Bartosz Wasag

TL;DR: This study shows the high frequency of KIT/PDGFRA kinase domain mutations in patients with secondary resistance and defines genomic amplification of Kit / PDGFRA as an alternative cause of resistance to the drug.

TL;DR: Findings indicate that the mutational status of the c-KIT/PDGFRA oncoproteins could be useful to predict the clinical response of patients imatinib therapy.

TL;DR: Seven gastrointestinal stromal neoplasms that presented clinicopathological features typical of GISTs but showed absence of CD117 expression as detected by immunohistochemistry are described, indicating that there is a subgroup of KIT‐negative GISTS that exhibit the same morphological, cytogenetic, and molecular features as KIT•positive tumours.

TL;DR: Treatment with dasatinib or the heat shock protein 90 inhibitor IPI-504 may provide a therapeutic alternative for GIST patients whose tumors carry the imatinib-resistant PDGFRAD842V mutant isoform.

TL;DR: It is suggested that loss of 14q is a relatively less frequent genetic event in the development of nongastric GISTs, the lack of which is most likely substituted by the accumulation of 1p/15q and other changes.