What drives the wheel towards long-term outcome in advanced GIST, its size, genotype or may be a pill or two of imatinib?
It is a rare event in the field of oncology therapeutics when a molecule with a selective and narrow spectrum of anti-cancer activity transforms the treatment landscape and outcomes in a previously ‘tough to treat’ disease. The initial case report, published in April 2001, documenting the remarkable response of a heavily pretreated metastatic patient with GIST to imatinib was one such event that marked a turning point in the biological, diagnostic, and therapeutic approaches to advanced GIST (1). It shows remarkable foresight on the part of the investigators of the EORTC-STBSG/AIGTG and the SWOG groups to start the parallel running large scale trials examining two different dose levels of imatinib (400 and 800 mg) with the advent of the use of imatinib in advanced GIST (2,3). The reasons for the continued relevance of these two studies is multifold: primarily, because of imatinib being active against GIST across varying doses with no clear-cut evidence of superiority of one dose level over another as per initial data. Secondly, the updated results of the EORTC-STBSG/AIGTG study have encompassed almost the entire learning curve of the management of advanced GIST over the last 15 years.