Adjuvant Imatinib in GIST: ESMO GI Oncology | September 2026

Introduction:

Adjuvant imatinib has clearly improved recurrence-free survival after complete resection of high-risk gastrointestinal stromal tumours (GISTs). However, important questions remain regarding who truly benefits, optimal treatment duration, and whether extending therapy beyond 3 years improves survival. This review emphasises that clinicopathological risk alone is no longer sufficient—molecular subtype increasingly matters.

Why is this important?

High-risk GIST can recur despite apparently curative surgery.

Three years of imatinib remains the standard, but relapse frequently occurs after stopping therapy.

Intermediate-risk GIST is heterogeneous and may be overtreated or undertreated.

KIT/PDGFRA genotype predicts both prognosis and imatinib sensitivity.

Key Takeaways:

Three years of adjuvant imatinib remains standard for high-risk, imatinib-sensitive GIST.

KIT exon 11 mutations, particularly deletions involving codons 557/558, are associated with higher recurrence risk but also strong imatinib sensitivity.

High-risk KIT exon 9 GIST can benefit from adjuvant imatinib; current evidence does not clearly support routine 800 mg dosing over 400 mg in the adjuvant setting.

PDGFRA D842V and SDH-deficient GIST are imatinib-resistant, so adjuvant imatinib should generally not be used.

Tumor rupture is a major adverse prognostic factor and should usually place patients in a very-high-risk category.

Intermediate-risk disease requires individualized decision-making based on tumor site, size, mitotic rate, rupture, genotype, and patient preference.

Extending imatinib beyond 3 years can delay recurrence in selected high-risk patients.

In IMADGIST, 6 years of therapy improved disease-free survival compared with 3 years, but no overall-survival advantage has yet been demonstrated.

Recurrence often clusters after stopping treatment, particularly within the first 6–18 months, supporting closer surveillance during this period.

Therapeutic drug monitoring may help selected patients with unexpected toxicity or inadequate drug exposure, but routine use is not yet established.

Clinical Impact:

The future of adjuvant GIST therapy is moving from a simple “high risk = 3 years of imatinib” model toward:

Clinicopathological risk + tumour rupture + molecular genotype → individualised duration and intensity of therapy.

For very-high-risk disease, especially after rupture, prolonged treatment may be reasonable, but this must be balanced against toxicity, adherence, cost, and the absence of proven OS benefit from indefinite therapy.

Bottom Line:

Adjuvant imatinib remains standard for high-risk, imatinib-sensitive GIST, but treatment should increasingly be genotype-driven. Three years is the current benchmark; longer therapy can delay recurrence in selected very-high-risk patients, although a survival advantage remains unproven. Molecular profiling is now essential—not optional—in deciding postoperative GIST therapy.