dasatinib

P2, N=40, Active, not recruiting, Washington University School of Medicine | Trial completion date: Aug 2026 --> Oct 2027 | Trial primary completion date: Aug 2026 --> Oct 2027

This study provided potential therapeutic possibilities for oxaliplatin resistance, contributing to CRC treatment.

P2, N=45, Not yet recruiting, University Health Network, Toronto

These findings highlight genomic context in shaping BH3 mimetic responses and point to rational combination of this class of drugs with anti-leukemic agents such as asparaginase.

Introduction of tyrosine kinase inhibitors (TKIs) targeting BCR::ABL1 fusion protein has revolutionized frontline therapy, with successive generations of TKIs-from imatinib to dasatinib and most recently ponatinib-achieving progressively deeper and more durable molecular responses. Concurrently, the integration of immunotherapy, particularly blinatumomab, has enabled chemotherapy-sparing approaches further improving tolerability and efficacy...Treatment-free remission strategies following prolonged TKI maintenance in non-transplant patients, and the integration of chimeric antigen receptor (CAR) T-cell therapy as bridge, consolidation, or salvage, represent emerging frontiers. This review critically examines the contemporary role of allogeneic HCT in Ph+ ALL and provides a framework for transplant decision-making in the contemporary era of targeted and cellular immunotherapy.

The CDK4/6 inhibitors abemaciclib and palbociclib have demonstrated promising results in patient-derived xenograft models of PM...While some cells showed sensitivity to Bcl-xL inhibitors, neither navitoclax nor the specific Bcl-xL inhibitor A-1331852, nor other BH3 mimetics targeting Bcl-2 (venetoclax) or Mcl-1 (S63845) increased cell death when combined with palbociclib...Therefore, we employed inhibitors of these pathways, such as dasatinib, momelotinib or Torin-1, which did not synergise with palbociclib to kill the cells...The differential effects of palbociclib and cisplatin on permanent growth arrest were verified by sorting PM cells based on size and β-galactosidase activity. Our findings underscore the importance of understanding the nature of therapy-induced senescence when assessing the effectiveness of senolytics in different tumour models.

The results of functional experiments showed that knockdown of LGALS3 could inhibit cell proliferation and invasion and promote apoptosis, while affecting drug sensitivity to Dasatinib. In summary, this study constructed a robust prognostic model based on T-HIERDEGs, systematically revealed the immune and molecular characteristics of different risk groups, explained the heterogeneity of T cell subpopulations in the hypoxic microenvironment and their potential role in immune escape, and provided a new theoretical basis and candidate targets for the prognosis assessment, immunotherapy, and combined strategies of HCC.

In SPIRIT2, which compared imatinib and dasatinib as first-line therapies, high BCL-XL expression was associated with treatment failure, poor early molecular response, and lower rates of MR2 and MR3 achievement in patients treated with imatinib. Notably, increases in BCL-XL were detectable 6 to 8 months prior to molecular relapse, suggesting it may serve as an early biomarker of unsuccessful TFR. We now propose a clinical diagnostic toolkit combining CIP2A and BCL-XL biomarkers to stratify CML patients by the risk of disease progression and likelihood of achieving successful TFR.

Dasatinib promotes apoptosis in EBV-positive gastric epithelial cells in association with coordinated suppression of SFK signaling and EBV-encoded BART miRNA expression, accompanied by derepression of pro-apoptotic cellular genes. These findings reveal a previously underappreciated vulnerability of EBV-positive epithelial cells and suggest that targeting host kinase signaling pathways that regulate viral microRNAs may represent a potential therapeutic strategy for EBV-associated malignancies.

Overall, compound 20 emerged as the most promising candidate from this study, warranting further investigation for its therapeutic potential.

Late autophagy inhibition using hydroxychloroquine broadly sensitized both morphotypes, reducing enlarged cells. Notably, the senolytics dasatinib preferentially eliminated E-state cells. These findings highlight the plasticity and heterogeneity of TMZ-induced senescent glioblastoma cells and emphasize the need for selective senotherapeutic strategies aiming to attenuate the pro-tumor effects exerted by SnCs on the tumor microenvironment.

Initial treatment included hydroxyurea and dasatinib; however, after chronic-phase CML was confirmed, therapy was transitioned to imatinib, resulting in resolution of B symptoms, normalization of WBC counts, and reduced leg swelling. This case underscores the importance of distinguishing CEH from aggressive disease states, such as blast-phase CML or myeloid sarcoma, through comprehensive histopathological and immunohistochemical analysis.