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Poster Display session

153P - Determinants of tumour-immune evolutionary trajectory in colorectal cancer

Date

27 Jun 2024

Session

Poster Display session

Presenters

Eszter Lakatos

Citation

Annals of Oncology (2024) 35 (suppl_1): S1-S74. 10.1016/annonc/annonc1477

Authors

E. Lakatos1, V. Gunasri2, L. Zapata3, J. Househam4, T. Heide5, N. Trahearn3, O. Swinyard6, C. Lynn3, G. Cresswell3, M. Mossner3, C. Kimberley6, I. Spiteri3, M. Jansen2, M. Rodriguez-Justo2, J.A. Bridgewater2, A. Baker7, A. Sottoriva5, T. Graham3

Author affiliations

  • 1 Chalmers University of Technology, Gothenburg/SE
  • 2 UCL Cancer Institute - Paul O'Gorman Building, London/GB
  • 3 The Institute of Cancer Research and Royal Marsden Hospital, Sutton/GB
  • 4 ICR - Institute of Cancer Research, London/GB
  • 5 Human Technopole, Milan/IT
  • 6 Cancer Research UK Barts Centre - Queen Mary University of London, London/GB
  • 7 ICR - Institute of Cancer Research, Sutton/GB

Resources

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Abstract 153P

Background

Immune system control is a major hurdle that cancer evolution must circumvent. The relative timing and evolutionary dynamics of subclones that have escaped immune control remain incompletely characterized, and how immune-mediated selection shapes the epigenome has received little attention. Here we infer the genome- and epigenome-driven evolutionary dynamics of tumour-immune coevolution within primary colorectal cancers (CRCs).

Methods

We leverage our existing CRC multi-region multi-omic dataset of 495 single glands (Heide et al., Nature, 2022), which we supplement with high-resolution targeted sequencing data and highly multiplexed imaging of the tumour microenvironment (TME) in 82 micro-biopsies, including the invasive margin and distant normal mucosa. We evaluate spatially-resolved normalised neoantigen burden, immune escape status, epigenetic alterations and immune infiltrate levels across and within 29 CRCs.

Results

Analysis of somatic chromatin accessibility alterations (SCAAs) reveals frequent somatic loss of accessibility at antigen presenting genes. SCAAs, together with transcriptional editing, emerge as a prevalent mechanism for silencing clonal neoantigens. We observe that strong immune escape and exclusion occur at the outset of CRC formation, and that within tumours, including at the microscopic level of individual tumour glands, localised alterations have negligible consequences for the immunophenotype of cancer cells. Localised immuno-editing occurs during local invasion and is associated with TME reorganisation, but that evolutionary bottleneck is relatively weak.

Conclusions

Collectively, we show that immune evasion in CRC follows a “Big Bang” evolutionary pattern, whereby genetic, epigenetic and TME-driven immune evasion acquired by the time of transformation defines subsequent cancer-immune evolution. Our findings suggest that epigenetic control could play a significant role in resistance to immune surveillance, and therefore epigenome modifying drugs could synergize with immunotherapy.

Legal entity responsible for the study

The authors.

Funding

Cancer Research UK, Wellcome Trust, Jean Shanks/Pathological Society, Chalmers Area of Advance Health Engineering.

Disclosure

A. Baker: Non-Financial Interests, Personal and Institutional, Ownership Interest: Patent. T. Graham: Financial Interests, Institutional, Other, Honorarium: Genentech; Non-Financial Interests, Personal and Institutional, Ownership Interest: Patent. All other authors have declared no conflicts of interest.

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