Poster Presentation 38th Lorne Cancer Conference 2026

Genomic guided therapies in oesophageal adenocarcinoma (#254)

Sowmya L Sharma 1 2 3 , Ho Yi Wong 1 3 , Rebecca L Johnston 3 , Lambros T Koufariotis 3 , Scott T Wood 3 , Georgina T Hollway 1 3 , Lauren G Aoude 4 , Aimee L Davidson 3 , John V Pearson 3 5 , Frank P Lin 6 7 , Andrew P Barbour 4 8 , Nicola Waddell 1 3 5
  1. School of Biomedical Sciences, University of Queensland, Brisbane, QLD, Australia
  2. ACL Pathology, Bellavista, NSW 2153, Australia
  3. QIMR Berghofer, Herston, QUEENSLAND, Australia
  4. Frazer Institute, University of Queensland, Woolloongabba, QLD 4102, Australia
  5. genomiQa, Brisbane, QLD 4006, Australia
  6. Garvan Institute of Medical Research, Sydney, NSW, Australia
  7. Department of Medical Oncology, Prince of Wales Hospital, Randwick, NSW, Australia
  8. Princess Alexandra Hospital, Woolloongabba, QLD 4102, Australia

Abstract:

Background and aims: Oesophageal adenocarcinoma (OAC) incidence continues to rise in developed countries. Despite advances in deciphering cancer genomes and oncogenic pathways, precision therapies for OAC remain limited.

Methods: We selected 109 actionable and/or potentially actionable genes based on pan-cancer drug information from open-source compendia and clinical trials for curation of genomic alterations. We determined the prevalence of alterations within these 109 genes using whole genome sequencing data of tumor DNA from n=217 OAC patients to discover approved treatments and potentially targetable alterations (PTAs). Additionally, matching RNA-seq from 210 of the patients was interrogated for select immune checkpoint inhibitor (ICI) targets (n=59), with expression findings validated in an independent OAC cohort (n=114).

Results: Approved actionable targets were revealed in 22.1% of patients; including HER-2 and MET antagonists, and immunotherapy directed by microsatellite instability and high tumor mutation burden. PTAs were noted in a further 72.8% of patients, with highest frequency in TP53; others were noted in APC, ARID1A, BRCA1, BRCA2, CCNE1, CDKN2A, EGFR, KRAS, MDM2, PIK3CA, PTEN, SMARCB1 and TSC2. Candidate co-occurring alterations included co-occurrence of PTEN loss and ERBB2 amplification and co-occurring variants in KRAS and TP53. For the remaining 5.1% of patients, no PTAs were detected. We identified and validated high expression of four genes encoding candidate ICI targets for OAC: CD24, VEGFA, PVR, and SLC3A2.

Conclusion: These PTAs and ICI targets will help to inform future clinical trials. Precision therapy may become available for all OAC in the near future.