The Role of RUNX1 in NF1-Related Tumors and Blood Disorders
Youjin Na1, Gang Huang1,2,3, and Jianqiang Wu1,4,*
1Division of Experimental Hematology and Cancer Biology, 2Divisions of Pathology and Experimental Hematology and Cancer Biology, Cancer & Blood Diseases Institute, Cincinnati Children’s Hospital Medical Center, Cincinnati, OH 45229, USA, 3Department of Pathology and Laboratory Medicine, 4Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, OH 45267, USA
Received November 27, 2019; Accepted December 12, 2019.; Published online January 15, 2020.
© Korean Society for Molecular and Cellular Biology. All rights reserved.

ABSTRACT
Neurofibromatosis type 1 (NF1) is an autosomal dominant disorder. NF1 patients are predisposed to formation of several type solid tumors as well as to juvenile myelomonocytic leukemia. Loss of NF1 results in dysregulation of MAPK, PI3K and other signaling cascades, to promote cell proliferation and to inhibit cell apoptosis. The RUNX1 gene is associated with stem cell function in many tissues, and plays a key role in the fate of stem cells. Aberrant RUNX1 expression leads to context-dependent tumor development, in which RUNX1 may serve as a tumor suppressor or an oncogene in specific tissue contexts. The co-occurrence of mutation of NF1 and RUNX1 is detected rarely in several cancers and signaling downstream of RAS-MAPK can alter RUNX1 function. Whether aberrant RUNX1 expression contributes to NF1related tumorigenesis is not fully understood. This review focuses on the role of RUNX1 in NF1-related tumors and blood disorders, and in sporadic cancers.
Keywords: cancer, mutation, neurofibromatosis type 1, RUNX1, tumor driver


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31 January 2020 Volume 43,
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