Neoadjuvant entrectinib for NTRK fusion-positive rectal gastrointestinal stromal tumor achieving partial response and sphincter preservation: a case report and literature review

Introduction

Gastrointestinal stromal tumor (GIST) is the most common mesenchymal tumor of the gastrointestinal tract, originating from the interstitial cells of Cajal. The development of GIST is typically associated with mutations in the c-KIT and PDGFRA genes. GISTs occur predominantly in the stomach (60%) and the small intestine (30%) (1). Rectal GIST is relatively rare, accounting for only 5% of all GIST cases (2).

NTRK genes (NTRK1, NTRK2, NTRK3) encode neurotrophic receptor tyrosine kinases (TKs) that mediate cellular responses via neurotrophin binding, such as NGF and BDNF (3,4). This interaction activates key pathways, including phosphatidylinositol 3-kinase (PI3K), mitogen-activated protein kinase (MAPK), and Janus kinase/signal transducer and activator of transcription (JAK/STAT), to regulate survival, proliferation, and differentiation (5). Genomic rearrangements causing NTRK fusions produce abnormal fusion proteins with constitutive kinase activity, driving oncogenic signaling via pathways like RAS-RAF-MEK-ERK and PI3K-AKT (6). This results in uncontrolled proliferation, apoptosis evasion, and increased migration, contributing to tumorigenesis (7).

NTRK fusion-positive GISTs represent an exceptionally rare subset, with an incidence of approximately 0.5–3% (8). These tumors are characterized by larger tumor size, an increased risk of recurrence and resistance to imatinib (8-10). TRK inhibitors such as entrectinib have demonstrated significant antitumor activity against NTRK fusion-positive GISTs (11). However, clinical data regarding their neoadjuvant use in GIST—particularly rectal GIST—remain extremely limited.

For large or anatomically challenging localized GISTs [e.g., rectum, esophagogastric junction (EGJ), duodenum], neoadjuvant imatinib can downsize tumors, increase R0 resections, and enable organ-/sphincter-preserving surgery. Prospective phase II data (RTOG 0132/ACRIN 6665) established the feasibility and safety of perioperative imatinib with high resectability and low complication rates (12). The current Chinese Society of Clinical Oncology (CSCO) (13), National Comprehensive Cancer Network (NCCN) (14), and European Society for Medical Oncology (ESMO)-European Reference Network for Rare Adult Solid Cancers (EURACAN)-Genetic Tumour Risk Syndromes (GENTURIS) guidelines (15) uniformly recommend mutation-guided neoadjuvant therapy (standard dose 400 mg; consider 800 mg for KIT exon 9); PDGFRA D842V-mutant tumors should not receive imatinib. In rectal GIST, multiple series and meta-analyses show higher rates of sphincter preservation and at least comparable oncologic outcomes versus upfront surgery (16-18). We report a rare case of rectal GIST harboring an ETV6-NTRK3 gene fusion, which achieved a near-pathological complete response and R0 resection following neoadjuvant entrectinib therapy. This case aims to expand current understanding of the therapeutic potential and clinical implications of TRK inhibition in NTRK-fusion GISTs and to provide insights into individualized management for this rare molecular subtype. We present this case in accordance with the CARE reporting checklist (available at https://gist.amegroups.com/article/view/10.21037/gist-2025-3/rc).

Case presentation

A 56-year-old male presented in May 2024 with altered bowel habits, narrowed stool caliber, and hematochezia, reporting the incidental discovery of a firm, fixed rectal mass after using Mayinglong ointment. No significant medical, surgical, familial, psychosocial, or genetic history was noted. Digital rectal examination identified a 5 cm mass 3 cm from the anal verge on the right rectal wall with indistinct margins, a smooth overlying mucosa, no luminal narrowing, an extrinsic growth pattern, and no blood staining. Chest, abdominal, and pelvic computed tomography (CT) scan showed a soft tissue mass was observed on the right lateral wall of the distal rectum, measuring approximately 55 mm × 50 mm × 49 mm. The mass exhibited well-defined margins, heterogeneous density with partial calcification, and heterogeneous enhancement on contrast imaging, consistent with a GIST, with no liver or lung involvement detected. Pelvic magnetic resonance imaging (MRI) revealed a 60 mm × 42 mm × 41 mm soft tissue mass on the right lateral rectal wall, 33 mm from the anal verge (Figure 1A,1B).

Figure 1 Pelvic MRI and histopathological findings before neoadjuvant entrectinib therapy. (A,B) Baseline MRI shows a 60 mm × 42 mm × 41 mm soft-tissue mass (yellow arrows) on the right lateral wall of the lower rectum, abutting the obturator internus muscle. (C) Pretreatment biopsy (H&E, ×200) shows spindle tumor cells arranged in an interlacing fascicular pattern with mild nuclear atypia and 4 mitoses per 5 mm² (50 HPF), without necrosis. Immunohistochemistry reveals DOG1(+), CD117(+), CD34(+), Desmin(−), S-100(−), SMA(−), and Ki-67 ≈5%. H&E, hematoxylin and eosin; HPF, high power field; MRI, magnetic resonance imaging.

