MYB as a Critical Transcription Factor and Potential Therapeutic Target in AML.
Adv Exp Med Biol
; 1459: 341-358, 2024.
Article
in En
| MEDLINE
| ID: mdl-39017851
ABSTRACT
Myb was identified over four decades ago as the transforming component of acute leukemia viruses in chickens. Since then it has become increasingly apparent that dysregulated MYB activity characterizes many blood cancers, including acute myeloid leukemia, and that it represents the most "addictive" oncoprotein in many, if not all, such diseases. As a consequence of this tumor-specific dependency for MYB, it has become a major focus of efforts to develop specific antileukemia drugs. Much attention is being given to ways to interrupt the interaction between MYB and cooperating factors, in particular EP300/KAT3B and CBP/KAT3A. Aside from candidates identified through screening of small molecules, the most exciting prospect for novel drugs seems to be the design of peptide mimetics that interfere directly at the interface between MYB and its cofactors. Such peptides combine a high degree of target specificity with good efficacy including minimal effects on normal hematopoietic cells.
Key words
Full text:
1
Collection:
01-internacional
Database:
MEDLINE
Main subject:
Leukemia, Myeloid, Acute
/
Proto-Oncogene Proteins c-myb
Limits:
Animals
/
Humans
Language:
En
Journal:
Adv Exp Med Biol
Year:
2024
Document type:
Article
Affiliation country:
Country of publication: