# Long-Term Survival Following Multimodal Therapy with Sunitinib and Surgery for Recurrent Duodenal Gastrointestinal Stromal Tumor

**Authors:** Manatsu Mizuno, Tsuyoshi Takahashi, Yoshito Tomimaru, Yukinori Kurokawa, Takuro Saito, Takaomi Hagi, Kota Momose, Kotaro Yamashita, Koji Tanaka, Tomoki Makino, Kiyokazu Nakajima, Tomomi Fujii, Eiichi Mori, Hidetoshi Eguchi, Yuichiro Doki

PMC · DOI: 10.70352/scrj.cr.25-0260 · 2025-06-27

## TL;DR

A patient with drug-resistant stomach tumor lived over 9 years after combining surgery with sunitinib treatment.

## Contribution

Demonstrates long-term survival using surgery plus sunitinib in a drug-resistant GIST case.

## Key findings

- Sunitinib maintained disease stability for 7 years before resistance developed.
- Surgical resection of resistant lesions allowed continued sunitinib control of remaining tumors for 9 years.
- Combining surgery with systemic therapy may prolong survival in resistant GIST cases.

## Abstract

Gastrointestinal stromal tumors (GISTs) are mesenchymal tumors often driven by KIT or PDGFRA mutations. Sunitinib, a second-line tyrosine kinase inhibitor (TKI), is effective in imatinib-resistant cases, particularly those with secondary KIT mutations in the ATP-binding domain. However, resistance to sunitinib poses challenges, and evidence supporting surgery during sunitinib treatment remains limited.

A 77-year-old male presented with multiple liver and peritoneal metastases from a duodenal GIST. Initial treatment with imatinib was discontinued due to adverse effects, and sunitinib was initiated, maintaining disease stability for 7 years. Disease progression as a solitary lesion in liver segment seven was identified via imaging and diagnosed as sunitinib-resistant. A laparoscopic partial hepatectomy was performed, achieving complete resection without complications. Postoperative resumption of sunitinib has controlled all other lesions for 9 years with no recurrence.

This case highlights the potential of combining sunitinib with surgery to manage drug-resistant GIST. Localized surgical resection of resistant lesions, integrated with systemic therapy, may offer prolonged survival in selected patients. Further studies are needed to define the optimal role of surgery in this context.

## Linked entities

- **Genes:** KIT (KIT proto-oncogene, receptor tyrosine kinase) [NCBI Gene 3815], PDGFRA (platelet derived growth factor receptor alpha) [NCBI Gene 5156]
- **Chemicals:** sunitinib (PubChem CID 5329102), imatinib (PubChem CID 5291)
- **Diseases:** GIST (MONDO:0011719), Gastrointestinal stromal tumors (MONDO:0011719)

## Full-text entities

- **Genes:** PDGFRA (platelet derived growth factor receptor alpha) [NCBI Gene 5156] {aka CD140A, PDGFR-2, PDGFR2}, KIT (KIT proto-oncogene, receptor tyrosine kinase) [NCBI Gene 3815] {aka C-Kit, CD117, MASTC, PBT, SCFR}, TXK (TXK tyrosine kinase) [NCBI Gene 7294] {aka BTKL, PSCTK5, PTK4, RLK, TKL}
- **Diseases:** metastases (MESH:D009362), mesenchymal tumors (MESH:C535700), Duodenal Gastrointestinal Stromal Tumor (MESH:D046152)
- **Chemicals:** imatinib (MESH:D000068877), ATP (MESH:D000255), Sunitinib (MESH:D000077210)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Figures

6 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12206549/full.md

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Source: https://tomesphere.com/paper/PMC12206549