The prognosis of patients with gastrointestinal stromal tumors harboring the KIT exon 11 mutation: a retrospective cohort study

Introduction

Gastrointestinal stromal tumors (GISTs) are the most common mesenchymal tumors of the gastrointestinal tract. Approximately 65% to 80% of these tumors have a gain-of-function mutation in the KIT proto-oncogene, including substitution, deletion, insertion, duplication, and insertion-deletion (indel) mutations (1,2). The structure of KIT receptor tyrosine kinase consists of an extracellular domain with immunoglobulin-like motifs, a juxta-membrane domain, an ATP-binding domain, and an activation loop domain (3). The most common mutation in GIST occurs in KIT exon 11, which affects the juxta-membrane domain and is considered to confer high sensitivity to imatinib in patients with metastatic or unresectable disease (4). In the BFR14 trial, imatinib treatment prolonged the median progress-free survival (PFS) of patients with metastatic or unresectable GIST with KIT exon 11 mutations to 39.4 months. Moreover, although the patients with mutations involving the 557 and/or 558 codons showed favorable sensitivity, they developed secondary resistance more rapidly than those without such mutations (5). The SWOG/S0033 trial also reported similar survival benefits from imatinib treatment for patients with exon 11 mutations but did not find significant differences in progression-free survival (PFS) across patients with different subsets of exon 11 mutations (6).

Surgical resection with negative margins is the primary treatment for localized GISTs. However, 30–40% patients eventually develop tumor recurrence after curative surgery (7). Several risk stratification models comprising combinations of clinical prognostic factors (including tumor size, tumor location, mitotic counts, and tumor rupture) have been established for determining recurrence risk (8-11). These can help to identify patients who may benefit from adjuvant imatinib treatment. Over the past two decades, several prospective studies have demonstrated the benefits of adjuvant imatinib treatment (12,13), and it is recommended that patients with high-risk GIST be treated with imatinib for at least 3 years postoperation (14,15). However, a portion of these patients experience tumor recurrence in the first year after the interruption of imatinib treatment. In the recent IMADGIST trial, prolongation of adjuvant imatinib treatment to 6 years was associated with a significant reduction in the recurrence risk among patients with high-risk GIST (16). Although genotype was not systematically examined as part of these studies’ design, patients with exon 11 mutations had the best prognosis after adjuvant imatinib treatment in the subgroup analysis (17,18). However, the specific duration of adjuvant imatinib treatment for patients with GISTs harboring exon 11 mutations and a high risk of recurrence has not been specifically examined.

Several studies have demonstrated the prognostic value of tumor mutation status, yet this has not been so effective as to replace conventional risk factors. Approximately 80% of KIT mutations occur in exon 11, a fact which was garnered heightened clinical interest in recent years. One study found that various exon 11 mutations in GISTs lead to different long-term prognoses after radical surgery (19,20). Some clinical trials have reported that deletion of exon 11 is linked to aggressive pathological features and that patients with deletions involving codons 557 and/or 558 benefit most from adjuvant imatinib treatment (17). However, there is no general consensuses on the association between the type of exon 11 mutation and long-term prognosis in adjuvant settings, with relatively few real-world studies being conducted on this subject. We therefore retrospectively reviewed patients with primary GIST harboring KIT exon 11 mutations who received surgical resection between January 2004 and December 2023 in our center. The aim of this study was to determine the prognostic significance of different exon 11 mutations in GISTs and inform therapeutic strategies for adjuvant imatinib treatment in patients with intermediate- or high-risk GISTs. We present this article in accordance with the STROBE reporting checklist (available at https://jgo.amegroups.com/article/view/10.21037/jgo-2026-0409/rc).

