Alternative splicing allows the generation of different protein isoforms, often with distinct and even opposite functions, from a single primary transcript. In this way, alternative splicing stands out as a major contributor to the proteomic diversity of complex organisms characterized by a limited number of protein-coding genes. It is therefore not surprising that the great plasticity that underpins the regulation of alternative splicing contributes to all areas of tumor cell biology. Notably, cancer-specific alternative splicing isoforms have been described. Many of these alternative splicing transcripts are novel. Some are expressed during embryonic development but virtually absent in mature/adult tissues. Hence, these novel transcripts may have a direct role in tumorigenesis and are powerful source to develop new diagnostic, prognostic, and therapeutic tools for human cancer. Despite the enormous amount of work already done, we have just uncovered the tip of the iceberg, and much remains to be achieved. In particular, a major goal of present alternative splicing research is to elucidate systematically the physiological (or pathological) roles of specific alternative splicing events, as well as to establish how alternative splicing regulation is coordinated with other steps in gene expression, in particular transcription, chromatin modification, and signaling pathways. Understanding the alterations of alternative splicing in cancer cells will lead to a better comprehension of several processes relevant to cancer biology.

We invite authors to contribute original research papers as well as review papers that will illustrate and stimulate the continuing effort to understand the molecular mechanisms underlying splicing deregulation in cancer and to exploit the use of cancer-associated alternative splicing variants as diagnostic/predictive biomarkers or potential targets for the development of innovative therapeutic strategies. Potential topics include, but are not limited to:

• Expression, activity, and function(s) of alternative splicing regulators involved in cancer development and progression, including splicing factors, splicing factor kinases and phosphatases
• Identification and functional characterization of alternative splicing variants implicated in major aspects of cancer cell biology or in the development of resistance to treatments
• The therapeutic potential of targeting cancer-associated alternative splicing isoforms
• Molecular mechanisms by which DNA damage and epigenetic chromatin changes can modulate alternative splicing
• Signaling pathways controlling alternative splicing choices and their alteration in cancer
• RNA-Seq applications and development of computational methods for the analysis of alternative splicing in cancer

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