Most human genes undergo alternative splicing (AS), and dysregulation of alternative splicing contributes to tumor initiation and progression. Computational analysis of genomic and transcriptomic data enables the systematic characterization of alternative splicing and its functional role in cancer. In this review, we summarize the latest computational approaches to studying alternative splicing in cancer and the current limitations of the most popular tools in this field. Finally, we describe some of the current computational challenges in the characterization of the role of alternative splicing in cancer.
Keywords: alternative splicing; cancer; computational analysis; spliceosomal mutations.
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