Journal
CURRENT OPINION IN HEMATOLOGY
Volume 9, Issue 4, Pages 288-293Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/00062752-200207000-00005
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- NCI NIH HHS [K01-CA74265] Funding Source: Medline
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The t(4;14)(p16.3;q32) translocation that occurs uniquely in a subset of multiple myeloma tumors results in ectopic expression of wild-type FGFR3 and enhanced expression of MMSET, a gene that is homologous to the MLL gene that is involved in acute myeloid leukemias. Wild-type FGFR3 appears to be weakly transforming in a hematopoietic murine model, whereas FGFR3 that contains kinase-activating mutations is strongly transforming in NIH3T3 cells and the hematopoietic model. The subsequent acquisition of FGFR3 kinase-activating mutations in some tumors with t(4;14) translocations confirms a role for FGFR3 in tumor progression. However, it remains to be proven if and how dysiregulation of FGFR3 or MMSET mediates an early oncogenic process in multiple myeloma. (C) 2002 Lippincott Williams Wilkins, Inc.
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