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Dynamics of Adaptation and Resistance in Cancer: MApping and conTrolling Transcriptional and Epigenetic Recurrence

Project description

Understanding drug resistance in tumours

Tumours evolve from early-stage, curable diseases into treatment-resistant cancers, with therapy resistance posing a major challenge in oncology. Much of this resistance is believed to arise from heritable epigenetic changes in cancer cells, often referred to as the ‘dark matter’ of cancer evolution. These genetic and epigenetic adaptations can occur simultaneously within the same tumour. However, the limited understanding of these mechanisms hinders the development of new treatments. The ERC-funded DARC MATTER project aims to explore drug resistance in colorectal cancer. Using patient-derived organoid models, the project will investigate how these organoids evolve under cancer treatment. Advanced techniques will be employed to identify new resistance mechanisms and develop predictive models, ultimately improving drug combination strategies and patient outcomes.

Objective

Tumours evolve, transforming from early-stage curable disease into treatment-refractory, deadly cancer. Therapy resistance is arguably the biggest problem in oncology today, and much of it remains unexplained.

The central hypothesis of this proposal is that a large proportion of unexplained drug resistance is due to heritable epigenetic alterations, and non-heritable transcriptional plasticity in cancer cells. I refer to these mechanisms as the dark matter of cancer evolution. Genetic, epigenetic and transcriptional adaptation, together with changes in the tumour microenvironment, may happen at the same time in the same tumour. Lack of knowledge of these mechanisms hinders the development of new treatments strategies. Tackling drug resistance requires a unique combination of clinical cohorts, experimental models, evolutionary biology and computational methods.

I will map and quantify the mechanisms and evolutionary dynamics of genetic and non-genetic drug resistance at unprecedented scale. I will focus on colorectal cancer, the third most common cancer and second leading cause of cancer-related death worldwide. I will use patient-derived organoid models, matched to clinical cohorts followed longitudinally. I will measure organoid evolution under the pressure of cancer drugs, with and without the tumour microenvironment. I will track cell lineages with lentiviral barcoding and perform longitudinal single cell multi-omics, measuring genomes, epigenomes and transcriptomes of the same cell. I will interpret the results within a unique computational framework that brings together evolutionary theory with machine learning to measure, predict and control resistance.

This project will identify new mechanisms and dynamics of cancer drug resistance, deliver new predictive models, and find novel collateral drug sensitivities. This will allow designing rational drug combinations and schedules that will prevent or delay resistance, drastically improving patient outcome.

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Topic(s)

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HORIZON-ERC - HORIZON ERC Grants

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Call for proposal

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(opens in new window) ERC-2023-COG

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Host institution

FONDAZIONE HUMAN TECHNOPOLE
Net EU contribution

Net EU financial contribution. The sum of money that the participant receives, deducted by the EU contribution to its linked third party. It considers the distribution of the EU financial contribution between direct beneficiaries of the project and other types of participants, like third-party participants.

€ 1 995 582,00
Address
VIALE LEVI MONTALCINI RITA 1
20157 Milano
Italy

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Region
Nord-Ovest Lombardia Milano
Activity type
Research Organisations
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Total cost

The total costs incurred by this organisation to participate in the project, including direct and indirect costs. This amount is a subset of the overall project budget.

€ 1 995 582,00

Beneficiaries (1)

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