Hervé Tiriac

This study uses patient-derived organoids to identify CFTR modulators as a therapeutic strategy for chronic pancreatitis.

This study shows HDAC inhibition reduces DDR gene expression in pancreatic tumors by altering transcriptional machinery distribution, enhancing sensitivity to DNA damage, and introduces a nanoparticle delivery system to reduce toxicity.

This study identifies CA19-9's role in remodeling the PDAC tumor microenvironment by inducing IL1a and TGFb, leading to immunosuppressive changes that can be mitigated by blocking these factors.

The paper uses 13C metabolic flux analysis on PDAC tumor slice cultures to identify metabolic pathways supporting glycosphingolipid synthesis and highlight the role of PIKfyve in lipid homeostasis.

This study shows CA19-9 promotes pancreatic cancer liver metastasis via E-selectin-mediated extravasation and AKT signaling, suggesting it as a therapeutic target.

This study identifies mevalonate biosynthesis as a therapeutic target and biomarker for gemcitabine-resistant pancreatic cancer.

This study develops ZBTB11 degraders to target metabolic vulnerabilities in K-Ras inhibitor-resistant PDAC, showing improved anti-cancer activity with reduced toxicity to neurons.

This study identifies metabolic adaptations in pancreatic cancer cells resistant to autophagy inhibitors and shows that targeting pyrimidine salvage can enhance treatment efficacy.

This study identifies MICAL2 as a super enhancer-associated gene that promotes pancreatic cancer growth and metastasis through multiple molecular mechanisms.

This study shows that combining SUMO inhibition with CD40 agonism enhances anti-tumor immunogenicity in PDAC by improving macrophage function and T-cell infiltration, leading to improved survival in a mouse model.