Oops, you're using an old version of your browser so some of the features on this page may not be displaying properly.

MINIMAL Requirements: Google Chrome 24+Mozilla Firefox 20+Internet Explorer 11Opera 15–18Apple Safari 7SeaMonkey 2.15-2.23

Poster display session

109P - Unraveling homologous recombination deficiency and therapeutic opportunities in soft tissue and bone sarcoma

Date

21 Mar 2023

Session

Poster display session

Presenters

Lara Planas-Paz

Citation

Annals of Oncology (2023) 8 (1suppl_3): 101026-101026. 10.1016/esmoop/esmoop101026

Authors

L. Planas-Paz1, A. Pliego-Mendieta2, C. Hagedorn2, D. Aguilera Garcia3, M. Haberecker4, F. Arnold5, M. Herzog2, L. Bankel6, R. Guggenberger7, S. Steiner8, Y. Chen2, A. Kahraman9, M. Zoche10, M.A. Rubin11, H. Moch12, C. Britschgi13, C. Pauli14

Author affiliations

  • 1 Institute For Pathology And Molecular Pathology, University Hospital Zürich, 8091 - Zurich/CH
  • 2 Institute For Pathology And Molecular Pathology, USZ - Institut für Pathologie und Molekularpathologie, 8091 - Zurich/CH
  • 3 Pathology And Molecular Pathology, University Hospital Zurich - Institute of Neuropathology, 8091 - Zurich/CH
  • 4 Institute For Pathology And Molecular Pathology, USZ - University Hospital Zurich - Institute of Pathology, 8091 - Zurich/CH
  • 5 Pathology, University Hospital Zurich, Zurich/CH
  • 6 Medical Oncology Department, USZ - University Hospital Zürich, 8091 - Zurich/CH
  • 7 Diagnostic And Interventional Radiology, USZ - University Hospital Zurich - Institut für Diagnostische und Interventionelle Radiologie, 8091 - Zurich/CH
  • 8 Pathology, University Hospital Zürich, 8091 - Zurich/CH
  • 9 Institute For Chemistry And Biochemical Analytics, Hochschule für Life Sciences FHNW - Institut für Medizintechnik und Medizininformatik, 4132 - Muttenz/CH
  • 10 Pathology Department, USZ - Institut für Pathologie und Molekularpathologie, 8091 - Zurich/CH
  • 11 Biomedical Research Dept., University of Bern - DBMR, 3008 - Bern/CH
  • 12 Department Of Pathology And Molecular Pathology, University Hospital Zurich - Institute of Neuropathology, 8091 - Zurich/CH
  • 13 Department Of Medical Oncology And Hematology, USZ - University Hospital Zürich, 8091 - Zurich/CH
  • 14 Pathology And Molecularpathology Department, USZ - University Hospital Zurich - Institute of Neuropathology, 8091 - Zurich/CH

Resources

This content is available to ESMO members and event participants.

Abstract 109P

Background

Defects in homologous recombination repair (HRR) in tumours correlate with poor prognosis and metastases development. Determining HRR deficiency (HRDness) is of major clinical relevance as it is associated with therapeutic vulnerabilities and remains poorly investigated in sarcoma. Sarcomas are rare mesenchymal cancers, accounting for approximately 1% of all malignancies. Standard of care mostly relies on chemotherapy but sarcoma often show chemoresistance and metastatic disease is associated with a poor prognosis. There is an increasing emphasis on understanding the cancer biology of individual sarcoma subtypes to inform the development of personalized targeted treatment approaches.

Methods

We investigated genomic and transcriptomic features of HRDness in sarcoma and cross-validated our findings among several datasets. We established and molecularly profiled eight patient-derived ex vivo sarcoma cell models. We functionally tested the sensitivity of our models to several targeted therapies including PARPi as gold standard treatment for HRDness and chemotherapies in six-point dose response curves either in monotherapy or in combination.

Results

We show that specific sarcoma entities exhibit high levels of genomic instability signatures and molecular alterations in HRR genes, while harbouring a complex pattern of chromosomal instability. Furthermore, sarcomas carrying HRDness traits exhibit a distinct SARC-HRD transcriptional signature that predicts PARPi sensitivity in patient-derived sarcoma cells. Concomitantly, HRDhigh sarcoma cells lack RAD51 nuclear foci formation upon DNA damage, further evidencing defects in HRR. We further identify the WEE1 kinase as a therapeutic vulnerability for sarcomas with HRDness and demonstrate the clinical benefit of combining DNA damaging agents and inhibitors of DNA repair pathways ex vivo and in the clinic.

Conclusions

We show that a subset of sarcoma entities exhibit features of HRDness at the genomic and transcriptomic level and highlight the need to characterize sarcoma patients with multiple parameters to better identify those with HRDness. In summary, we provide a personalized oncological approach to treat sarcoma patients successfully.

Clinical trial identification

Editorial acknowledgement

Legal entity responsible for the study

The authors.

Funding

Swiss Cancer Research Foundation [KFS-5270-02-2021] and the Olga Mayenfisch Foundation.

Disclosure

All authors have declared no conflicts of interest.

This site uses cookies. Some of these cookies are essential, while others help us improve your experience by providing insights into how the site is being used.

For more detailed information on the cookies we use, please check our Privacy Policy.

Customise settings
  • Necessary cookies enable core functionality. The website cannot function properly without these cookies, and you can only disable them by changing your browser preferences.