Modeling SF3B1 Mutations in Cancer: Advances, Challenges, and Opportunities.
In this issue of Cancer Cell, Obeng et al. identify the consequences of expressing the most common mutation in the spliceosomal gene SF3B1 on hematopoiesis. The knockin mouse model described represents a valuable tool to dissect the effects of SF3B1 mutations on transformation, splicing, and less well-characterized functions of SF3B1.
Human Oncology and Pathogenesis Program, Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA.
Daichi
D
Inoue
Human Oncology and Pathogenesis Program, Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA; Leukemia Service, Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA. Electronic address: abdelwao@mskcc.org.
Omar
O
Abdel-Wahab
D000818:Animals; D009154:Mutation; D010750:Phosphoproteins / Q000235:genetics*; D012326:RNA Splicing; D000072260:RNA Splicing Factors; D017381:Spliceosomes / Q000235:genetics
D010750:Phosphoproteins; D000072260:RNA Splicing Factors