High-risk patients exhibited heightened sensitivity to targeted therapies (e.g., dasatinib and olaparib), suggesting actionable therapeutic vulnerabilities. Functional studies identified YTHDF3 as a novel oncogenic driver that is significantly overexpressed in AML, where its knockdown suppressed proliferation, induced apoptosis, and stabilized leukemogenic transcripts (ZZZ3, KLHL11) via the regulation of mRNA stability. This integrative study reveals the m6A reader network as a central orchestrator of AML progression, provides a validated prognostic framework for risk-adapted therapy, and positions YTHDF3 as a potential diagnostic and therapeutic target, bridging RNA epigenetics with clinical translation in AML.

By conjugating the BCR-ABL inhibitor dasatinib with the LC3B-binding ligand GW5074, we engineered eight distinct ATTEC variants with diverse linkers...The activity of DS-PPE-GW was further enhanced by the autophagy activator rapamycin, confirming its autophagy dependence. Notably, DS-PPE-GW did not increase global autophagic flux, suggesting selective engagement of pre-existing autophagosomes. These findings demonstrate that strategically designed ATTECs can efficiently degrade BCR-ABL, targeting both its catalytic and non-catalytic functions, and provide a promising strategy for next-generation CML therapy.

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.