A brand new editorial perspective titled “C/EBPβ cooperates with MYB to maintain the oncogenic program of AML cells” has been printed in Oncotarget.
On this new paper, researcher Karl-Heinz Klempnauer from Westfälische-Wilhelms-Universität discusses latest research on the function of transcription issue MYB in acute myeloid leukemia (AML). MYB has been recognized as a key regulator of a transcriptional program for self-renewal of AML cells.
The MYB gene initially attracted consideration because the progenitor of a retrovirally-transduced oncogene that induces a myeloid leukemia in chickens. MYB encodes a transcription issue with important roles within the growth of the hematopoietic system and the proliferation and differentiation of hematopoietic progenitor cells. Subsequent work recognized MYB additionally as an important participant within the growth and upkeep of leukemia in people.
“Current work summarized right here has now highlighted the CCAAT-box/enhancer binding protein beta (C/EBPβ) as a necessary issue and potential therapeutic goal that cooperates with MYB and coactivator p300 within the upkeep of the leukemic cells,” the paper states.
Karl-Heinz Klempnauer, C/EBPβ cooperates with MYB to keep up the oncogenic program of AML cells, Oncotarget (2023). DOI: 10.18632/oncotarget.28377
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C/EBPβ cooperates with MYB to keep up the oncogenic program of AML cells (2023, November 13)
retrieved 13 November 2023
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