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MeSH Review

Leukemia, Myeloid

 
 
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Disease relevance of Leukemia, Myeloid

 

Psychiatry related information on Leukemia, Myeloid

 

High impact information on Leukemia, Myeloid

 

Chemical compound and disease context of Leukemia, Myeloid

  • About 65 percent of previously untreated adults with primary acute myeloid leukemia (AML) enter complete remission when treated with cytarabine and an anthracycline [13].
  • To determine the clinical importance of this property, we measured the uptake of tritiated thymidine by leukemic cells in serum-free and cytokine-free cultures as a means of determining the rate of spontaneous proliferation in 114 patients with newly diagnosed acute myeloid leukemia [14].
  • The results genetically define a connection between the Bcr-Abl cytoplasmic tyrosine kinase and Ras and add to the accumulating evidence that deregulation of Ras is a central event in the genesis of a number of molecularly distinct forms of human myeloid leukemia [15].
  • Taken together, these results demonstrate that in vivo activation of cAMP signaling contributes to APL clearance, independently of its RA-sensitivity, thus raising hopes that other myeloid leukemias may benefit from this therapeutic approach [16].
  • Ara-C treatment was also associated with increases in c-jun transcripts in U-937, THP-1, and HL-60 myeloid leukemia cells [17].
  • These observations reveal a significant cross-talk between Ca(2+) and retinoic acid signaling pathways that regulates the differentiation of myeloid leukemia cells, and they suggest that CaMKIIgamma may provide a new therapeutic target for the treatment of certain human myeloid leukemias [18].
 

Biological context of Leukemia, Myeloid

 

Anatomical context of Leukemia, Myeloid

 

Gene context of Leukemia, Myeloid

  • In addition, the CD14 gene is included in the "critical" region that is frequently deleted in certain myeloid leukemias [28].
  • One of its components, CAN/Nup214, is an FXFG repeat-containing protein known to be involved in myeloid leukemia in humans [29].
  • ETO, fusion partner in t(8;21) acute myeloid leukemia, represses transcription by interaction with the human N-CoR/mSin3/HDAC1 complex [30].
  • In addition, we have identified a third chimeric transcript, AML1/EVI1, in one of the therapy-related acute myeloid leukemia patients [31].
  • Likewise, in murine myeloid leukemia, transcriptional coactivation of Meis1 with HoxA7/A9 suggests that Meis1-HoxA7/9 heterodimers may evoke aberrant gene transcription [32].
 

Analytical, diagnostic and therapeutic context of Leukemia, Myeloid

References

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  18. CaMKII regulates retinoic acid receptor transcriptional activity and the differentiation of myeloid leukemia cells. Si, J., Mueller, L., Collins, S.J. J. Clin. Invest. (2007) [Pubmed]
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