A 54-year-old woman undergoes resection of a gastric gastrointestinal stromal tumour with a mitotic count of 8 per 50 high power fields. Adjuvant therapy with imatinib is planned. Its therapeutic target in this tumour is:

• A HER2/neu tyrosine kinase
• B BCR-ABL fusion protein
• C VEGFR-2 extracellular domain
• D Mutated c-KIT (CD117) tyrosine kinase ✓

Explanation

About 85 to 90 percent of GISTs carry activating mutations of the c-KIT proto-oncogene, and most of the remainder have PDGFRA mutations. Both are type III receptor tyrosine kinases inhibited by imatinib mesylate, making it first-line therapy for advanced and high-risk resected GIST. BCR-ABL inhibition explains imatinib's success in chronic myeloid leukaemia but is irrelevant here, since GISTs are mesenchymal tumours unrelated to the Philadelphia chromosome.

Reference: Robbins and Cotran Pathologic Basis of Disease, 10th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.