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Poster Display & Cocktail

53P - Exploring the clinical and therapeutic implications of non-hotspot mutations in POLE

Date

03 Mar 2025

Session

Poster Display & Cocktail

Presenters

Marta Amann Arevalo

Citation

Annals of Oncology (2025) 10 (suppl_2): 1-8. 10.1016/esmoop/esmoop104198

Authors

M. Amann Arevalo1, M.D.C. Garijo Martínez2, I. Moreno1, A. Manzano Fernández3, P. Pérez Segura1, A. Escudero1, J. De La Macorra1, J. Bartolomé Arcilla1

Author affiliations

  • 1 Medical Oncology, Hospital Clinico Universitario San Carlos, 28040 - Madrid/ES
  • 2 Medical Oncology, University Hospital of Salamanca, 37007 - Salamanca/ES
  • 3 Medical Oncology, Hospital Universitario 12 de Octubre, 28040 - Madrid/ES

Resources

This content is available to ESMO members and event participants.

Abstract 53P

Background

POLE gene encodes DNA polymerase ε, which exhibits polymerase and exonuclease activities, including proofreading. Mutations in POLE's exonuclease domain lead to high tumor mutation burden (TMB) in various cancers, regardless of microsatellite stability. Mutations outside this domain are poorly understood.

Methods

We conducted an observational retrospective study in 1257 advanced solid tumor patients undergoing NGS testing of their disease between July 2019 and February 2024. We analyzed clinical data, treatment responses, TMB, and genetic alterations in POLE altered tumors.

Results

55 patients with POLE altered tumors were identified, mostly with lung cancer (13%), followed by endometrial (11%), ovarian (9%) and colorectal cancer (7%). Gender distribution was balanced, with 24 male (44%) and 31 female (56%) patients, the majority over 50 years old (72%). POLE alterations predominantly consisted of point mutations (96%) and two splicing events (4%); all non-hotspot alterations located outside the exonuclease domain. 35% of patients exhibited TMB high, and 15% showed an ultramutated phenotype with TMB>50 mut/Mb. Only two patients had MSI-H status. As expected, co-occurring genetic alterations were frequently observed, including genes of the cell growth pathway (TP53, 78%; PIK3CA, 31%; PTEN, 27.%; KRAS, 22%; MTOR, 22%; NF1, 22%; NOTCH1-3, 22%), the homologous recombination repair pathway (BRCA2, 26%; ATM, 20%), and the chromatin modulation pathway (MLL2, 55%; ARID1A, 27%; SPEN, 22%...). Immune checkpoint inhibitors were administered to 16 patients. None exhibited MSI-H or dMMR. Of those treated, 11 achieved disease control, including three with partial response, six with complete response, and three with stable disease. Six patients demonstrated prolonged responses to immunotherapy, exceeding 30 months.

Conclusions

In our cohort, patients with POLE mutated tumors showed a tendency towards high TMB and a favorable response to immunotherapy despite being non-hotspot mutations, outside the exonuclease domain. Insights from comprehensive genomic profiling reports hold significant promise in tailoring personalized treatment strategies.

Clinical trial identification

Editorial acknowledgement

Legal entity responsible for the study

The authors.

Funding

Has not received any funding.

Disclosure

All authors have declared no conflicts of interest.

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