An ultrasound-guided biopsy of the rectal mass revealed spindle-shaped tumor cells in a woven pattern with cytologic atypia, occasional mitoses, and no necrosis. Immunohistochemistry (IHC) showed DOG1 (+), CD34 (+), CD117 (+), and Ki-67 (~5%), confirming the diagnosis of a GIST (Figure 1C). Sanger sequencing results showed that both the KIT and PDGFRA genes were wild-type. Further next-generation sequencing (NGS) analysis of 556 hotspot genes identified an ETV6 (exon 5)-NTRK3 (exon 14) fusion (Figure 2), microsatellite stability (MSS), and a tumor mutational burden (TMB) of 0.7 mutations/Mb. As illustrated in Figure 3, the 3' end of ETV6 exon 5 (chr12p13) is fused in-frame to the 5' region of NTRK3 exon 14 (chr15q25), forming a continuous open reading frame. The resulting fusion protein preserves the ETV6 sterile alpha motif (SAM) and the NTRK3 TK domain, suggesting constitutive kinase activation as the primary oncogenic mechanism.

Figure 2 ETV6(ex5)::NTRK3(ex14) fusion schematic. The fusion involves ETV6 exon 5 (chr12p13) and NTRK3 exon 14 (chr15q25). The DNA/RNA junction sequence (5' → 3') is shown, with the 3' end of ETV6 exon 5 (… CCTTCCACCAGCGGAGGAT) directly fused to the 5' start of NTRK3 exon 14 (TAAGAGAAAACCCTCAGC …). The chimeric protein retains the SAM domain of ETV6 and the TK domain of NTRK3, leading to constitutive activation of downstream signaling pathways such as MAPK. MAPK, mitogen-activated protein kinase; NTRK, neurotrophic tyrosine receptor kinase; SAM, sterile alpha motif; TK, tyrosine kinase.

Figure 3 Pelvic MRI and histopathological findings after neoadjuvant entrectinib therapy. (A,B) After 3 months of entrectinib, the lesion markedly decreased in size (38 mm × 27 mm × 30 mm) with clearer margins (yellow arrows), loss of diffusion restriction, and no obvious enhancement, indicating a significant radiologic response. The tumor size was reduced by 36.7%, and the therapeutic response was evaluated as PR according to RECIST version 1.1. (C) Post-neoadjuvant resection specimen (H&E, ×200) demonstrates extensive collagenization with very few residual spindle cells and no visible mitotic figures, consistent with treatment-related regression and near-complete response. H&E, hematoxylin and eosin; MRI, magnetic resonance imaging; PR, partial response; RECIST, Response Evaluation Criteria in Solid Tumors.

The patient received oral neoadjuvant therapy with entrectinib from June 6, 2024 to September 13, 2024. Initially administered orally at 600 mg daily, the dosage was adjusted to 500 mg on July 4, 2024, due to adverse effects, including blurred vision, fatigue, constipation, and memory impairment. Symptomatic management alleviated these side effects. Follow-up MRI on July 26, 2024 and September 13, 2024, demonstrated partial response (PR) (Figure 3A,3B) according to Response Evaluation Criteria in Solid Tumors (RECIST) version 1.1. The baseline CT scan was performed at an outside institution, and the original DICOM data were unavailable; therefore, attenuation values could not be retrieved, and Choi response evaluation was not feasible. On September 15, 2024, the patient underwent laparoscopic intersphincteric resection (ISR), ileostomy, and regional lymphadenectomy. Postoperative pathology revealed well-demarcated collagen nodules within the intestinal wall tissue, containing sparse spindle cells with no definitive mitotic figures observed (Figure 3C). Evidence of chronic hemorrhage was noted. Based on the clinical history, the findings are consistent with post-treatment changes of a gastrointestinal stromal tumor (GIST). No tumor involvement was identified at the resection margins on either side of the intestinal segment. Examination of regional lymph nodes (para-aortic, central intermediate, and mesenteric perienteric) showed no evidence of metastasis (0/4, 0/11, 0/15). The patient continued oral administration of entrectinib for 3 months postoperatively.

On February 11, 2025, the patient underwent ileostomy closure. In November 2025, the patient underwent anorectal manometry, which revealed a normal rectoanal inhibitory reflex (RAIR), normal anal resting and squeeze pressures, normal rectoanal coordination, and increased rectal sensitivity. Contrast-enhanced CT of the chest, abdomen, and pelvis, as well as pelvic MRI (Figure 4), showed no evidence of tumor recurrence.

