The sum is greater than the FGFR1 partner.
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.
Braun
Benjamin S
BS
Department of Pediatrics and Comprehensive Cancer Center, University of California San Fransisco, San Francisco, CA 94143 USA.
Shannon
Kevin
K
D001853:Bone Marrow / Q000378:metabolism; D043171:Chromosomal Instability; D002880:Chromosomes, Human, Pair 11 / Q000235:genetics; D004791:Enzyme Inhibitors / Q000494:pharmacology; D006801:Humans; D007951:Leukemia, Myeloid / Q000378:metabolism*; D023421:Models, Animal; D020794:Receptor Protein-Tyrosine Kinases / Q000378:metabolism*; D051496:Receptor, Fibroblast Growth Factor, Type 1; D017468:Receptors, Fibroblast Growth Factor / Q000378:metabolism*; D019737:Transplants
D004791:Enzyme Inhibitors; D017468:Receptors, Fibroblast Growth Factor; C496348:FGFR1 protein, human; D020794:Receptor Protein-Tyrosine Kinases; D051496:Receptor, Fibroblast Growth Factor, Type 1