Abstract
Mutations in spliceosomal components are prevalent in myelodysplastic syndromes, but less so in acute myeloid leukemia (AML). However, aberrant splicing is prolific in AML, suggesting deregulated splicing could contribute broadly to tumorigenesis. Elevated stress responses correlate with splicing dysfunction across myeloid malignancies, representing potentially novel therapeutic targets.See related article by Anande et al., p. 3597.