The sum is greater than the FGFR1 partner

Department of Pediatrics and Comprehensive Cancer Center, University of California San Fransisco, San Francisco, CA 94143 USA.
Cancer Cell (Impact Factor: 23.52). 04/2004; 5(3):203-4. DOI: 10.1016/S1535-6108(04)00060-1
Source: PubMed


Cancer-associated chromosomal translocations create chimeric oncoproteins that contribute to aberrant growth by dominant or dominant negative mechanisms. Interestingly, genes such as MLL, RARA, and EWS are fused to multiple partners. This molecular promiscuity can provide important functional information, as specific translocations may be associated with discrete clinical and molecular features. In this issue of Cancer Cell, use a murine retroviral transduction/transplantation system to analyze two FGFR1 fusions found in hematologic malignancies. Their results show that these chromosomal rearrangements play a central role in pathogenesis, underscore the role of partner genes in modulating disease phenotypes, and uncover potential therapeutic targets.

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    • "These encode the RNA - binding protein LSM1 ( Fraser et al . , 2005 ) , the receptor tyrosine kinase FGFR1 ( Braun and Shannon , 2004 ) , the cell - cycle - regulatory protein TACC1 ( Still et al . , 1999 ) , the metalloproteinase ADAM9 ( Maz - zocca et al . "
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