Methods

Patients

The clinical data of patients who received surgical resection for primary GIST with KIT exon 11 mutation at The First Affiliated Hospital, Zhejiang University, between January 2004 to December 2023 were retrospectively reviewed. Resection status was classified as R0 resection (negative margins), R1 resection (microscopic residual tumor), or R2 resection (macroscopic residual tumor). No sample size calculation was performed due to the retrospective nature of the study design. The pathological diagnosis was based on a combination of histopathological evaluation and immunohistochemistry (IHC) staining for CD117 and/or DOG-1. Mitotic count was measured in the area with highest proliferation of the tumor (surgical specimens), and the number of mitoses in 50 high-power fields (HPFs; 400×) was calculated. Paraffin-embedded tissue samples were examined for somatic mutations in KIT (exons 9, 11, 13, and 17) and PDGFRA (exons 12, 14 and 18) via polymerase chain reaction amplification and Sanger sequencing. Data on gender, age, pathological characteristics, genotypes, therapeutic strategy, and post-operative treatment were collected. The postoperative recurrence risk assessment of GISTs was based on the modified National Institute of Health (NIH) consensus classification system (14).

The major inclusion criteria were as follows: (I) surgical resection for primary GIST with KIT exon 11 mutation, (II) an Eastern Cooperative Oncology Group (ECOG) performance status score 2 or less, and (III) survival of more than 1 month after surgery. Patients with metastatic disease or other malignant tumors were excluded. The study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments. The study was approved by the Ethics Committee of The First Affiliated Hospital, Zhejiang University School of Medicine (No. 2024-0904), and the informed consent was exempted because of the retrospective nature of this study.

Follow-up

All patients were followed up every 3–6 months for 1-2 years, every 6–12 months for 3–5 years, and then annually after 5 years. The follow-up included a combination of laboratory tests, radiographic imaging (computed tomography or magnetic resonance imaging), or gastrointestinal endoscopy if necessary.

Statistical analysis

The Chi-squared test was used to analyze categorical variables, while analysis of variance was used to compare differences in continuous variables. DFS was defined as the time from the resection of GIST to tumor recurrence or death (regardless of the cause), whichever occurred first. Overall survival (OS) was defined as the time from the pathological or operative diagnose of GIST to death of any cause. Patients who were alive and free of tumor recurrence in June 2025 were censored from the DFS analysis. Survival curves were analyzed via the Kaplan-Meier method, with differences being compared with the log-rank test. A Cox proportional hazard model was used to identify the independent predictors of DFS. A two-sided P value <0.05 was considered statistically significant. All the statistical analyses were performed with SPSS version 29.0 (IBM Corporation, Armonk, NY, USA).

Results

Patient characteristics

As shown in Figure 1, a total of 647 patients were included in the study, with 370 (57.2%) men and 277 (42.8%) women (Table 1). The median age was 59 (range 23–85) years. Among the patients, 67 (10.4%) received neoadjuvant imatinib treatment, 366 (56.7%) received adjuvant imatinib treatment, and 214 (33.1%) received surgery only (Table 1). There were 637(98.5%) patients who received R0 resection of the tumor (Table 1). The most common tumor location was the stomach (n=385, 59.5%), followed by small intestine (n=231, 35.7%), rectum (n=24, 3.7%), and other locations (n=7, 1.1%). Regarding postoperative specimens, the median tumor size was 5.3 (range 0.8–40.0) cm. According to the modified NIH consensus classification, 22 (3.4%), 160 (24.7%), 149 (23.0%), and 245 (37.9%) patients were categorized as very low risk, low risk, intermediate risk, and high-risk, respectively (Table 1). Moreover, 67 (10.4%) patients received neoadjuvant imatinib treatment, and 4 (0.6%) patients with unknown mitotic counts were placed into the undefined-risk group (Table 1). Among the 67 patients who received neoadjuvant imatinib treatment, the median duration of preoperative imatinib was 7 (range 0.2–24) months, and 61 of these patients continued to receive postoperative imatinib treatment, with a median duration of 34 (0.5–110) months. Of the 366 patients who received adjuvant imatinib treatment, the median duration of imatinib treatment was 24 (range 1–141) months. The details of the clinical characteristics of all patients are shown in Table 1.

