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Exploring the non-genetic (i.e. ePIgenetic) mechanisms that contribute to therapy Escape in melanoma

Project description

Epigenetic mechanisms contributing to therapy resistance in melanoma

Resistance to anticancer drugs is thought to mainly occur due to genetic alterations. Recent evidence indicates that it may also be acquired in the absence of genetic changes. It is unclear whether genetic or non-genetic mechanisms of resistance are selected in a stochastic manner and what the epigenetic mechanisms underlying the transition from drug tolerance to resistance are. The EU-funded EscaPI project aims to identify the drug-tolerant subpopulations that drive non-genetic resistance by performing lineage tracing and depletion experiments in preclinical models. The project will capitalise on modern technologies of in vivo barcoding and single-cell multi-omics approaches, providing a dynamic and integrated view of the evolution of epigenomic profiles at a single-cell resolution. Moreover, it will search for predictive biomarkers to assess the percentage of melanoma patients that exhibit non-genetic resistance through a combination of multiplexed staining and targeted DNA sequencing.

Objective

Resistance to anticancer drugs, which often develops from a heterogeneous pool of drug-tolerant cells known as minimal residual disease (MRD), is thought to mainly occur through acquisition of genetic alterations. Emerging evidence indicates that drug resistance may also be acquired in absence of a genetic cause. It remains unclear, however, whether genetic versus non-genetic mechanisms of resistance are selected in a stochastic manner, and what are the epigenomics mechanisms underlying the transition from drug-tolerance to resistance. This project aims at identifying the drug-tolerant subpopulation(s) that drive non-genetic resistance by performing lineage tracing and depletion experiments in pre-clinical models. Taking advantage of up-to-date technologies combining in vivo barcoding and single-cell multi-omics approaches, this project aims to provide a dynamic and integrated view of the evolution of epigenomic profiles -at single-cell resolution- before, during and after acquisition of drug resistance phenotypes in a in vivo clinically-relevant context. A third objective of this proposal is to search for predictive biomarkers of non-genetic resistance and to assess the percentage of melanoma patients that undergo non-genetic resistance through combination of multiplexed staining and targeted DNA sequencing. The success of this project is ensured by my personal background in epigenetics and related data computational analysis, the achievements of the JCM lab in melanoma epigenetic reprogramming and the close collaborations with experts in single-cell multi-omics fields. I anticipate that my involvement in this project will broaden my skills and knowledge and help me become a high-qualified European independent scientist.

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Programme(s)

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Topic(s)

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Funding Scheme

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MSCA-IF - Marie Skłodowska-Curie Individual Fellowships (IF)

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Call for proposal

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(opens in new window) H2020-MSCA-IF-2019

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Coordinator

VIB VZW
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.

€ 178 320,00
Address
SUZANNE TASSIERSTRAAT 1
9052 ZWIJNAARDE - GENT
Belgium

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Region
Vlaams Gewest Prov. Oost-Vlaanderen Arr. Gent
Activity type
Research Organisations
Links
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.

€ 178 320,00
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