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Poster Display session

63P - Systemic therapy for KIT/PDGFRA wild-type GIST

Date

15 Mar 2024

Session

Poster Display session

Presenters

Margaux Dupont

Citation

Annals of Oncology (2024) 9 (suppl_2): 1-32. 10.1016/esmoop/esmoop102441

Authors

M. Dupont1, M. Lamkhioued1, D. Pissaloux2, A. Meurgey3, M. Brahmi4

Author affiliations

  • 1 Medical Oncology Dept, Centre Léon Bérard, 69008 - Lyon/FR
  • 2 Biopathology Dept, Centre Léon Bérard, 69008 - Lyon/FR
  • 3 Pathology Dept, Centre Léon Bérard, 69008 - Lyon/FR
  • 4 Medical Oncology Dept., Centre Léon Bérard, 69008 - Lyon/FR

Resources

This content is available to ESMO members and event participants.

Abstract 63P

Background

KIT/PDGFR wild-type (KPWT) gastrointestinal stromal tumors (GIST) constitute a minority of all metastatic GIST cases. Most studies to date involve case reports or small series, and treatment approaches vary widely among teams. Additional research is needed to define the optimal management of metastatic KPWT GIST patients. This retrospective study aimed to assess the outcomes of KPWT GIST patients treated with Tyrosine Kinase Inhibitors (TKI) at our institution.

Methods

We conducted a retrospective study at the Centre Léon Bérard (CLB). The NetSarc national sarcoma database was queried for KPWT GIST patients at CLB. Data were extracted from individual patient files and reviewed by an expert sarcoma pathologist. Whole exome-RNAseq was performed with FFPE material in the absence of known neurofibromatosis type 1 (NF1) or SDH-deficiency.

Results

A total of 78 KPWT GIST patients were identified. Four molecular groups could be formed, NF1-associated GIST (N=29), SDHB-deficient GIST (N=13), other rare alterations (N=7 with 3 BRAF V600E mutation, 1 NTRK3 rearrangement, 1 TSC1 variant, 1 FLNA mutation, and 1 FGFR2 mutation), and wild-type GIST (N=29). SDHB-deficient GIST patients were significantly younger (p-value = 0.0006), and NF1-associated GIST were more likely to be primarily located in the small intestine (p-value < 0.0001). Median PFS with imatinib was 9.5 months (with a noteworthy PFS of 199 months in a wild-type GIST), and 10 months with sunitinib. Regorafenib was significantly less effective with a median PFS of 3 months (p-value = 0.01). Pazopanib showed the highest median PFS of 30 months (with a notable PFS of 116 months in an SDHB-deficient GIST). Overall survival was of 190 months for NF1-patients, 246 months for SDHB-patients, 45.7 months with other molecular alterations, and 185 months for wild-type GIST (p-value = 0.5).

Conclusions

This retrospective series is one of the largest describing clinical characteristics and treatment response of KPWT GIST, a rare disease. Imatinib and sunitinib demonstrated good responses, while regorafenib showed no efficacy. Long responders were reported with multi-targeted TKI, warranting further investigation through prospective trials to validate those results.

Clinical trial identification

Editorial acknowledgement

Legal entity responsible for the study

M. Dupont.

Funding

Has not received any funding.

Disclosure

All authors have declared no conflicts of interest.

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