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Poster Display session

668P - The Impact of MTAP loss on response to immune checkpoint inhibitors in stage IV NSCLC: A prospective real-world analysis

Date

07 Dec 2024

Session

Poster Display session

Presenters

Aya El-Helali

Citation

Annals of Oncology (2024) 35 (suppl_4): S1632-S1678. 10.1016/annonc/annonc1698

Authors

A. El-Helali1, E.Y. Ko2, C.H.L. Wong2, M. Lecoultre1, M.K.L. Chiu2, I. Ho3, D. Leung3, A.W.M. Lee4, V.H.F. Lee1

Author affiliations

  • 1 Clinical Oncology, HKU - The University of Hong Kong, 0000 - Hong Kong/HK
  • 2 Clinical Oncology, HKU - The University of Hong Kong, Hong Kong/HK
  • 3 Clinical Oncology, Queen Mary Hospital, Hong Kong/HK
  • 4 Clinical Oncology, The University of Hong Kong - Shenzhen Hospital, 518053 - Shenzhen/CN

Resources

This content is available to ESMO members and event participants.

Abstract 668P

Background

Methylthioadenosine phosphorylase (MTAP) is a key enzyme involved in the salvage pathway of purine metabolism. MTAP loss occurs in approximately 15% of non-small cell lung cancer (NSCLC). Given the prevalence of MTAP loss in NSCLC and its association with poor prognosis, targeting MTAP may represent a promising therapeutic strategy. We, therefore, aim to explore the association between MTAP loss and response to immune checkpoint inhibitors (ICI) in advanced NSCLC.

Methods

The present study was conducted as a part of an ongoing multi-center prospective precision oncology genomic sequencing programme in Hong Kong. Comprehensive target panel next-generation sequencing (cTP-NGS) was performed using Foundation One CDx in newly diagnosed advanced non-squamous NSCLC. The genomic landscape of MTAP-loss and MTAP-proficient tumors was described. We compared the clinical characteristics, genomic landscape, and survival outcomes of patients harboring MTAP-loss and MTAP-proficient tumors.

Results

205 consecutively recruited patients were analyzed. MTAP loss was observed in 18% (n=37) of our cohort. MTAP loss was correlated with never-smokers (p = 0.034), and negative PD-L1 expression (TPS <1%) (p = 0.00022). There was no significant association with age, gender, actionable alterations, and TMB in the MTAP loss cohort. EGFR was the most frequently altered gene (Loss: 46% vs Proficient: 35%). CDKN2A/B loss was comutated with MTAP loss, while TEK loss was only reported in 19% of MTAP loss. The median follow-up time was 14 months. Among patients who received systemic therapy, the median OS (mOS) of the MTAP loss and proficient cohorts was 24.9 and 22.5 months (p = 0.95), respectively. However, among the patients who received ICI +/- chemotherapy (n=56), the mOS in the MTAP loss cohort was 6.3, while the mOS was 27.6 months in the MTAP proficient cohort (HR: 3.31; 95% CI: 1.21-9.04; p = 0.020).

Conclusions

Our study underscores the clinical significance of MTAP loss and its association with poor response to ICIs in advanced-stage NSCLC. These findings highlight the potential prognostic value of MTAP status in patients who receive ICI +/- chemotherapy and suggest that MTAP loss may be a predictor of poorer outcomes.

Clinical trial identification

Editorial acknowledgement

Legal entity responsible for the study

The authors.

Funding

Innovation and Technology Commission (ITC)–Hong Kong under the Partnership Research Programme scheme (PRP/067/20FX).

Disclosure

All authors have declared no conflicts of interest.

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