Alternative splicing is the main mechanism increasing the proteome diversity coded by a limited number of genes and therefore likely plays a role in cancer. The understanding of the role of alternative splicing in cancer is reaching a novel level thanks to the use of new tools including splicing-sensitive microarrays allowing to analyze splicing at a large-scale level. Using original approaches, we performed genome-wide analyses of the expression of splicing variants and we demonstrated that alteration of splicing programs together with transcriptional programs occurs during tumor progression. Our mains goals are to identify the molecular mechanisms responsible for splicing alteration during tumor progression and to better understand how alternative splicing contributes to the phenotypic plasticity of cancer cells.

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News : publication dans Nucleic Acids Research
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