Role of co-repressors in transcriptional repression mediated by the t(8;21), t(16;21), t(12;21), and inv(16) fusion proteins

S W Hiebert; B Lutterbach; J Amann

doi:10.1097/00062752-200107000-00003

Role of co-repressors in transcriptional repression mediated by the t(8;21), t(16;21), t(12;21), and inv(16) fusion proteins

Curr Opin Hematol. 2001 Jul;8(4):197-200. doi: 10.1097/00062752-200107000-00003.

Authors

S W Hiebert¹, B Lutterbach, J Amann

Affiliation

¹ Department of Biochemistry, Vanderbilt-Ingram Cancer Center, Vanderbilt University School of Medicine, 23rd and Pierce Avenue, Nashville, TN 37232, USA. scott.hiebert@mcmail.vanderbilt.edu

PMID: 11561155
DOI: 10.1097/00062752-200107000-00003

Abstract

The t(8;21), t(16;21), inv(16), and t(12;21) are some of the most frequent chromosomal translocations found in acute myeloid and acute lymphoblastic leukemia. The fusion proteins created by these chromosomal translocations are transcriptional repressors. A full understanding of the types of proteins that these fusion proteins recruit to repress transcription will not only clarify understanding of the molecular mechanism of action of these fusion proteins but also provide further targets for therapeutic intervention.

Publication types

Review

MeSH terms

Acute Disease
Core Binding Factor Alpha 2 Subunit
Gene Expression Regulation, Neoplastic
Humans
Leukemia, Myeloid / genetics*
Oncogene Proteins, Fusion / physiology*
Precursor Cell Lymphoblastic Leukemia-Lymphoma / genetics*
RUNX1 Translocation Partner 1 Protein
Repressor Proteins / physiology
Transcription Factors / physiology
Transcription, Genetic
Translocation, Genetic

Substances

AML1-ETO fusion protein, human
AML1-MTG16 protein, human
CBFbeta-MYH11 fusion protein
Core Binding Factor Alpha 2 Subunit
Oncogene Proteins, Fusion
RUNX1 Translocation Partner 1 Protein
Repressor Proteins
TEL-AML1 fusion protein
Transcription Factors