Figure 1 Flowchart of patient selection. The diagram illustrates the inclusion and exclusion process of patients undergoing surgery for primary GIST with KIT exon 11 mutations. *, 58 patients with synchronous metastasis were excluded. GIST, gastrointestinal stromal tumor.

Mutational subtypes

Figure 2 shows a pie chart of the cumulative mutations by codon, and a total of 155 different exon 11 mutations were identified. The most frequently mutated codon was 557 (n=259, 40.0%), followed by 559 (n=229, 35.4%), 558 (n=227, 35.1%), and 560 (n=178, 27.5%) (Figure 2). The most common mutation type was deletion (n=233, 36.0%), followed by substitution (n=222, 34.3%), insertion-deletion (indel; n=132, 20.4%), insertion (n=38, 5.9%), and duplication (n=22, 3.4%) (Table 1). Substitution mutations, as compared to deletion or indel mutations, occurred more frequently in the stomach (63.5% vs. 52.1%; P=0.007) and were more likely to have a low mitotic count (74.8% vs. 62.5%; P=0.002) (Table 1). A higher proportion of tumors with deletion or indel mutations were considered high-risk GISTs as compared to those with other mutations (43.0% vs. 31.2%; P=0.002). However, tumor size did not differ significantly across the five mutation types examined in this study (P=0.228; Table 1).

Figure 2 Distribution of KIT exon 11 mutation codons. Pie chart showing the relative frequency of different codons identified within KIT exon 11.

Survival analysis

The median follow-up time of this study was 55 (range 12–255) months. At last follow-up, 96 (14.8%) patients had experienced postoperative tumor recurrence. The most common site of recurrence was the liver (n=47, 7.3%), followed by the peritoneum (n=41, 6.3%). Of the 96 patients with recurrence, 30 died from GIST. The 5-year DFS and OS of the entire cohort was 83.4% and 96.5%, respectively. Survival analysis was performed on the 637 (98.5%) patients who underwent R0 resection. According to Kaplan–Meier analysis, mutation type was significantly associated with the prognosis of in the entire cohort (log-rank P=0.013; Figure S1), especially for patients who received surgery only (log-rank P=0.002, Figure 3A) or adjuvant imatinib treatment (log-rank P=0.005; Figure 3B). The 5-year DFS of imatinib-naïve patients carrying deletion or indel mutation involving codons 557 and/or 558 was 76.2%, which was lower than that of patients carrying deletion or indel mutations that did not involve codons 557 or 558 (log-rank P=0.021; Figure 4A), the difference was adjusted by imatinib treatment (log-rank P=0.308; Figure 4B). Of the 146 intermediate-risk patients, 127 received adjuvant imatinib treatment, which was associated with better prognosis as compared to non–adjuvant imatinib treatment (5-year DFS rate: 96.4% vs. 91.7%; log-rank P<0.001; Figure S2A). However, there was no additional survival benefit from prolonged imatinib treatment for intermediate-risk patients (Figure 5A). The 5-year DFS rate of high-risk patients who underwent surgery only was 28.6%, which was lower than that of those who received adjuvant imatinib treatment (5-year DFS: 76.4%; log-rank P<0.001; Figure S2B). Of the 215 high-risk patients who received adjuvant imatinib treatment, only 4 (4/215, 1.86%) experienced tumor recurrence during imatinib treatment, and the prolonged duration (≥5 years) of imatinib treatment was associated with a better prognosis (log-rank P<0.001; Figure 5B). Of the 67 patients underwent neoadjuvant imatinib treatment, 42 were considered to have high-risk GIST according to pretherapeutic radiological examination (tumor size > 10.0 cm in any location or tumor size > 5.0 cm in a nongastric location). The 5-year DFS rate of patients with high-risk GISTs who received neoadjuvant imatinib treatment was 73.2%, which was comparable to that of those with high-risk GISTs who received upfront resection followed by adjuvant imatinib treatment (5-year DFS rate: 76.4%; log-rank P=0.947; Figure S2B).

