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Cocktail and Poster Display session

87P - Enhancing treatment strategies for metastatic high-grade neuroendocrine neoplasms: Insights from extensive genomic profiling through WES and WGS in a phase I clinical setting

Date

26 Feb 2024

Session

Cocktail and Poster Display session

Topics

Pathology/Molecular Biology

Tumour Site

Presenters

Sara Krogshede

Citation

Annals of Oncology (2024) 9 (suppl_1): 1-9. 10.1016/esmoop/esmoop102310

Authors

S.K. Krogshede1, I.K. Buhl2, L. Perino2, C. Baudet2, C.W. Yde2, M.M. Clausen3, I.E.V. Tuxen1, M. Hoejgaard1, S.W. Langer1, I. Spanggaard1, K.S. Rohrberg1

Author affiliations

  • 1 Department Of Oncology, Rigshospitalet, 2100 - Copenhagen/DK
  • 2 Center For Genomic Medicine, Rigshospitalet, 2100 - Copenhagen/DK
  • 3 Department Of Clinical Physiology And Nuclear Medicine, Rigshospitalet, 2100 - Copenhagen/DK

Resources

This content is available to ESMO members and event participants.

Abstract 87P

Background

HG-NEN is a heterogeneous group of rare cancers, including neuroendocrine carcinoma (NEC) and high-grade neuroendocrine tumors (NET G3). HG-NENs are characterized by poor differentiation, rapid growth, limited treatment options and poor prognosis. The aim of this study was to investigate the potential of WES/WGS to inform treatment of metastatic HG-NEN.

Methods

Blood and tumor biopsies from 49 patients (pts) with HG-NEN referred to the phase 1 Unit at Department of Oncology, Copenhagen University Hospital – Rigshospitalet, Denmark were analyzed with WES (n=30) or WGS (n=19) in the framework of the CoPPO project in the period 2013- 2022. Tumor mutational burden (TMB) was calculated as number of non-synonymous mutations per mega base (Mb).

Results

45 pts had somatic mutations in 61 selected different cancer associated genes. Most frequent somatic mutations included TP53 (33/49), APC (13/49), KRAS (9/49), BRAF (9/49), and RB1 (8/49). When compared, NET G3 (n=11) and NEC (n=38) appeared as molecularly distinct i.e., only one NET G3 was TP53 mutated compared to 33 NEC. Overall, the NET G3 contained fewer oncogenic mutations (median=1) compared to NEC (median=4). We identified 29 pts (59%) with actionable genomic variants (most frequently BRAF V600E, n=7 and TMB-high defined as >10 mutations per Mb n=24).

Conclusions

Extensive genomic profiling in pts with HG-NEN holds potential as more than half of the pts presented with potential treatment targets extending therapeutic options.

Clinical trial identification

Editorial acknowledgement

Legal entity responsible for the study

The authors.

Funding

Has not received any funding.

Disclosure

I.K. Buhl: Financial Interests, Personal, Full or part-time Employment: Aida Oncology Aps (shares). M. Hoejgaard: Financial Interests, Personal, Other, Advisory role for various diagnostic companies/investors: LingoMedical; Financial Interests, Personal, Stocks/Shares, Stocks, I. Spanggaard: Financial Interests, Institutional, Invited Speaker: Roche, Puma Biotechnology, MSD, Genentech, Incyte, AstraZeneca, Orion, Pfizer; Non-Financial Interests, Personal, Principal Investigator: Roche, Puma Biotechnology, MSD, Genentech, Incyte, AstraZeneca, Orion, Pfizer. K.S. Rohrberg: Financial Interests, Personal, Invited Speaker: Bayer, Amgen, MSD, GSK; Financial Interests, Personal, Advisory Board: AbbVie, Genmab; Financial Interests, Institutional, Invited Speaker, Compensation for conduction of clinical trial: Lilly, Roche/Genentech, Bristol Myers Squibb, Symphogen, Pfizer, Novartis, Alligator Bioscience, Genmab, BioInvent, Monta Bioscience, Amgen, Navire; Financial Interests, Institutional, Other, Compensation for conduction of clinical trial: Bayer, Incyte, Puma Biotechnology, Orion Clinical. All other authors have declared no conflicts of interest.

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