Lower-risk myelodysplastic syndromes (MDS) and chronic myelomonocytic leukemia (CMML) are commonly managed with erythropoiesis-stimulating agents, luspatercept, or hypomethylating agents. There were no dose-limiting toxicities. Although safe, fostamatinib demonstrated no clinical benefit, underscoring the need for alternative strategies to modulate inflammatory signaling in MDS/CMML.

Our results identify PHF23 as a critical oncogenic driver in glioma and support the PHF23-RPS for risk stratification. Entospletinib may offer a potential immunomodulatory option for high-risk gliomas.

P2/3, N=110, Active, not recruiting, Hutchison Medipharma Limited | Trial primary completion date: Sep 2026 --> Nov 2025 | Recruiting --> Active, not recruiting

Dual targeting of FLT3/SYK (TAK-659) and the proteasome (Ixazomib) showed strong synergy across genetically defined AML subsets, irrespective of FLT3 mutant status. These findings define a therapeutically targetable axis linking FLT3/SYK/β-catenin signaling to stress adaptation, provide a mechanistic basis for combinatorial targeting in high-risk AML. Trial registration: NCT04079738, Date of registration 03 September 2019.

P1, N=18, Completed, Hutchmed | Recruiting --> Completed

P1, N=54, Completed, Hutchmed | Recruiting --> Completed | Trial primary completion date: Feb 2026 --> Nov 2025

P2, N=40, Not yet recruiting, Inova Health Care Services | Trial completion date: Oct 2026 --> Oct 2027 | Trial primary completion date: May 2026 --> May 2027

P1, N=18, Recruiting, Hutchmed

P1, N=54, Recruiting, Hutchmed

Collectively, our study establishes miR-31 as a novel biomarker for LUAD proliferative potential and implicates the miR-31/CDK1-E2F2 network as a promising target for disrupting LUAD progression. These findings establish a miRNA-centric precision therapeutic paradigm for effectively suppressing oncogenic proliferation in LUAD.

Severe anemia and neutropenia induced by R788 in the sickle mouse model suggests that concomitant use of Syk inhibitors with hydroxyurea in patients with SCD should be approached cautiously. Further research is required to clarify the benefits and risks of selective Syk inhibition in SCD and other hemolytic conditions exhibiting stress hematopoiesis.

Additionally, fostamatinib inhibited PDAC cell proliferation even in the absence of viral infection, while ruxolitinib did not. Our data suggest that fostamatinib may be repurposed as an effective drug that enhances OV therapy in PDAC by promoting OV replication and suppressing tumor growth.