Treatment with imatinib, a tyrosine kinase inhibitor, resulted in a continuous complete molecular response (CMR). To our knowledge, this is the first report to demonstrate the clinical and cytogenetic manifestations of BCR::PDGFRA positive myeloid neoplasm coexisting PDGFRA mutations. Furthermore, it emphasizes the effectiveness of targeted therapy and the significance of personalized management.

Both primary patient and Ba/F3 cells carrying TPR::ABL2 exhibited kinase activation and sensitivity to tyrosine kinase inhibitors (TKIs). This study expands the repertoire of ABL2 fusions identified in ALL and supports the incorporation of TKIs into T-ALL treatment regimens to improve outcomes for this subtype.

In the event of molecular relapse, carefully considered use of imatinib or nilotinib at the lowest effective dose may be employed exclusively in the second or third trimester following multidisciplinary counseling, whereas dasatinib should be avoided throughout gestation. We emphasize structured algorithms, explicit intervention thresholds, and monthly BCR-ABL1 (IS) testing, as well as collaboration with obstetrics, neonatology, and reproductive medicine, including assisted reproductive technologies. Finally, we discuss practical pathways applicable to resource-limited settings to balance maternal-fetal safety with patient values and to support informed, preference-concordant decision-making.

For resistance, assessment of BCR::ABL1 mutations is essential, and second-line agents should be chosen according to the initial TKI and mutation sensitivity. This article summarizes the criteria and timing for switching to second-line therapy and key considerations for selecting and managing second-line TKIs, and briefly reviews the evidence for asciminib and ponatinib in second-line and later settings.

P2, N=20, Not yet recruiting, Institute of Hematology & Blood Diseases Hospital, China

We present two cases of family members affected with multifocal GIST tumors who underwent germline genetic analysis and were found to have germline pathogenic variants in Exon 11 of the KIT gene [c.1735_1737del (p.Asp579del)]. Both patients were treated with Imatinib with good response.

Conditional knockdown of Pim1 in CD4+ T cells (Pim1 cKO) or using the Pim1 inhibitor AZD1208 alleviated the development of inflammatory arthritis in association with decreasing the proportion of Th17 cells. Through molecular docking and dynamic simulation, nilotinib, a Food-and-Drug-Administration-approved drug, was identified as a selective substitute for the currently clinically nonapproved Pim1 inhibitors, which impeded Th17 cell differentiation and was well tolerated during the treatment of Pim1 cKO mice and 2 inflammatory arthritis mouse models. Our study contributes to a better understanding of the mechanism through which Pim1 promotes Th17 cell differentiation and advances the clinical application of Pim1 as an effective target for treating inflammatory arthritis.

P1, N=47, Completed, National Cancer Institute (NCI) | Recruiting --> Completed | N=70 --> 47 | Trial completion date: Jun 2026 --> Feb 2026 | Trial primary completion date: Jun 2026 --> Apr 2025

The combined ponatinib and VK2 treatment synergistically impairs AML cell survival by enhancing apoptosis, suppressing clonogenic growth, and disrupting mitochondrial function. This dual targeting of oncogenic kinase signaling and metabolic integrity supports the ponatinib-VK2 combination as a promising therapeutic strategy for AML.

Neoadjuvant imatinib has been increasingly adopted for locally advanced or anatomically complex tumors to facilitate resectability and organ preservation, although optimal treatment duration and patient selection remain controversial...Nevertheless, duodenum-specific data remain limited, and consensus on optimal management strategies is lacking. This review summarizes current evidence and evolving strategies in the diagnosis and treatment of dGISTs, with a focus on surgical decision-making, perioperative systemic therapy, and ongoing clinical trials, and highlights critical unmet needs requiring future investigation.

Furthermore, we observed a positive correlation between G6PD overexpression and the resistance of CML cells to imatinib. Subsequent mechanistic investigations revealed that the complex formed by the interaction of phosphorylated STAT3 (p-STAT3) and hypoxia-inducible factor 1α (HIF-1α) functions as a novel transcriptional regulator of G6PD, thereby driving its increased expression. Collectively, this study provides compelling evidence that strategies directly targeting p-STAT3/HIF-1α-G6PD may represent an effective therapeutic approach to suppress CML cells proliferation and overcome drug resistance, offering new insights into the diagnosis and clinical management of CML patients.

Critically, the terpene moiety dictated downstream pathway bias: 6a preferentially attenuated CREB activation, whereas 6d more effectively suppressed the PI3K/Akt oncogenic axis and strongly activated proapoptotic p53-mediated stress responses. Our findings establish terpene-engineered imatinib analogues as tunable modulators and promising candidates for targeting downstream BCR-ABL signaling pathways in leukemia treatment.