Intermediate A demonstrated superior antiproliferative activity compared to derivatives 1-12 and exhibited cytotoxicity comparable to imatinib in K562 cells (IC50 = 6.15 ± 1.26 µM vs. 5.14 ± 1.44 µM, respectively)...The compound showed acceptable predicted physicochemical and ADME characteristics based on in silico analysis. Intermediate A emerges as a significant anti-CML candidate exhibiting potent cytotoxic, apoptotic, and moderate ABL TK inhibitory activity, together with a favorable selectivity profile.

The cumulative risk score based on m6A pathway variants showed a strong association with PFS. These findings provide preliminary, hypothesis-generating evidence that genetic variations may contribute to inter-patient variability in outcomes and warrant further investigation as potential biomarkers in IM-treated GIST.

A literature review of all children with PDGFRB rearrangement was collated in our analysis. The challenges of diagnosis, treatment, and follow-up posed by such a rare genetic disorder with no pediatric guidelines are being discussed.

The results of the study provide essential pharmacokinetic information for the clinical use of radotinib in the treatment of CML patients. ClinicalTrials.gov, Identifier NCT06461078, NCT03722420.

P1, N=18, Recruiting, University of California, San Diego | Not yet recruiting --> Recruiting | Initiation date: Dec 2025 --> Jun 2026

P2, N=125, Active, not recruiting, University of Jena | Not yet recruiting --> Active, not recruiting

P=N/A, N=100, Not yet recruiting, Institute of Hematology & Blood Diseases Hospital, China

P3, N=21, Terminated, University of Maryland, Baltimore | Completed --> Terminated; The Principal Investigator left the institution. The study was halted prematurely.

P2, N=45, Not yet recruiting, The University of Hong Kong

The median overall survival of 5 patients with available follow-up was 11 months. We conclude that the reciprocal translocation t(5;12)(q32;p13) requires a careful and step-wise diagnostic work-up to differentiate between an underlying ETV6::PDGFRB fusion gene with associated excellent prognosis on imatinib and an ETV6::ACSL6 fusion gene, for which the prognosis is poor and alloHCT appears to be a promising therapeutic option.

We report that imatinib-treated neutrophils can process and release IL-1β independently of NLRP3 inflammasome assembly and the expression/activity of caspase-1 or Gasdermin D. Mechanistically, imatinib induces azurophilic granule permeabilization to drive robust cytosolic accumulation of granule-derived neutral serine proteases, serine protease-mediated processing of proIL-1β, and release of mature IL-1β. Together these findings elucidate a novel mechanism by which disruption of neutrophil granules can bypass the NLRP3 inflammasome pathway to drive serine protease-mediated IL-1β processing and release.

Despite low mitotic activity, the tumor was classified as high risk due to its size (>10 cm), and the patient was commenced on adjuvant imatinib therapy. This case highlights a gastric GIST masquerading as a giant gastric diverticulum and emphasizes the importance of considering GIST as a differential diagnosis of large gastric masses.