한빛사논문
- 조회3,428
Abstract
Seung-Hee Jo1, Jonathan Schatz2, Jaime Acquaviva1, Harinder Singh2 and Ruibao Ren1,*
1 Rosenstiel Basic Medical Sciences Research Center and Department of Biology, Brandeis University, Waltham, MA, United States; 2 Department of Molecular Genetics and Cell Biology, Howard Hughes Medical Institute, The University of Chicago, Chicago, IL, United States
* Corresponding author
Abstract
Interferon regulatory factor 4 (IRF-4) plays important functions in B and T cell development and immune response regulation and was originally identified as the product of a proto-oncogene involved in chromosomal translocations in multiple myeloma. Though IRF-4 is expressed in myeloid cells, its function in that lineage is not known. The closely related family member IRF-8 is a critical regulator of myelopoiesis, which when deleted in mice results in a syndrome highly similar to human chronic myelogenous leukemia (CML). In early lymphoid development, we have shown previously that IRF-4 and IRF-8 can function redundantly. We therefore investigated the effects of a combined loss of IRF-4 and IRF-8 on hematologic tumorigenesis. We found that mice deficient in both IRF-4 and IRF-8 develop from a very early age a more aggressive CML-like disease than mice deficient in IRF-8 alone, correlating with a greater expansion of granulocyte-monocyte progenitors (GMPs). While these results demonstrate for the first time that IRF-4 can function as tumor suppressor in myeloid cells, interestingly, all mice deficient in both IRF-4 and IRF-8 eventually develop and succumb to a B-lymphoblastic leukemia/lymphoma. Combined losses of IRF-4 and IRF-8 therefore can cooperate in the development of both myeloid and lymphoid tumors.
논문정보
- Research article
- 2010년 07월 (BRIC 등록일 )
- 국외 연구진
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