MYB oncoproteins: emerging players and potential therapeutic targets in human cancer

MYB transcription factors are highly conserved from plants to vertebrates, indicating that their functions embrace fundamental mechanisms in the biology of cells and organisms. In humans, the MYB gene family is composed of three members: MYB , MYBL1 and MYBL2 , encoding the transcription factors MYB...

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Published in:Oncogenesis (New York, NY) Vol. 10; no. 2; pp. 19 - 15
Main Authors: Cicirò, Ylenia, Sala, Arturo
Format: Journal Article
Language:English
Published: London Nature Publishing Group UK 26.02.2021
Nature Publishing Group
Subjects:
631/67
631/67/395
Apoptosis
c-Myb protein
Cancer
Cell Biology
Human Genetics
Internal Medicine
Leukemia
Medicine
Medicine & Public Health
MYB gene
MYB protein
Oncology
Oncoproteins
Review
Review Article
Therapeutic applications
Therapeutic targets
Transcription factors
ISSN:2157-9024, 2157-9024
Online Access:Get full text
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Summary:MYB transcription factors are highly conserved from plants to vertebrates, indicating that their functions embrace fundamental mechanisms in the biology of cells and organisms. In humans, the MYB gene family is composed of three members: MYB , MYBL1 and MYBL2 , encoding the transcription factors MYB, MYBL1, and MYBL2 (also known as c-MYB, A-MYB, and B-MYB), respectively. A truncated version of MYB, the prototype member of the MYB family, was originally identified as the product of the retroviral oncogene v-myb , which causes leukaemia in birds. This led to the hypothesis that aberrant activation of vertebrate MYB could also cause cancer. Despite more than three decades have elapsed since the isolation of v-myb, only recently investigators were able to detect MYB genes rearrangements and mutations, smoking gun evidence of the involvement of MYB family members in human cancer. In this review, we will highlight studies linking the activity of MYB family members to human malignancies and experimental therapeutic interventions tailored for MYB -expressing cancers.
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ISSN:2157-9024
2157-9024
DOI:10.1038/s41389-021-00309-y