The enigma of ectopic expression of FGFR3 in multiple myeloma: a critical initiating event or just a target for mutational activation during tumor progression
M Chesi, PL Bergsagel, WM Kuehl - Current opinion in …, 2002 - journals.lww.com
M Chesi, PL Bergsagel, WM Kuehl
Current opinion in hematology, 2002•journals.lww.comAbstract 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 …
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 …
Abstract
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 dysregulation of FGFR3 or MMSET mediates an early oncogenic process in multiple myeloma.
Lippincott Williams & Wilkins