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

167P - Copy number intratumour heterogeneity in the context of metastatic seeding

Date

22 Mar 2024

Session

Poster Display session

Topics

Tumour Site

Thoracic Malignancies

Presenters

Shania Makker

Citation

Annals of Oncology (2024) 9 (suppl_3): 1-4. 10.1016/esmoop/esmoop102575

Authors

S. Makker1, C. Martinez-Ruiz2, K. Grigoriadis3, J.R.M. Black4, N. McGranahan5

Author affiliations

  • 1 Queen Mary University of London, London/GB
  • 2 UCL - University College London, London/GB
  • 3 The Francis Crick Institute, London/GB
  • 4 UCL Cancer Institute - UCL - London's Global University, London/GB
  • 5 UCL Cancer Institute - Paul O'Gorman Building, London/GB

Resources

Login to get immediate access to this content.

If you do not have an ESMO account, please create one for free.

Abstract 167P

Background

Intra-tumour heterogeneity (ITH) fuels tumour evolution and copy number (CN) ITH has been shown to be a prognostic indicator in non-small cell lung cancer (NSCLC). We aimed to better understand the tumour landscape and genomic underpinnings of prognostic ITH in NSCLC, with a particular focus on CN ITH.

Methods

We performed an analysis of CN profiles of 1385 tumour regions taken from 421 tumour samples in the TRACERx421 dataset of paired primary and metastatic NSCLC tumours which had undergone multi-region sampling and high depth whole exome sequencing. TRACERx421 provides a unique longitudinal cohort of patients tracked through disease from primary to relapse and metastasis, facilitating the evaluation of tumour evolution and ITH over time. Tumour region level CN estimates were used to calculate a measure of CN ITH.

Results

We found that in a cohort of metastatic tumours only, regions with mutations which seeded metastases (seeding regions) had significantly lower CN diversity than non-seeding regions (p = 4.4 x10-5). This was largely driven by tumours with metastasis-seeding mutations present in all cancer cells of the primary tumour (homogeneous seeding tumours). This may be explained by these tumours undergoing multiple successive clonal sweeps, shown by significantly higher branch ratio (proportion of mutations present in all tumour cells relative to mutations present only in the most recent clones) (p = 0.0098), and was not explained by smoking. Critically, in a cohort of metastatic and non-metastatic tumours, tumours comprising both non-seeding and seeding regions (heterogeneous seeding tumours) had significantly higher CN diversity than non-metastatic and homogeneous seeding tumours (p = 2.2 x10-9 and p = 3.2 x10-5 respectively). The higher CN ITH may be explained by increased subclonal expansion (p = 3.4 x10-5).

Conclusions

This work highlights previously unknown associations of seeding patterns with CN ITH and suggests mechanisms for the link with propensity for metastasis, and consequently poor prognosis. This research suggests the clinical importance of CN ITH which shows promise for future practice, such as through its implementation in stratification of patients into risk groups for treatment and monitoring.

Legal entity responsible for the study

CRUK.

Funding

Achilles.

Disclosure

N. McGranahan: Financial Interests, Personal, Invited Speaker: Achilles. All other 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.