A pilot study of alternative TrkAIII splicing in Merkel cell carcinoma: a potential oncogenic mechanism and novel therapeutic target.
Lucia CappabiancaStefano GuadagniRita MaccaroneMichela SebastianoAlessandro ChiomintoAntonietta Rosella FarinaAndrew Reay MackayPublished in: Journal of experimental & clinical cancer research : CR (2019)
MCPyV positive MCCs but not MCPyV negative MCC, BCCs and SCCs exhibit predominant alternative TrkAIII splicing, with evidence of intracellular TrkAIII activation. This establishes a new potential MCC subset, unveils a novel potential MCPyV oncogenic mechanism and identifies TrkAIII as a novel potential therapeutic target in MCPyV positive MCC.