Figure 4 Axial (A) and sagittal (B) T2-weighted MRI images showing postoperative changes after rectal GIST resection, with no obvious abnormality in the surgical site. GIST, gastrointestinal stromal tumor; MRI, magnetic resonance imaging.

The patient’s clinical course is summarized in Figure 5 (timeline).

Figure 5 Timeline of the patient’s clinical course. The patient was diagnosed with a rectal GIST harboring an ETV6::NTRK3 fusion. He received neoadjuvant entrectinib therapy followed by laparoscopic ISR and adjuvant entrectinib treatment. Subsequently, the patient underwent ileostomy closure and regular follow-up, with no evidence of recurrence. GIST, gastrointestinal stromal tumor; ISR, intersphincteric resection; MRI, magnetic resonance imaging; NTRK, neurotrophic tyrosine receptor kinase.

All procedures performed in this study were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Declaration of Helsinki and its subsequent amendments. Written informed consent was obtained from the patient for publication of this case report and accompanying images. A copy of the written consent is available for review by the editorial office of this journal.

Discussion

This case report presents a 56-year-old male patient with a low rectal GIST with wild-type KIT and PDGFRA genes, harboring an ETV6-NTRK3 gene fusion. The tumor had a maximum diameter of 60 mm and showed ill-defined borders with the right obturator internus muscle. The patient underwent three months of neoadjuvant therapy with entrectinib, achieving PR with manageable toxicity. Subsequently, an R0 resection was performed, resulting in well-preserved anorectal function postoperatively. The pathological examination revealed significant tumor regression, with findings consistent with near-complete response. This case provides comprehensive molecular, imaging, and pathological evidence supporting the efficacy of entrectinib as neoadjuvant targeted therapy in NTRK fusion-driven GISTs. Moreover, longitudinal imaging and functional follow-up demonstrated sustained remission and favorable postoperative recovery. To our knowledge, this represents the first reported case of neoadjuvant entrectinib treatment in an NTRK fusion-positive rectal GIST.

This is the first case of NTRK-positive rectal GIST among more than 200 cases at The Sixth Affiliated Hospital of Sun Yat-sen University. Relevant case reports were identified through PubMed and Google Scholar searches (updated to October 2025); only studies with available full texts were included. To date, we have identified only 14 cases of GISTs with NTRK fusions in the literature across seven published studies (8,10,19-21). We have summarized the clinicopathological parameters, immunohistochemical characteristics, and genetic features of 13 previously reported GIST cases (Cases #2–#14) along with our NTRK fusion-positive patient (Case #1) in Table 1. Among the 14 patients, the male-to-female ratio was 4:3. Except for one 20-year-old patient, all others were over 40 years of age (mean age: 50±12 years). The tumor locations included the rectum (5/14), small intestine (2/14), duodenum (1/14), colon (1/14), and mesentery (1/14), with the majority located in the intestinal tract. The remaining cases involved the stomach (2/14) and an unknown site (1/14). Excluding three patients with unknown tumor sizes, among the remaining 11 patients, the maximum tumor diameter was >10 cm in 4 cases (4/11), 5.1–10.0 cm in 3 cases (3/11), 2.1–5.0 cm in another 3 cases (3/11), and <2.0 cm in 1 case (1/11).

The presence of an ETV6-NTRK3 fusion, specifically joining ETV6 exon 5 to NTRK3 exon 14, represents a canonical oncogenic configuration identical to that reported in previously described ETV6-NTRK3-positive GISTs and other NTRK fusion-driven malignancies such as secretory carcinoma, congenital fibrosarcoma, and cellular mesoblastic nephroma (6). This conserved fusion pattern yields a chimeric protein that retains the SAM domain of ETV6 and the TK domain of NTRK3. The ETV6 SAM domain mediates self-association (dimerization), which in turn facilitates ligand-independent activation of the NTRK3 kinase domain (7). This molecular architecture underlies constitutive activation of downstream signaling cascades, including the RAS-RAF-MAPK and PI3K-AKT pathways, consistent with the biological behavior observed in this rectal GIST. Importantly, such fusions are extremely rare in GIST and are predominantly found in the KIT/PDGFRA-wild-type subset, defining a distinct molecular subgroup driven by TRK signaling rather than classical receptor TK mutations (22,23). The preservation of this structural configuration across tumor types underscores its functional significance as a universal oncogenic driver. Moreover, the favorable clinical responses to TRK inhibitors (e.g., entrectinib, larotrectinib) reported in ETV6-NTRK3-positive tumors—including GIST—further highlight the biological and therapeutic relevance of this fusion as a targetable biomarker (3,11).

