Alternative splicing (AS) has many important roles in the pathogenesis of leukemia. Recent papers suggest that one of its key aspects is exclusion of 3'-terminal exons in favor of premature termination using intronic polyadenylation signals. This process generates leukemia suppressor isoforms with truncated C termini and acting in loss-of-function or dominant-negative manners.
Keywords: RNA processing; alternative splicing; cancer; intronic polyadenylation; leukemia; protein diversity.
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