H2020Индивидуална стипендия2020–2022

MetEpiC · P53-dependent Metabolic and Epigenetic Reprogramming in Carcinogenesis

„Хоризонт 2020“ — Действия „Мария Склодовска-Кюри“

Период: 2020-04-01 → 2022-05-31
Финансиране от ЕС: 196 708 €
Участници: 1
Схема: MSCA-IF

Линиите свързват координатора с партньорите.

Накратко на български

Мутациите в гена TP53 променят метаболизма и генетичните механизми на клетките, което води до развитие на рак и синдрома Ли-Фраумени. Разбирането на тези процеси помага за откриването на нови биомаркери и мишени за лекарства, за да се подобри грижата за пациентите.

Този кратък обзор е генериран от изкуствен интелект

Кратко обяснение, генерирано от езиков модел по текста на CORDIS. Оригиналът е по-долу.

Резултати накратко

P53-dependent Metabolic and Epigenetic Reprogramming in Carcinogenesis

Cancer is a multifactorial and complex disease, but some alterations are frequently observed in tumors. Mutations of the tumor suppressor gene TP53, a guardian of our cells, are the most frequent alterations in cancers cells, with about half of tumors harboring this mutational event. Moreover, heritable TP53 mutations leads to predisposition to early, rare and multiple cancers in patients, a condition referred as the Li-Fraumeni Syndrome. The project aimed at characterizing downstream events associated with TP53 mutations, using state-of-the-art omics technologies, in order to find molecular signatures that could participate to cancer development and to seek for cancer biomarkers and drug targets. Cancer represent a major cause of death in our society, thus it is crucial to better understand the causes of cancer development and to find therapeutic options that will improve cancer care management in the future.

Текст от CORDIS, на английски · Данни: CORDIS, © Европейски съюз

Цел на проекта

Carcinogenesis is a multi-factorial disease which combines genetic mutations, aberrant epigenetic landscape and altered cell metabolism. TP53 which is the most mutated gene in human cancers, is known to regulate cell metabolism. It has been recently established that the metabolic status of cells can modulate the epigenetic landscape. The goal of this proposal is to characterize metabolic-driven modulation of epigenetic landscape during carcinogenesis using TP53 mutated cancers as models. In this project, we plan to address how TP53 mutations alter cell metabolism and the epigenome, thus creating abnormal gene expression facilitating carcinogenesis. Thanks to our preliminary data we will focus our attention on Acetyl-CoA metabolism and histone acetylations. This project will take advantage of state-of-the art approaches such as metabolomics, epigenomics and transcriptomics. My expertise on epigenetics and metabolism, as well as the expertise of the supervisor in the field of TP53 and carcinogenesis, are major assets for this project. Altogether, we expect that unraveling novel mechanisms interconnecting TP53 mutations, cellular metabolism and epigenome will provide new insights for understanding cancer development. Moreover, we expect to propose innovative strategies to tackle cancers harboring mutated TP53 thanks to combination of drugs targeting metabolism and the epigenome. This fellowship will definitively help me to conduct a unique and promising research line in the European Community with the final goal to establish myself as an independent scientist.

Оригинален текст от CORDIS (на английски).

Участници

INSTITUT NATIONAL DE LA SANTE ET DE LA RECHERCHE MEDICALE · ParisКоординаторФранция