@entity4373 ( @entity4373 ), the process of removing introns from pre-mRNA and re-arrangement of exons to give several types of mature transcripts, has been described more than 40 years ago. However, until recently, it has not been clear how extensive it is. Genome-wide studies have now conclusively shown that more than 90% of genes are alternatively spliced in @entity1 . This makes @entity4373 one of the main drivers of proteomic diversity and, consequently, determinant of cellular function repertoire. Unsurprisingly, given its extent, numerous splice isoforms have been described to be associated with several diseases including @entity5 . Many of them have antagonistic functions, e.g., pro- and anti-angiogenic or pro- and anti-apoptotic. Additionally several splice factors have been recently described to have oncogene or @entity5 suppressors activities, like @entity19982 which is frequently mutated in @entity2590 . Beside the implications for @entity5 pathogenesis, de-regulated @entity4373 is recognized as one of the novel areas of cell biology where therapeutic manipulations may be designed. This editorial discusses the possibilities of manipulation of @entity4373 for therapeutic benefit in @entity5 . Approaches involving the use of oligonucleotides as well as small molecule splicing modulators are presented as well as thoughts on how specificity might be accomplished in splicing therapeutics.

Modulators of alternative splicing as novel therapeutics in XXXX .

@entity1 :: ('9606', 'Species') :: ['humans'] @entity5 :: ('MESH:D009369', 'Disease') :: ['cancer', 'tumour'] @entity4373 :: ('MESH:C536589', 'Disease') :: ['Alternative splicing', 'AS'] @entity2590 :: ('MESH:D009190', 'Disease') :: ['myelodysplastic syndromes'] @entity19982 :: ('23451', 'Gene') :: ['SF3B1']
@entity5 :: (MESH:D009369,Disease) :: ['cancer']