Figure 3 DFS by KIT exon 11 mutation subtype. Kaplan-Meier survival analysis comparing DFS across patients with different exon 11 mutations. Analyses are shown for patients treated with surgery alone (A) and those receiving adjuvant imatinib treatment (B). DFS, disease-free survival.

Figure 4 DFS in patients with deletion or indel mutations at KIT exon 11. (A) Surgery alone. (B) adjuvant imatinib treatment. DFS, disease-free survival.

Figure 5 DFS according to risk stratification and duration of adjuvant imatinib. Kaplan-Meier curves showing the DFS of patients with intermediate-risk (A) and high-risk (B) GIST receiving different durations of adjuvant imatinib therapy. DFS, disease-free survival; GIST, gastrointestinal stromal tumor; IM-AT, adjuvant imatinib treatment.

Among the 637 (98.5%) with R0 resection, the factors associated with the long-term prognosis were tumor size (log-rank P<0.001; Figure S3A), mitotic count (log-rank P<0.001; Figure S3B), tumor location (log-rank P<0.001; Figure S3C), and tumor rupture (log-rank P<0.001; Figure S3D). After adjustments were made for these above-mentioned variables in the Cox proportional hazard model, the independent predictors of prognosis were tumor size (P<0.001), tumor location (P=0.001), mitotic counts (P<0.001), tumor rupture (P<0.001), exon 11 mutation subtype (P=0.006), and adjuvant imatinib treatment (P<0.001) (Table 2).

Discussion

In recent years, the genetic landscape of GISTs has been extensively characterized. Among the mutations in GISTs, those at exon 11 are the most common and tend to involve codons 550–590 (21). Although the prognostic role of genotype has been examined in several studies, only a few have focused on exon 11 mutations. In our study, we reviewed 647 patients with GIST harboring exon 11 mutations who received surgery over a 20-year period at our hospital and found that mutational status was associated with patient prognosis.

The clinicopathological characteristics of the patients included in this study were consistent with those of previous reports (1), with the most common location being the stomach, followed by the small intestine. Of the 155 different mutations examined in this study, the majority occurred in the hot spot region of codons between 550 to 560, and deletion was the most common mutation. Studies have found that the deletion mutations of KIT exon 11 are associated with a lower DFS but that they confer high sensitivity to front-line imatinib treatment (17,22). Consistent with this, we found that a greater proportion of GISTs with deletion or indel mutations were high risk as compared to GISTs with other mutations. Furthermore, imatinib-naïve patients with deletion or indel mutations involving codons 557 and/or 558 had a worse DFS than did those carrying deletions or indels that did not involve codons 557 or 558, and the poor prognosis was improved by adjuvant imatinib treatment.

The principal treatment for patients with localized GISTs is surgical resection, but a portion of these patients experience tumor recurrence within the first 5 years. Therefore, adjuvant imatinib treatment is considered to be a key strategy for improving prognosis for patients with intermediate-to-high-risk GIST. Three randomized controlled trials [RCTs; ACOSOG-Z9001 (12), SSG/XVIII (13), and IMADGIST (16)] confirmed the efficacy of adjuvant imatinib treatment for patients with GISTs. These studies further conducted survival analysis to determine the associations between KIT mutations and DFS. Patients with a tumor size ≥3 cm were included in ACOSOG-Z9001 trial, and adjuvant imatinib treatment was associated with better DFS in patients with the KIT exon 11 deletion (18). The SSG/XVIII trial demonstrated that patients with high-risk GIST harboring KIT exon 11 mutations receive greater benefit from a 3-year duration of adjuvant imatinib treatment than from 1-year treatment, as do those with deletion or indel mutations (23). The IMADGIST trial investigated a longer duration (6 years) of adjuvant imatinib treatment for patients with GIST at a high risk of relapse >35%. Although it was concluded that extending the adjuvant imatinib treatment from the recommended 3 years to 6 years resulted in a significant reduction of the recurrence risk, the sample size was limited. Moreover, the definition of high-risk group according to the National Comprehensive Cancer Network (NCCN) Task Force on GIST guidelines at the time of these trials was less well defined than it is now (16). These three studies do not uniformly indicate a definite survival benefit for patients with KIT exon 9 mutations from adjuvant imatinib treatment but do suggest that adjuvant imatinib treatment may be associated with mutation type. In our study, the 5-year DFS rate of high-risk patients who underwent surgery only was just 28.6%, and improved DFS was associated with the extended duration of adjuvant imatinib treatment. Therefore, we propose that patients with high-risk GISTs harboring exon 11 mutations receive at least 5 years of adjuvant imatinib treatment, but the exact duration time remains to be clarified in further research.

