P=N/A, N=600, Active, not recruiting, Pfizer | Not yet recruiting --> Active, not recruiting | Trial completion date: Dec 2029 --> Jun 2028 | Trial primary completion date: Dec 2029 --> Jun 2028

Our findings suggest that AURKB serves as a crucial biomarker in the development and progression of OA and is significantly associated with immune infiltration, offering a novel perspective for elucidating the pathogenesis of OA.

Our study leverages single-cell profiling to elucidate HPV-driven immunological remodeling in HNSCC. The derived prognostic signature effectively captures the essence of the TIME, serving as a reliable biomarker for predicting patient survival and informing precision therapy, potentially bridging the gap between HPV status and clinical decision-making.

Maslinic acid (MA), a plant-derived pentacyclic triterpene, was compared to the FDA-approved drugs dasatinib (DAS) and doxorubicin (DOX) to determine its antileukemic potential. Thus, these results illustrate that MA may act as a natural scaffold with antileukemic properties and call for additional experimental confirmation. The online version contains supplementary material available at 10.1007/s40203-025-00478-3.

Among 289 patients with clinical follow-up, HLA-DQB1*06:04 (aHR [95% CI] = 3.71 [1.57-8.77]) and DRB1*13:02 (aHR = 3.95 [1.77-8.81]) were associated with faster MR4 achievement in imatinib-treated patients (FDR < 0.01), while B*44:02 (aHR = 4.83 [1.62-14.41]) predicted favorable response to dasatinib (FDR < 0.05). Conversely, a higher HED score for HLA-C was associated with improved TFR in dasatinib-treated patients (P = 0.0067). These findings suggest that HLA genotype and class-specific HED may influence CML susceptibility and outcomes and could inform TKI selection and discontinuation strategies.

Dasatinib, an FDA-approved SRC/EPHA2 inhibitor, effectively reduced p-PI3KβY962 and inhibited tumor progression in PTEN-null but not PTEN-WT tumors. These findings establish p-PI3KβY962 as a druggable target and biomarker for developing targeted therapy in PTEN-deficient cancers beyond conventional PI3K kinase inhibition.

She ultimately achieved Major Molecular Response (MMR) after haploidentical hematopoietic stem-cell transplantation (haplo-HSCT). This case highlights the importance of comprehensive molecular profiling at diagnosis and the need to develop alternative therapeutic strategies for rare BCR::ABL1 variants.

The optimized machine learning model (glmBoost+Stepglm) generated a parsimonious 14-gene signature demonstrating exceptional cross-cohort accuracy (mean AUC=0.991), while pharmacological screening prioritized kinase inhibitors (e.g., dasatinib, p=2.1×10⁻⁸) and immunomodulators as therapeutic candidates. Our study establishes FCGR2A-mediated myeloid reprogramming as a critical interface between metabolic dysfunction and ccRCC progression, serving as both a prognostic biomarker and therapeutic target. This dual-disease modeling paradigm provides actionable insights for precision management of obesity-associated malignancies.

Our results show that the multitargeted SRC TKI dasatinib significantly enhanced the efficacy of RET TKIs in RET fusion-positive (RET+) NSCLC and PTC cells...Importantly, synergy was also observed with eCF506 (NXP900), a next-generation clinical SRC inhibitor. Finally, both SRC TKIs restored sensitivity in selpercatinib-resistant RET+ PTC cells. These results elucidate RET and SRC signaling crosstalk in RET+ NSCLC and PTC, suggesting that co-inhibiting SRC has clinical potential in TKI-naïve and -resistant RET+ cancers.

Comprehensive multi-omics mapping links heightened TGF-β activity and a distinct consensus-clustering subtype to unfavourable outcomes and immunotherapy resistance in CRC. The externally validated TGFRS offers a practical prognostic and predictive tool. RCN3⁺ CAFs constitute key stromal drivers, and dasatinib emerges as a repurposable agent to disrupt this axis, warranting clinical exploration.

It was found to inhibit the c-Src-mediated kinase activity (IC50: 517 nM) in comparison to the positive control, bosutinib (IC50: 408 nM). The compound was also able to increase the oxidative stress and induce apoptosis in the colorectal cancer cells employed. The study thus may pave the way for exploration of the top identified ligands further to develop and establish their potential as c-Src kinase inhibitors with anticancer potential.

P3, N=5949, Active, not recruiting, National Cancer Institute (NCI) | Trial completion date: Oct 2025 --> Oct 2026