SMAD4 could be used as the diagnostic biomarker for pancreatic adenocarcinomas. There is combined classification accuracy of 98.9%, suggesting that they are a sensitive and specific approach for adenocarcinomas in limited material of EUS-FNAs and that combined panel approach was significantly more accurate than any other individual approach.
1 day ago
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SMAD4 (SMAD family member 4) • S100P (S100 calcium binding protein P)
Peroxisomes act as pivotal regulators of digestive cancer progression by modulating signaling pathways, the TIME, therapeutic resistance, and lipid metabolism. Targeting peroxisomal function, particularly in high-risk subgroups of HCC and CRC, warrants further exploration as a promising therapeutic strategy.
P1, N=46, Recruiting, University of Illinois at Chicago | Trial completion date: Jan 2026 --> Jan 2028 | Trial primary completion date: Nov 2025 --> Nov 2027
9 days ago
Trial completion date • Trial primary completion date
We found that CLCA1 modulates the SIRT1/HIF-1α pathway, suppressing tumor proliferation, and might enhance gemcitabine sensitivity in pancreatic cancer cells. This investigation points to CLCA1 as a viable therapeutic target for tackling hypoxia-induced chemoresistance and enhancing treatment success in PDAC. Further exploration of CLCA1-based therapies could offer new opportunities for clinical translation.
9 days ago
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LDHA (Lactate dehydrogenase A) • HIF1A (Hypoxia inducible factor 1, alpha subunit) • CLCA1 (Chloride Channel Accessory 1) • SLC2A1 (Solute Carrier Family 2 Member 1)
Combined MEK and autophagy inhibition showed limited tolerability in human PDAC. Divergent efficacy between preclinical and clinical settings likely reflects differences in tumor cell state heterogeneity between models. Integration of diverse, representative preclinical models is critical to guide development of effective therapies in PDAC.
Targeting CSF1R might be a PAAD treatment. Inhibiting CSF1R activity or TGF-β binding to CSF1R inhibits tumour growth and immune escape. Investigating the link between CSF1R, TGF-β, and the immune system opens new opportunities for combining targeted medicines with immunotherapy.