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.

suck abstract from ncbi


10.1038/onc.2015.174

http://scihub22266oqcxt.onion/10.1038/onc.2015.174
suck pdf from google scholar
C4666810!4666810!26028034
unlimited free pdf from europmc26028034    free
PDF from PMC    free
html from PMC    free

suck abstract from ncbi


Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534

Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534

Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534
pmid26028034      Oncogene 2016 ; 35 (9): 1090-8
Nephropedia Template TP

gab.com Text

Twit Text FOAVip

Twit Text #

English Wikipedia


  • Role of HOXA9 in leukemia: dysregulation, cofactors and essential targets #MMPMID26028034
  • Collins CT; Hess JL
  • Oncogene 2016[Mar]; 35 (9): 1090-8 PMID26028034show ga
  • HOXA9 is a homeodomain-containing transcription factor that plays an important role in hematopoietic stem cell expansion and is commonly deregulated in acute leukemias. A variety of upstream genetic alterations in acute myeloid leukemia (AML) lead to overexpression of HOXA9, which is a strong predictor of poor prognosis. In many cases, HOXA9 has been shown to be necessary for maintaining leukemic transformation, however the molecular mechanisms through which it promotes leukemogenesis remain elusive. Recent work has established that HOXA9 regulates downstream gene expression through binding at promoter distal enhancers along with a subset of cell-specific cofactor and collaborator proteins. Increasing efforts are being made to identify both the critical cofactors and target genes required for maintaining transformation in HOXA9-overexpressing leukemias. With continued advances in understanding HOXA9-mediated transformation, there is a wealth of opportunity for developing novel therapeutics that would be applicable for the greater than 50% of AML with overexpression of HOXA9.
  • ä


  • DeepDyve
  • Pubget Overpricing
  • suck abstract from ncbi

    Linkout box