Actualités
Séminaires

Romain LEVAYER

Institut Pasteur, Department of Developmental and Stem Cell Biology

Toward a predictive understanding of epithelial cell death

contact : Alexandre Djiane (IRCM)

Katarzyna SIUDEJA

INSERM U1280

Institute for Integrative Biology of the Cell (I2BC)

University Paris-Saclay-CEA-CNRS; Gif/Yvette

Endogenous retroviral activity in the fly intestine - towards the mechanisms of action of selfish DNA in the soma

contact : Alexandre Djiane (Inserm-IRCM)

Valéria NAIM

CNRS UMR 9019 Paris-Saclay

Intégrité du génome et cancer

Gustave Roussy, Villejuif

"Understanding genome instability from S-phase to mitosis"

contact : Eric JULIEN (Inserm/CNRS)

Replication stress resulting from slowing or stalling of DNA replication forks is a major driver of genome instability during cancer initiation and progression. DNA replication can be challenged as a consequence of oncogene activation or by agents that interfere with DNA synthesis, such as the ones used in chemotherapy. To accomplish genome duplication and prevent chromosomal instability, cells have evolved mechanisms that protect, stabilize and/or restart replication forks while delaying cell cycle progression, which avoids entering mitosis with under-replicated DNA. Over the last years, however, work from several laboratories including ours has shown that cells can progress into mitosis with under-replicated DNA. This led to the identification of mechanisms, mediated by the Fanconi anemia (FA) and Homologous Recombination (HR) repair pathways, that promote post-replication repair and rescue of under-replicated DNA in mitosis, allowing cells to divide and continue proliferating. I will discuss how these findings have advanced our understanding of the link between replication stress and genome instability; I will present a molecular pathway that connects mitochondrial stress and functions of FA proteins in genome maintenance; finally, I will show that mechanisms involved in mitotic rescue of under-replicated DNA may represent promising targets to selectively kill cancer cells that sustain intrinsically high levels of replication stress.

Attention ! séminaire décalé au 09 juin 14h.

Rafael J. Argüello

Centre d'Immunologie de Marseille-Luminy (CMIL), CNRS-INSERM, Université Aix-Marseille

"One Cell At a Time : A Change of Perspective for metabolic Studies"

contact : Laurent Le Cam (Inserm)

MATTHIAS DROSTEN

Centro de Investigación del Cáncer (CIC) and Instituto de Biología Molecular y Celular del Cáncer (IBMCC), CSIC-USAL, Salamanca, Spain

"Targeting RAS signaling in lung cancer"

contact : Antonio Maraver (Inserm) -ATTENTION Séminaire décalé au vendredi 02 Juin à 14h

KRAS oncogenes have been identified in a quarter of all human lung tumors. Recently, several inhibitors were developed that target specific mutant KRAS isoforms and two of them, directed against the KRAS G12C oncoprotein, have just been approved. However, most patients develop resistance against these inhibitors and no actual survival benefits have been observed in clinical trials. Thus, it is urgently required to identify novel therapeutic options applicable to most if not all patients with KRAS-mutant tumors. I will discuss what we have learned from genetically engineered mouse models about the development of resistance to KRAS inhibition. Moreover, I will present novel insights into the mechanisms of KRAS signaling in lung cancer and how a better understanding of KRAS signaling may help to overcome resistance to targeting either KRAS itself or its MAPK effector pathway.

SABINE COLNOT

Centre de Recherche des Cordeliers, INSERM UMRS1138, Paris

"Beta-catenin signaling, metabolism and epigenetics: a node for theranostics in primary liver cancers"

contact : Florence Cammas (Inserm/CNRS)

WILLIAM AMOYAL

Vizgen, MEng, MBA, Regional Account Manager

Decipher Tissue Complexity with Spatial Genomics: Single Cell Spatially Resolved Transcriptomic Imaging with MERSCOPE Powered by MERFISH

contact : Laurent Le Cam (Inserm)

Biological systems are composed of numerous cell types, intricately organized to form functional tissues and organs. While recent advancements in genomics technologies have made it possible to characterize cell types through careful analysis of the transcriptome, they are unable to resolve how gene expression and cell types are spatially arranged. In this presentation, we introduce you to Vizgen’s all-in-one in situ genomics platform MERSCOPE, which enables the direct profiling of the spatial organization of intact tissue with genomic scale
throughput. The instrument, the MERFISH chemistry and use cases will be presented as well.