Skip to main content
Ir a la página de inicio de la Comisión Europea (se abrirá en una nueva ventana)
español es
CORDIS - Resultados de investigaciones de la UE
CORDIS

Integrating DNA Methylation and Drug Abundance at Single-Cell Resolution to Predict Cancer Drug Sensitivity

Objetivo

One of the greatest challenges in cancer therapy is treatment resistance, which arises from the selection of pre-existing cell states carrying survival advantages during treatment. Although genetic alterations have been extensively studied, genetics alone accounts for only a subset of relapses observed in clinical settings. EPI-SENSOR proposes that therapy response is driven by epigenetic divergence – the extent to which a tumor cell’s epigenetic state deviates from its cell-of-origin. I hypothesize that pre-existing epigenetic divergence determines whether individual cancer cells are sensitive or resistant to therapy. Testing this hypothesis requires a joint characterization of genetic mutations, differentiation state, epigenetic patterns, and drug abundance within a single cell - a level of integration that has not previously been possible. This underscores the need for novel research methods. We have developed innovative single-cell epigenomic technologies and computational tools that enable us to test our hypothesis. Using acute myeloid leukemia as a cancer model system, EPI-SENSOR will profile longitudinal patient samples at diagnosis and during cancer treatment, utilizing joint profiling of DNA methylation, somatic mutations, and surface protein expression in single cells. This approach will enable us to understand which molecular mechanisms determine sensitive or resistant cell phenotypes. Furthermore, we will develop a novel approach that tags cancer drugs with an oligonucleotide compatible with single-cell readouts. This approach will quantify cancer drug abundance and DNA methylation states at the single-cell level. Finally, we will develop a prognostic tool based on bulk DNA methylation data to implement EPI-SENSOR in clinical practice. All of these approaches combined will reveal non-genetic mechanisms of therapy resistance, define predictive DNA methylation signatures, and provide translational tools for personalized cancer treatment.

Ámbito científico (EuroSciVoc)

Este proyecto aún no se ha clasificado con EuroSciVoc.
Sugiera los ámbitos científicos que considere más relevantes y ayúdenos a mejorar nuestro servicio de clasificación.

Palabras clave

Programa(s)

Tema(s)

Régimen de financiación

HORIZON-ERC - HORIZON ERC Grants

Ver todos los proyectos financiados en el marco de este régimen de financiación

Convocatoria de propuestas

(se abrirá en una nueva ventana) ERC-2026-STG

Ver todos los proyectos financiados en el marco de esta convocatoria

Institución de acogida

DEUTSCHES KREBSFORSCHUNGSZENTRUM HEIDELBERG
Aportación neta de la UEn
€ 1 499 423,00
Dirección
IM NEUENHEIMER FELD 280
69120 Heidelberg
Alemania
Región
Baden-Württemberg Karlsruhe Heidelberg, Stadtkreis
Tipo de actividad
Research Organisations
Enlaces
Coste total
€ 1 499 423,00

Beneficiarios (1)