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Abstract

Alternative splicing is a tightly regulated process that can be disrupted in cancer. Established cancer genes express splice isoforms with distinct properties and their differential expression is associated with tumour progression. Although prostate adenocarcinoma (PCa) is effectively managed at early stage by therapies targeting the androgen receptor signaling axis, up to 30% of late stage prostate cancers progress to a treatment-resistant form of the disease called neuroendocrine prostate cancer (NEPC), for which there are few therapeutic options. It is histologically distinct from PCa, expresses a neuronal gene signature and is associated with poor survival (