P1, N=20, Recruiting, M.D. Anderson Cancer Center | Trial primary completion date: Sep 2025 --> Sep 2027

P1/2, N=46, Active, not recruiting, M.D. Anderson Cancer Center | Trial completion date: Dec 2025 --> Dec 2028 | Trial primary completion date: Dec 2025 --> Dec 2028

P1/2, N=67, Active, not recruiting, D3 Bio (Wuxi) Co., Ltd | Phase classification: P1 --> P1/2 | Trial completion date: Nov 2025 --> Apr 2028 | Trial primary completion date: Nov 2025 --> Apr 2028

It exhibited strong binding affinities with VX-11e, irinotecan, and dactinomycin. Endothelial cells were identified as key cells; the occurrence of PTC reduced their quantity and affected the frequency/intensity of their interactions with mast cells. In conclusion, PTPN11 holds promise as a prognostic marker for PTC and is of great value for clinical management.

This pan-cancer study elucidates the pivotal role of ENTPD6 in tumor progression and establishes its potential as a therapeutic target for immunotherapeutic approaches in specific malignancies.

Clinically, low GCKR expression predicted poorer survival and reduced immunotherapy benefit, while higher expression indicated selective sensitivity to MEK inhibitors including refametinib and PD0325901. These findings define GCKR as both a mutation- and expression-driven biomarker that connects metabolic regulation with immune remodeling, offering translational value for prognosis and precision therapy in gastric cancer.

Here, we investigated the role of SCAMP3 in ERK1/2 signaling and therapeutic response using TMT-based LC-MS/MS phosphoproteomics of wild-type (WT) and SCAMP3 knockout (SC3KO) SUM-149 cells under basal conditions, after epidermal growth factor (EGF) stimulation, and during ERK1/2 inhibition with MK-8353...These findings position SCAMP3 as a central coordinator of ERK signaling and autophagy. Our results support SCAMP3 as a potential therapeutic target to enhance ERK1/2 inhibitor clinical efficacy and overcome adaptive resistance mechanisms in TNBC.

Our findings establish RAD21-mediated epigenetic regulation as a novel mechanism driving LUAD progression. The efficacy of ulixertinib in suppressing cancer metastasis in preclinical models highlights its translational potential for LUAD therapy.

We screened datasets associated with Gilteritinib and Quizartinib in the Gene Expression Omnibus (GEO) database for enrichment analysis and validated potential key pathways that may limit their therapeutic efficacy through qPCR and Western blot. Transcriptome sequencing revealed that these synergistic effects may stem from the regulation of gene expression such as PKD1, NR2E3, KDF1, and PRSS8 as well as modulation of ion channel activity. This in vitro study identifies aberrant activation of the RAS/MAPK pathway as a critical factor limiting the efficacy of FLT3 inhibitors in FLT3-ITD-positive AML and demonstrates the potent synergistic effects of Ulixertinib combined with FLT3 inhibitors in FLT3-ITD-positive AML cells, providing a novel therapeutic strategy for AML.

P1, N=45, Recruiting, UNC Lineberger Comprehensive Cancer Center | Trial primary completion date: Aug 2025 --> Jul 2026

P2, N=35, Active, not recruiting, National Cancer Institute (NCI) | Trial primary completion date: Dec 2025 --> Dec 2026 | Trial completion date: Dec 2025 --> Dec 2026