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10.3324/haematol.2017.167288 http://scihub22266oqcxt.onion/10.3324/haematol.2017.167288 C5865438!5865438!29326122     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=29326122&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 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Haematologica 2018 ; 103 (4): 614-25 Nephropedia Template TP {{tp|p=29326122|t=2018. Gfi1b: a key player in the genesis and maintenance of acute myeloid leukemia and myelodysplastic syndrome |pdf=|usr=}}{{29326122}} gab.com Text Gfi1b: a key player in the genesis and maintenance of acute myeloid leukemia and myelodysplastic syndrome JO: Haematologica http://www.kidney.de/pget.php?&tw=1&pmid=29326122 #FOAvip Differentiation of hematopoietic stem cells is regulated by a concert of different transcription factors. Disturbed transcription factor function can be the basis of (pre)malignancies such as myelodysplastic syndrome (MDS) or acute myeloid leukemia (AML). Growth factor independence 1b (Gfi1b) is a repressing transcription factor regulating quiescence of hematopoietic stem cells and differentiation of erythrocytes and platelets. Here, we show that low expression of Gfi1b in blast cells is associated with an inferior prognosis of MDS and AML patients. Using different models of human MDS or AML, we demonstrate that AML development was accelerated with heterozygous loss of Gfi1b, and latency was further decreased when Gfi1b was conditionally deleted. Loss of Gfi1b significantly increased the number of leukemic stem cells with upregulation of genes involved in leukemia development. On a molecular level, we found that loss of Gfi1b led to epigenetic changes, increased levels of reactive oxygen species, as well as alteration in the p38/Akt/FoXO pathways. These results demonstrate that Gfi1b functions as an oncosuppressor in MDS and AML development. Twit Text FOAVip Gfi1b: a key player in the genesis and maintenance of acute myeloid leukemia and myelodysplastic syndrome ????Haematologica http://www.kidney.de/pget.php?&tw=1&pmid=29326122 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29326122 #FOAvip English Wikipedia <ref>{{Cite pmid|29326122}}</ref> Gfi1b: a key player in the genesis and maintenance of acute myeloid leukemia and myelodysplastic syndrome #MMPMID29326122 Thivakaran A; Botezatu L; Hönes JM; Schütte J; Vassen L; Al-Matary YS; Patnana P; Zeller A; Heuser M; Thol F; Gabdoulline R; Olberding N; Frank D; Suslo M; Köster R; Lennartz K; Görgens A; Giebel B; Opalka B; Dührsen U; Khandanpour C Haematologica 2018[Apr]; 103 (4): 614-25 PMID29326122show ga Differentiation of hematopoietic stem cells is regulated by a concert of different transcription factors. Disturbed transcription factor function can be the basis of (pre)malignancies such as myelodysplastic syndrome (MDS) or acute myeloid leukemia (AML). Growth factor independence 1b (Gfi1b) is a repressing transcription factor regulating quiescence of hematopoietic stem cells and differentiation of erythrocytes and platelets. Here, we show that low expression of Gfi1b in blast cells is associated with an inferior prognosis of MDS and AML patients. Using different models of human MDS or AML, we demonstrate that AML development was accelerated with heterozygous loss of Gfi1b, and latency was further decreased when Gfi1b was conditionally deleted. Loss of Gfi1b significantly increased the number of leukemic stem cells with upregulation of genes involved in leukemia development. On a molecular level, we found that loss of Gfi1b led to epigenetic changes, increased levels of reactive oxygen species, as well as alteration in the p38/Akt/FoXO pathways. These results demonstrate that Gfi1b functions as an oncosuppressor in MDS and AML development. äGfi1b: a key player in the genesis and maintenance of acute myeloid le(epmc).pdf DeepDyve Pubget Overpricing