Open AccessGenetic compensation of RUNX family transcription factors in leukemia
Author(s) -
Kamikubo Yasuhiko
Publication year - 2018
Publication title -
cancer science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.035
H-Index - 141
eISSN - 1349-7006
pISSN - 1347-9032
DOI - 10.1111/cas.13664
Subject(s) - myeloid leukemia , runx1 , leukemia , cancer research , transcription factor , haematopoiesis , biology , core binding factor , genetics , gene , stem cell
Runt (Runt domain)‐related transcription factor 1 ( RUNX 1) is a transcription factor belonging to the core‐binding factor ( CBF ) family. It is considered to be a master regulator of hematopoiesis and has been regarded as a tumor suppressor because it is essential for definitive hematopoiesis in vertebrates. It is one of the most frequent target genes of chromosomal translocation in leukemia, and germ line mutation of RUNX 1 causes familial platelet disorder with associated myeloid malignancies. Somatic cell mutations and chromosomal abnormalities, including those of RUNX 1, are observed in myelodysplastic syndrome, acute myeloid leukemia, acute lymphoblastic leukemia, and chronic myelomonocytic leukemia at a high frequency. In addition, recent studies reported by us and other groups suggested that WT RUNX 1 is needed for survival and proliferation of certain types of leukemia. In this review, we describe the significance and paradoxical requirement of RUNX 1 tumor suppressor in hematological malignancies based on recent findings such as “Genetic compensation of RUNX family transcription factors in leukemia,” “ RUNX 1 inhibition‐induced inhibitory effects on leukemia cells through p53 activation” and our novel promising theory “Cluster regulation of RUNX ( CROX )” through the RUNX gene switch method using pyrrole‐imidazole polyamides as a new technique that could contribute to the next generation of leukemia treatment strategies.