The enigma of ectopic expression of FGFR3 in multiple myeloma: A critical initiating event or just a target for mutational activation during tumor progression

Marta Chesi, P. Leif Bergsagel, W. Michael Kuehl

Research output: Contribution to journalReview article

32 Scopus citations

Abstract

The t(4;14)(pl 6.3;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 multiplemyeloma.

Original languageEnglish (US)
Pages (from-to)288-293
Number of pages6
JournalCurrent opinion in hematology
Volume9
Issue number4
DOIs
StatePublished - Jan 1 2002

ASJC Scopus subject areas

  • Hematology

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