NTRK fusion testing has now become an integral part of the molecular diagnostic work-up for KIT/PDGFRA-wild-type GISTs, as recommended by recent World Sarcoma Network consensus guidelines (24). Our case provides additional clinical evidence supporting this recommendation, demonstrating that systematic molecular screening for NTRK rearrangements allows the identification of a small but clinically actionable subset of GISTs that may benefit from TRK-targeted therapy. This finding reinforces the importance of including NTRK fusion analysis within the diagnostic algorithm of wild-type GISTs and further validates the global consensus that comprehensive molecular profiling is essential for accurate classification and precision treatment in this rare subgroup. In diagnosing KIT/PDGFRA-wild-type GISTs, IHC offers a convenient and inexpensive screening method but may yield false results, while fluorescence in situ hybridization (FISH) is highly specific yet can miss complex fusions. RNA-based NGS provides the most comprehensive and accurate detection of NTRK rearrangements, making it the preferred approach for confirming fusions and guiding targeted therapy (25).

Entrectinib is a multi-targeted small-molecule TK inhibitor and a highly potent ATP-competitive inhibitor, primarily targeting TRKA/B/C (encoded by the NTRK1/2/3 genes), ROS1, and ALK TKs (26). One of the approved indications for entrectinib in China is the treatment of locally advanced or metastatic solid tumors with NTRK fusion. In the study supporting the approved indication, the efficacy analysis population consisted of 54 patients, including 13 cases of sarcoma and one case of GIST. Most patients harbored NTRK1 or NTRK3 fusions, with the most common gene fusion being ETV6-NTRK3, accounting for 46% of cases. Among patients with the ETV6-NTRK3 subtype, the efficacy rate reached 68%. The overall response rate (ORR) was 57%, including a complete response rate of 7% (4). This case demonstrated a significant therapeutic effect of entrectinib, with a high likelihood of achieving complete remission if the treatment duration is further extended, while maintaining manageable toxicity. This finding highlights the potential of personalized, molecular-targeted cancer therapy in rare GIST subtypes. For wild-type-GIST, NGS should be utilized as the preferred diagnostic tool to accurately identify molecular features, such as NTRK fusions, thereby facilitating the implementation of tailored targeted therapies (27,28).

This case provides molecular and clinical evidence that the ETV6-NTRK3 fusion functions as an oncogenic driver in wild-type GIST. The near-complete pathological response after a short course of neoadjuvant entrectinib indicates that TRK inhibition can effectively induce tumor regression even in locally advanced rectal lesions. The conserved fusion structure across tumor types highlights its biological stability and therapeutic relevance, supporting the pan-tumor use of TRK inhibitors. The mild and manageable adverse events observed—blurred vision, fatigue, and constipation—align with previous safety data, confirming entrectinib’s favorable tolerability. This case underscores the importance of routine NTRK fusion testing in KIT/PDGFRA-wild-type GISTs, as advocated by major guidelines (World Sarcoma Network, CSCO, NCCN, and ESMO-EURACAN-GENTURIS). Incorporation of NGS into diagnostic workflows enables the identification of rare but actionable targets, guiding personalized TRK-directed therapy. Larger, multicenter studies with extended follow-up are needed to define the optimal timing and duration of neoadjuvant TRK inhibition and to establish standardized postoperative management, thereby advancing precision oncology for this ultra-rare molecular subset.

Nevertheless, this study is limited by its single-patient nature and the relatively short follow-up duration. Furthermore, the absence of baseline DICOM CT data precluded quantitative response assessment using Choi criteria. Despite these limitations, the case contributes valuable real-world evidence supporting entrectinib use in this rare subset of GIST.

Conclusions

This case suggests the potential therapeutic efficacy and manageable safety profile of neoadjuvant entrectinib in the treatment of NTRK fusion-positive rectal GIST. Furthermore, it supports the pivotal role of next-generation molecular profiling in accurately identifying of actionable genetic alterations, which may help guide precise and personalized therapeutic strategies for wild-type GIST.

Acknowledgments

The authors would like to express their sincere gratitude to the patient and his family for their trust and cooperation, and for providing consent to publish this case report. We also thank our colleagues from the Department of Pathology for their technical support in immunohistochemical and next-generation sequencing analyses, as well as our colleagues from the Department of Radiology for their assistance in the imaging evaluation.

Footnote

Reporting Checklist: The authors have completed the CARE reporting checklist. Available at https://gist.amegroups.com/article/view/10.21037/gist-2025-3/rc

Peer Review File: Available at https://gist.amegroups.com/article/view/10.21037/gist-2025-3/prf

Funding: None.

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://gist.amegroups.com/article/view/10.21037/gist-2025-3/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. All procedures performed in this study were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Declaration of Helsinki and its subsequent amendments. Written informed consent was obtained from the patient for publication of this case report and accompanying images. A copy of the written consent is available for review by the editorial office of this journal.

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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