P2, N=60, Recruiting, Memorial Sloan Kettering Cancer Center | Trial completion date: May 2026 --> May 2027 | Trial primary completion date: May 2026 --> May 2027
2 days ago
Trial completion date • Trial primary completion date
Quercetin-3-rhamnoside, quercetin-3-glucoside, quercetin-3-O-galactoside, and quercetin-3-rutinoside demonstrated superior binding affinities (-9.5 to -11.089 kcal/mol) compared to control drug Luvixasertib (-8.869 kcal/mol), with enhanced electronic properties (electrophilicity index: 3.53-4.67 compared to control 2.70)...Additionally, toxicity profiling revealed favorable safety profiles with no hepatotoxic, carcinogenic, or mutagenic potential for most derivatives. Therefore, Quercetin derivatives from A. indica leaf represent promising lead compounds for targeted TTK inhibitors in lung and pancreatic adenocarcinomas, highlighting their potential for further experimental validation against TTK.
Comprehensive genomic profiling is essential for patients with PAAD and carries both prognostic and predictive value. MTAP loss KRAS-mutant PAAD represents a subgroup of immune-excluded PAADs with a poor prognosis.
The patient did not respond to gemcitabine and cisplatin-based systemic chemotherapy. Selpercatinib, a selective inhibitor of receptor tyrosine kinase RET, blocks RET kinase activity by binding to its adenosine triphosphate-binding site, thus preventing the kinase from phosphorylating substrates and halting oncogenic signaling. The patient was treated with selpercatinib, which produced a durable response lasting over 15 months in this chemotherapy-refractory patient, highlighting the efficacy of selpercatinib in HOOK3-RET fusion-positive pancreatic cancer.
6 days ago
Journal
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RET (Ret Proto-Oncogene) • AFP (Alpha-fetoprotein)
It functions as a driver of stromal activation, immune checkpoint engagement, and tumor progression. EXT1 represents a clinically relevant biomarker and a promising therapeutic target in inflammation-driven cancers like PAAD and LUAD.
Its integrated visual tools enhance interpretability and support more informed clinical decision-making. The package is freely available on Bioconductor (https://bioconductor.org/packages/devel/bioc/html/CPSM.html) and GitHub (https://github.com/hks5august/CPSM).
Our findings reveal that YARS2 mediates PARPi resistance via the MYC/E2F1 pathway in PDAC, highlighting YARS2 may serve as a potential target for therapy to counteract PARPi resistance.
Intravenous injection of VDS produces the same responses as an intratumoral injection, and outperforms direct injection of H-1 parvovirus (H-1PV), which minimally affects immune responses and tumor volume. Combining bacteria and OVs creates a therapy that activates the immune system, generates antitumor immunity, and provides a promising platform for treating solid tumors.