Highlights
- Inflammatory signature which outperforms gene signatures centred on T cell inflammation or IFN-γ-signalling
- Predictive even in cancer types in which TMB or PDL1 are not associated with response
- Widely prognostic even when adjusted for age, gender, tumour stage and other disease-specific features
The opportunity
Inflammation can either support or restrain cancer progression and response to therapy. Yet, how different types of inflammatory tumour microenvironments are established is unclear. Dr Zelenay and the team have shown a critical role of COX-2-dependent inflammation in initiating a cancer-promoting inflammatory response. Strong proof of concept data is available on overall patient survival predictions across various malignancies.
The cyclooxygenase inflammation signature (COX-IS) is widely prognostic even when adjusted for age, gender, tumour stage and other disease-specific features. Strong proof of concept data is available on treatment outcome predictions for both PD-1/PD-L1 or CTLA-4 blockade therapy across multiple different patient cohorts in several cancer types. The COX-IS outperforms gene signatures centred on T cell inflammation or IFN-γ-signalling and is predictive even in cancer types in which TMB or PDL1 are not associated with response.
The COX-2 IS includes a multigene expression ratio combining pro- and anti-tumorigenic factors increasing its predictive power. Proof of concept data – ICI treatment response: Melanoma P<0.05, Bladder Cancer P<0.001. The COX-IS associates with treatment response even in cases where TMB or PDL1 fail to do so.
More information and data available under CDA.
Contact
Jonathan Brown is a Business Development Executive in the Business Development and Transaction team of Cancer Research Horizons. He spent the majority of his career in a variety of regional and global commercial roles at AstraZeneca, Roche and AbbVie.