Functional genomics and cancer
Systems biology of cell fate decisions in normal and tumor cells
Our interest is to understand the mechanisms and dynamics of signal transduction, epigenetic (de)regulation and chromatin structure, which coordinate global gene expression programs in normal and cancer cells. Based on our expertise on nuclear receptors action we develop technologies and global systems biology approaches to identify comprehensive RNA profiles, transcription factor binding sites, epigenomes and chromatin interactomes from ultra-small sample sizes, and use integrative bioinformatics to identify functional gene “hubs” and decision points that dynamically coordinate gene programming. Our studies involve a plethora of genome-wide technologies and the corresponding development of bioinformatics tools.
A particular interest of our team is the integrative analysis of aberrations affecting signaling, epigenome, chromatin architecture and transcriptome upon tumorigenic transformation. In this context we identify targets and mechanisms, which are relevant for the development of novel therapeutic paradigms, and study the mechanisms and therapeutic potential of signaling drugs and epigenetic modulators.
Another emphasis of our work is to decipher the mechanisms underlying the cancer-selectivity of apoptogenic TRAIL signaling. Studies on the role of the senescence-mediated secretome on TRAIL action and the epigenetic alterations during cellular senescence address the link between cancer and aging.
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Current projects
- Study of the molecular mechanisms controlling the modulation of TRAIL-dependent signaling by non-muscle myosins.
- Deciphering the molecular Mechanisms Underlying the modulation of TRAIL-induced signaling by non-muscular myosins. AICR
- Characterization of a novel epigenetic putative regulator of gene expression in breast cancer. Project funded by INCa.
- Analysis Of interactions between ndsRNAs recently discovered, and the factors / complex epigenetic during tumorigenesis. Project EpiCaR (Epigenetics, Cancer and ndsRNAs) funded by the Cancer Plan.
- Identification of modulators and gene expression signatures of TRAIL sensitivity. Project funded by ARC
- Epigenetic regulation of tumour-cell specific apoptosis. Project financed by the INCa -
Collaborations
- Dr. Peter MULLIGAN, Centre de Recherche en Cancérologie de Lyon (CRCL), UMR Inserm 1052 CNRS 5286 Centre Léon Bérard.
- Dr. Laurence Vandel, Centre de Biologie du Developpement, UMR5547 du CNRS/Universite Paul Sabatier, Toulouse, FRANCE -
Prizes/Awards
- Hinrich GRONEMEYER - René & Andrée Duquesne prize - Ligue contre le cancer - 2015
- Hinrich GRONEMEYER - Scientific Excellence Award - Inserm - 2010
- Hinrich GRONEMEYER - European Medal - The Endocrine Society - 1996
- Hinrich GRONEMEYER - Member of the European Molecular Biology Organization (EMBO) - European Molecular Biology Organization (EMBO) - 1995
- Hinrich GRONEMEYER - Scientific Prize - Société Française d'Endocrinologie (SFE) - 1991
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News
- Dec. 20, 2017 - Chemotherapy implicated in the appearance of certain metastases
- Sept. 20, 2016 - The power of cell fate modeling
- Oct. 29, 2015 - TARDIS: a universal method at everyone hands to identify rare RNAs
- Sept. 14, 2015 - Hinrich Gronemeyer distinguished for his work on cancer
- March 16, 2015 - Epigenetic erosion of inactive X chromosome in breast cancer
- Dec. 15, 2014 - Discovery of a novel RNA class
- Nov. 24, 2014 - 2 IGBMC researchers among the world’s most influential
- June 6, 2011 - Smaller and smaller samples
- June 1, 2011 - The oestradiol secret code
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Publications
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A comprehensive resource for retrieving, visualizing, and integrating functional genomics data.
Life Sci Alliance Jan 2020 ; 3: .
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Inference from RNA interference: Suggestions to our authors.
Int J Cancer Aug. 27, 2019 .
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Mol Cell March 21, 2019 ; 73:1217-1231 .
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Sci Rep Aug. 22, 2018 ; 8:12629 .
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Modeling gene-regulatory networks to describe cell fate transitions and predict master regulators.
NPJ Syst Biol Appl Aug. 2, 2018 ; 4:29 .
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Development of biotin-retinoid conjugates as chemical probes for analysis of retinoid function.
Bioorg Med Chem Lett Aug. 1, 2018 ; 28:2442-2445 .
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Nat Cell Biol Apr 2018 ; 20:432-442 .
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Cell Death Differ Jan. 23, 2018 ; 25:486-541 .
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Senescence-associated reprogramming promotes cancer stemness.
Nature Jan. 4, 2018 ; 553:96-100 .
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Dual role of DR5 in death and survival signaling leads to TRAIL resistance in cancer cells
Cell Death and Disease 31 August 2017 2017 ; 8:e3025 .
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Job opportunities
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Alumni
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