acting as dominant negative for wild-type protein, or ?gain of function? specifically promoting cancer survival. The gain of function is achieved by shifting p53 binding partner proteins, or changed genomic binding landscape leading to a cancer-promoting transcriptome. Another example of genetic change of TF causing malignancy is the AML-ETO fusion protein in the human t(8;21)-leukemia. The fusion protein is an active TF, and more interestingly, new studies link the disease causing role of AML-ETO to the unique transcriptome in the hematopoietic stem cells. Nuclear receptors (NR) are a group of ligand-dependent TFs governing the expression of genes involved in a broad range of reproductive, developmental and metabolic programs. Genetic changes and epigenetic modifications of NRs lead to cancers and metabolic diseases. Androgen receptor (AR), estrogen receptor (ER) and progesterone receptor (PR) are well studied NRs in prostate, breast and endometrial cancers. The development in sequencing technology and computational genomics enable us to investigate the transcription programs of these master TFs in an unprecedented level. This Research Topic aims to present the most up-to-date progress in the field of transcription regulation in cancers and metabolic diseases.
610   $asenescence
610   $aCell Cycle
610   $aCancer stem cell
610   $anuclear receptor
610   $amicroRNA
610   $ap63
610   $aexosome
610   $atran
610   $aepigenetics
610   $ap53
700   $aCarol Prives$4auth$01296294
702   $aWen Zhou$4auth
906   $aBOOK
912   $a9910136797603321
996   $aTranscriptional Regulation in Cancers and Metabolic Diseases$93023968
997   $aUNINA