News
Seminar

Jeudi 09 Avril 2026 de 14h00 à 15h00
SEMINAIRE IRCM Jeudi 09 AVRIL


Professor Jifang Zhou, MD, PhD, MPH  & Dr. Yue Zhai, MD, PhD,  (Lecturer)

School of International Business, China Pharmaceutical University (CPU), China

"Reimbursement of Anticancer Drugs in Asia and France: A Comparative Analysis of Health Technology Assessment Frameworks and Real-World Evidence

This presentation offers a comparative overview of drug reimbursement policies for anticancer therapies across Asia and France, with a particular focus on oncology. Drawing on large-scale health insurance databases and electronic health record (EHR) systems, our team examines how reimbursement criteria and pharmaceutical benefits are shaped by real-world evidence, including safety profiles and treatment efficacy observed in patient cohorts. We aim to highlight key similarities and differences across health systems, and to discuss implications for policy and clinical practice

host: Prof E. DESHAYES (ICM)


Vendredi 10 Avril 2026 de 14h00 à 15h00
SEMINAIRE IRCM Vendredi 10 AVRIL 14h


Thomas DUPIC, PhD

Centre d'Immunology Marseille-Luminy (CIML), Inserm

"Dynamics of the spike-specific B-cell repertoire following SARS-CoV-2 Vaccination"

Host : P. Martineau (IRCM)

We longitudinally tracked the B-cell repertoires of 10 individuals after SARS-CoV-2 infection and repeated vaccinations. We reconstructed in vitro the naive sequences of a curated selection of 10,000 clonal lineages and measured their affinity for the spike protein binding domain of SARS-CoV-2. Our findings reveal that while the overall properties of the repertoire, including diversity, expansion, and V-gene usage, remained stable and similar to healthy individuals, the 'binder' lineages, whose naive sequence is capable of antigen binding, expanded more and had higher mutation rates. Their evolutionary patterns also differed markedly from non-binders. Among the binders, the high-affinity binder lineages showed the most activity and diversified more across the time points. We also demonstrate that lineages with identical naive sequences in different individuals evolve in similar ways. This comprehensive dataset of antibody-spike interactions in a real-world setting provides insights into detecting reacting clones within a repertoire and helps us understand how the functional diversity of the naive repertoire shapes the adaptive immune response to vaccination.


Mercredi 22 Avril 2026 de 14h00 à 15h00
SEMINAIRE IRCM Mercredi 22 avril


Pierre Lemieux

Angiogenesis Research Group, School of Kinesiology and Health Science, 

Muscle Health Research Centre, Faculty of Health, York University, Toronto, ON, Canada

"The Epigenetic Landscape of Exercising Muscle: A Role for MDM2"

host : L Linares (IRCM)


Vendredi 24 Avril 2026 de 14h00 à 15h00
SEMINAIRE IRCM 24 Avril 14h


Vincent LOUBIERE, PhD

Institut de Génétique Humaine (IGH), UMR 9002

CNRS - Université de Montpellier

"Decoding Persistent Gene Networks in Epigenetic Cancer models"

host : E. JULIEN(IRCM)


Vendredi 19 Juin 2026 de 14h00 à 15h00
SEMINAIRE IRCM 19 Juin


Valérie de Crécy-Lagard, PhD

Distinguished Professor, AAAS & ASM fellow

Microbiology and Cell Science, University of Florida 

"From Bacteria to Humans: Using Comparative Genomics to Reveal Hidden Gene Functions"

host: A . David (IRCM)

This talk highlights how comparative genomics, combined with biochemistry, structural biology, and machine learning, can uncover the functions of genes across all domains of life. It explains why functional annotation remains one of biology’s biggest challenges—due to paralogs, missing genes, inconsistent curation, and the limits of sequence?based prediction.

Through case studies, the presentation shows how bacterial model systems help solve long?standing mysteries in human biology. Examples include the discovery of the t6A tRNA?modification pathway, the functional and medical relevance of the PLPBP/YggS protein family, and the identification of the long?missing queuine/queuosine transporter in eukaryotes (SLC35F2). The talk emphasizes that accurate gene?function discovery requires integrative approaches and community?driven curation, as AI alone cannot yet resolve complex functional questions.


Vendredi 26 Juin 2026 de 14h00 à 15h00
SEMINAIRE IRCM 26 juin 14h


Daniel MUNOZ-ESPIN, PhD

CRUK Cambridge Centre Early Detection Programme, 

Hutchison/MRC Research Centre; Cambridge University

"Aging, senescence and reprogramming in lung cancer: therapeutic interventions"

host: A. Maraver (IRCM)


Vendredi 03 Juillet 2026 de 14h00 à 15h30
SEMINAIRE IRCM 3 Juillet 14h


David PEPIN, PhD

Harvard Medical School - Massachusetts General Hospital (USA)

"Role of Cancer associated Mesothelial cells in Tumor Microenvironment"

hôte : Nathalie Bonnefoy & Maeva Chauvin (IRCM)

Pr. David Pépin, Ph.D., is an Associate Professor of Surgery at Harvard Medical School and Massachusetts General Hospital. He trained as a molecular and developmental biologist, earning his doctorate at the University of Ottawa and completing postdoctoral training in reproductive biology and ovarian cancer research at MGH. His laboratory is focused on women’s health, from fertility to ovarian cancer. His team has pioneered research on the role of developmental hormone signals, such as anti?Müllerian hormone (AMH), in regulating the tumor microenvironment through stromal cells such as cancer?associated mesothelial cells (CAMCs). Pr. Pépin’s work combines advanced preclinical models and biological insights to uncover novel therapeutic targets for ovarian cancer and women’s health, bridging basic science with clinical applications.


