Institut Cochin

@institutcochin.bsky.social

Biomedical research center located in the heart of Paris, affiliated to Inserm, CNRS and Université Paris Cité. #cancer, #immunology, #endocrinology-#metabolism, #microbiology, cellular #plasticity and #reproduction. https://institutcochin.fr/en

A new publication by Fumigalli & Pendino is out ! Research on CAR-T cell therapies is advancing every day! DOI: 10.1016/j.ymthe.2026.04.009 institutcochin.fr/en/equipes/c... @cnrs.fr @inserm.fr @upcite.bsky.social

Cancer Immunotherapy and Cell Reprogramming

Our team, "Cancer Immunotherapy and Cellular Reprogramming," investigates the co-evolution of cancer and immune cells to enhance the immune system's efficacy, overcome therapeutic resistance, and counteract metastatic progression. At the intersection of the Immunology and Cancer research axes of Institut Cochin, our work stands out for its focus on tumor and immune cell factors that either promote or inhibit tumor progression, particularly in the context of anticancer therapies. Using molecular targets identified in our research, we aim to elucidate their roles in cellular regulation in both mouse models and human studies. We are exploring the role of the epigenetic factor RINF in the reprogramming of (CAR)T cells, stromal cells, and tumor cells, as well as the impact of the enzyme IL4I1. The catabolic activity of IL4I1 impair immune cell effectiveness, particularly macrophages, in tumor control. Additionally, we investigate the cellular dynamics influenced by key cytokines (IFNs, TGFβ and GCSF), which modulate both the tumor microenvironment and metastatic progression. In parallel, we aim to identify predictive biomarkers for immunotherapy success or failure. Our research underscores the critical need for myeloid cell reprogramming, complementing T lymphocyte-based approaches, to improve cancer treatments. We also analyze the synergistic interactions between these cell populations following anti-PD1/PDL1 therapies or interferon-inducing treatments. Our ultimate goal is to lay the groundwork for targeting key factors in tumor evolution while refining Immunotherapy approaches, to develop innovative clinical solutions and transform cancer care.

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🔬 Covid-19: block the door, not the virus Institut Pasteur developed B07-Fc, an alpaca-derived antibody targeting ACE2 — the viral entry point that doesn't mutate. Effective against all tested variants. Nasal administration. Preclinical validation needed. 📄 Nature Communications #SARS-CoV-2

COVID-19: a new strategy under investigation to tackle all variants

Scientists at the Institut Pasteur have developed an innovative strategy to combat SARS-CoV-2. Rather than targeting a virus in constant mutation, they propose blocking the gateway used by the virus t...

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#seminar on February 5 at noon by Serena Janho dit Hreich (Stroma & Immunity Team-Immunity and Cancer, @institutcurie.bsky.social): Interplay of Cancer-Associated Fibroblasts and invasive clusters of tumor cells drives progression in early stages of bladder cancer institutcochin.fr/en/agenda/in...

Interplay of Cancer-Associated Fibroblasts and invasive clusters of tumor cells drives progression in early stages of bladder cancer

Bladder cancer progression from non-muscle invasive (NMIBC), particularly the T1 stage, to muscle invasive disease (MIBC) represents a critical clinical transition requiring aggressive therapy due to high metastatic recurrence risk. Risk of progression of T1 tumors is mainly based on the presence of invasive tumor cells breaching the urothelial layer and invading the lamina propria. However, cellular and molecular events occurring in the tumor microenvironment (TME) that drive this progression remain poorly defined. To address this knowledge gap, we investigated the changes within the TME associated with the progression of bladder cancer. Single-cell RNA sequencing (scRNAseq) analysis of untreated NMIBC and MIBC human samples, alongside multiplexed imaging, revealed extensive cancer-associated fibroblast (CAF) remodeling as a key feature associated with disease progression. We show that activated CAFs are present in small focal patches in T1 tumors that surround a subset of invasive tumor cells. Both cell types were more strongly associated with progression into MIBC than either population alone, supporting the interaction of these two cell types to promote tumor progression. I will address the implicated cross-talk using multiplex imaging, spatial transcriptomics, scRNAseq and in vitro assays. Overall, we highlight the importance of the stromal compartment and the cross-talk between specific populations of CAFs and tumor cells that may serve as a prognostic biomarker and therapeutic target in NMIBC. Paris post-doc seminar series.

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