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Abstract
Alternative splicing changes are frequently observed in cancer and are starting to
be recognized as important signatures for tumor progression and therapy. However,
their functional impact and relevance to tumorigenesis remain mostly unknown. We carried
out a systematic analysis to characterize the potential functional consequences of
alternative splicing changes in thousands of tumor samples. This analysis revealed
that a subset of alternative splicing changes affect protein domain families that
are frequently mutated in tumors and potentially disrupt protein-protein interactions
in cancer-related pathways. Moreover, there was a negative correlation between the
number of these alternative splicing changes in a sample and the number of somatic
mutations in drivers. We propose that a subset of the alternative splicing changes
observed in tumors may represent independent oncogenic processes that could be relevant
to explain the functional transformations in cancer, and some of them could potentially
be considered alternative splicing drivers (AS drivers).