Case Report: Genotype-informed management after clinically necessary cytoreduction for giant recurrent gastric gastrointestinal stromal tumor with prior rupture and KIT exon 17 N822Y mutation

Advanced recurrent gastrointestinal stromal tumor (GIST) after prolonged tyrosine kinase inhibitor (TKI) exposure requires integration of surgical oncology, molecular reassessment, and continuous systemic therapy. We report a 72-year-old man with a 21-year history of gastric GIST who underwent initial resection in 2005, resection of recurrent disease in 2009, and long-term imatinib therapy. After years of apparent disease stability, he independently reduced imatinib and had a prolonged surveillance gap before recurrence was detected in 2024. Following tumor rupture and short-interval progression on sunitinib and regorafenib, he received ripretinib. In January 2026, clinically necessary maximal cytoreductive surgery was performed for bulky recurrent peritoneal disease with bleeding, anemia, abdominal-wall involvement, high risk of re-rupture, and invasion or close involvement of the right colon. Pathology confirmed recurrent high-risk spindle-cell GIST. Postoperative next-generation sequencing identified a founding KIT exon 11 deletion and a secondary KIT exon 17 p.Asn822Tyr activation-loop mutation; ripretinib was resumed after recovery of oral intake. Three-month CT showed recurrent peritoneal tumors, while a right hepatic subcapsular low-enhancement nodule was favored to represent post-ablation change. This case illustrates that surgery in resistant recurrent GIST may be necessary for local complication control and tissue acquisition, but even after maximal macroscopic cytoreduction, durable management depends on continuous genotype-informed systemic therapy and close surveillance.