Vendredi 27 Mars 2026 de 14h00 à 15h00
SEMINAIRE EXTERNE IRCM


Ana Pardo-Saganta, PhD

Professor Lung Inflammation and Repair

Institute for Lung Health - Justus Liebig University

German Center for Lung Research, GIESSEN (Germany)

"Coordinated healing: heterotypic cellular interactions in lung injury and repair"

host : A. MARAVER (IRCM)

Chronic lung disease such as IPF or COPD develops over extended periods of time and are
characterized by failure in mechanisms of repair (1,2). Both pathologies are considered age-related
diseases exhibiting most of the hallmarks of aging including stem cell exhaustion and altered
intercellular communication (3). In the last years, novel epithelial progenitor cells have been identified
and demonstrated to contribute to lung repair. In fact, distinct subpopulations of alveolar type (AT) 2
cells have been shown to have higher regenerative capacity (4-8). Recent findings shed light to the
mechanisms of regeneration of the alveolar epithelium (8-11); however, a better understanding of the
coordinated processes of tissue repair from different stem cell pools after injury is crucial to restore
the delicate lung architecture. Our research focuses on the study of the interplay between these
epithelial progenitor populations and neighboring cell types of their microenvironment in the
development of lung disease.
It is now generally accepted that epithelial cell loss or dysfunction drives the development of lung
fibrosis (12-15). We have identified an additional function for AT2 cells that in addition to serve as
adult stem cells of the alveolar epithelium can play a profibrotic role directly activating adjacent
fibroblast. This communication is mediated by the Notch pathway and their blockade seems to
attenuate the fibrotic phenotype, revealing a potential therapy for IPF, a fatal disease with no cure, a
median survival of 3-5 years post-diagnosis and whose incidence in increasing in the last years (1).
Thus, our findings support the notion that the pathophysiology of pulmonary fibrosis relies in part, on
the Notch-regulated interaction between aberrant cellular populations of the fibrotic lung and that
unravelling this complex microenvironment is critical to find efficient treatments for IPF.
References
1. Schneider JL, et al. The aging lung: physiology, disease and immunity. Cell. 2021 Apr
15;184(8):1990-2019. doi: 10.1016/j.cell.2021.03.005.
2. Han S, et al. Alveolar epithelial regeneration in the aging lung. .J Clin Invest. 2023 Oct
16;133(20):e170504. doi: 10.1172/JCI170504
3. Lopez-Otin C. et al. Hallmarks of aging: An expanding universe. Cell 2023, Jan 19;186(2):243-278.
doi: 10.1016/j.cell.2022.11.001
4. Zacharias WJ. et al, Nature 2018 Mar 8;555(7695):251-255. doi: 10.1038/nature25786.
5. Nabhan AN. et al., Science 2018 Mar 9;359(6380):1118-1123. doi: 10.1126/science.aam6603
6. Chen et al., Am J Physiol Lung Cell Mol Physiol. 2017 Jul 1;313(1):L41-L51. doi:
10.1152/ajplung.00564.2016.
7. Ahmadvand N. et al., Eur Respir J. 2021 Nov 4;58(5):2004168. doi: 10.1183/13993003.04168-
2020.
8. Choi J. et al., Cell Stem Cell 2020 Sep 3;27(3):366-382.e7. doi: 10.1016/j.stem.2020.06.020.
9. Kobayashi Y. et al, Nat Cell Biol 2020 Aug;22(8):934-946. doi: 10.1038/s41556-020-0542-8.
10. Strunz M. et al., Nat Comm 2020. Jul 16;11(1):3559. doi: 10.1038/s41467-020-17358-3.
11. Jiang P. et al., Am J Respir Crit Care Med. 2020 Jun 1;201(11):1443-1447. doi:
10.1164/rccm.201909-1726LE.
12. Sakai, N. & Tager, A. M. Fibrosis of two: Epithelial cell-fibroblast interactions in pulmonary
fibrosis. Biochim. Biophys. Acta - Mol. Basis Dis. 1832, 911–921 (2013).
13. Barkauskas, C. E. & Noble, P. W. Cellular Mechanisms of Tissue Fibrosis. 7. New insights into the
cellular mechanisms of pulmonary fibrosis. AJP Cell Physiol. 306, C987–C996 (2014).
14. Xie T. et al. Abnormal respiratory progenitors in fibrotic lung injury. Stem Cell Res Ther.;13(1):64
(2022).
15. Konkimalla A, et al. Lung Regeneration: Cells, Models, and Mechanisms. Cold Spring Harb
Perspect Biol.; a040873 (2021).



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