How much molecular pathology is required to treat GI stromal tumours?

摘要

The discovery in the late 1990s of the critical role of constitutive activation of the KIT receptor, most often due to KIT mutation, in gastrointestinal stromal tumours (GISTs) followed closely by the remarkable success of the selective KIT tyrosine kinase inhibitor, imatinib, has led to rapid expanding research into the underlying biology of these mutations and their implications for both prognosis and response to treatment. There would appear to be accumulating evidence of the importance of these mutations; however, the role of mutational analysis of KIT or PDGFRA in tailoring the treatment strategy for an individual patient is far from clear.