Neoadjuvant imatinib treatment can improve the likelihood of radical resection by decreasing tumor size, and several studies have confirmed the efficacy and safety of this strategy (24,25). Neoadjuvant treatment is recommended for imatinib-sensitive GISTs with huge tumor size or special anatomic sites, and exon 11 mutations were considered as the most suitable type for treatment (14). However, only a few retrospective studies have compared the survival of patients who received neoadjuvant imatinib treatment followed by resection and adjuvant imatinib treatment to that of those patients who receive upfront resection followed by adjuvant imatinib treatment (26). Our study included 67 patients who received neoadjuvant imatinib treatment, 42 of whom were considered to have high-risk GISTs according to radiological examination before treatment (tumor size >10.0 cm with any location or tumor size >5.0 cm with a nongastric location). The 5-year DFS rate of high-risk patients who received neoadjuvant imatinib treatment was 73.2%, which was comparable to that of those with high-risk GISTs who received upfront resection followed by adjuvant imatinib treatment. Therefore, neoadjuvant imatinib treatment may be an effective strategy for treating huge GISTs with KIT exon 11 mutations and should be examined in future RCTs.

This study involved several limitations that should be addressed. First, selection bias was inevitable, as not all patients diagnosed with GISTs undergo genetic testing. Second, patients who were recommended to receive adjuvant imatinib treatment were more likely to undergo genetic testing, and the proportion of patients with intermediate-to-high-risk GISTs could be expanded. Third, as we employed a single-center retrospective design, the results remain to be further verified in prospective multicenter RCTs.

Conclusions

This study examined the genetic landscape of GISTs with exon 11 mutations, and the mutational type was associated with long-term prognosis. Patients with deletion or indel mutations at exon 11 had worse prognosis compared to patients with other mutations. Adjuvant imatinib treatment demonstrated efficacy for patients with intermediate-to-high-risk GISTs harboring KIT exon 11 mutations, and patients with high-risk GISTs who received at least 5 years of imatinib treatment postoperation had a favorable prognosis. Large-scale prospective studies are needed to determine the optimal duration of adjuvant imatinib treatment for patients with different recurrence risks and mutations.

Acknowledgments

The authors are most grateful to all the patients whose data were used in this study.

Footnote

Reporting Checklist: The authors have completed the STROBE reporting checklist. Available at https://jgo.amegroups.com/article/view/10.21037/jgo-2026-0409/rc

Data Sharing Statement: Available at https://jgo.amegroups.com/article/view/10.21037/jgo-2026-0409/dss

Peer Review File: Available at https://jgo.amegroups.com/article/view/10.21037/jgo-2026-0409/prf

Funding: None.

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://jgo.amegroups.com/article/view/10.21037/jgo-2026-0409/coif). The authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. The study was conducted in accordance with the Declaration of Helsinki and its subsequent amendments. The study was approved by the Ethics Committee of the First Affiliated Hospital, Zhejiang University School of Medicine (No. 2024-0904), and the informed consent was exempted because of the retrospective nature of this study.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

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