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Particular prognostic parameters are known in both CM and UM (Damato et al, 2011), however, predictive biomarkers that can foretell response to therapies are of paramount importance.

In both uveal and cutaneous melanoma cell lines, SRPK1 was highly expressed, and inhibition of SRPK1 by knockdown or with pharmacological inhibitors reduced pro-angiogenic VEGF expression maintaining the production of anti-angiogenic VEGF isoforms.

Both pharmacological SRPK1 inhibitors and SRPK1 knockdown reduced growth of human melanomas in vivo, but neither affected cell proliferation in vitro.

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Although VEGF is upregulated in melanoma, its overall expression has been shown to correlate poorly with metastatic spread (Stefanou et al, 2004).

However, VEGF can be generated as two isoform families, the pro-angiogenic VEGF-Ab expression in primary tumours that had gone on to metastasise.

Tumour progression also requires angiogenesis, which is regulated by VEGF-A, itself alternatively spliced to form two families of isoforms, pro- and anti-angiogenic.