Our multi-layered omics framework provided genetically anchored evidence for the role of THBS3, RORC, and TNFRSF25 as druggable targets in IBD. The identified candidate drugs offered new avenues for therapeutic intervention. Further clinical validation is warranted to harness these targets for the development of effective IBD treatments.

Since 2004, patients receiving imatinib with relapse in non-marrow sites were given dasatinib to preserve control of leukemic marrow. Dasatinib is a potentially practice-changing targeted therapy for EML. Finding and eradicating EML could increase the possibility of lengthy disease-free survival.

These findings underscore the necessity for vigilant, protocol-driven monitoring of blood counts and cardiac function (including echocardiography) during dasatinib therapy. Proactive management strategies should be considered to mitigate these risks and improve treatment safety.

P2, N=40, Not yet recruiting, M.D. Anderson Cancer Center

P1, N=30, Not yet recruiting, Ohio State University

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.

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.