Consistently, SRC inhibitor dasatinib rescued enzalutamide sensitivity and inhibited the proliferation of enzalutamide-resistant cancer cells. Taken together, our findings demonstrate a substantial role for FMNL2/SRC interaction in the regulation of AR translocation, suggesting that targeting FMNL2-mediated SRC activation might be a potential therapeutic strategy for enzalutamide-resistant PCa and dasatinib could be an option.

This case highlights the aggressive progression of CML to acute mixed lineage leukemia and underscores the challenges in managing patients with resistant disease. The patient's gastrointestinal bleeding and recurrent infections further complicated treatment, emphasizing the need for early intervention and close monitoring of high-risk CML patients.

We found that TKIs, such as imatinib, nilotinib, and dasatinib, increased the gene expression of PRDX2 in K562 cells; however, only dasatinib increased the cytoplasmic protein expression of PRDX2. This discrepancy was linked to post-translational regulation through SUMOylation in cooperation with dasatinib. Our results suggest that the antioxidants PRDX1 and PRDX2 could serve as potential targets for TKIs in the treatment of CML.

The distinct T cell populations that respond to first and subsequent CD3 bispecific treatment offer an explanation to the first-dose effect, wherein the risk of CRS associated with CD3 bispecific treatment is mainly limited to the initial dose. Furthermore, our work suggests that tumor killing capacity and cytokine production of T cells could be uncoupled, as demonstrated here by utilizing different T cell populations as effector cells. These findings could be further explored for designing mechanism-based strategies to mitigate the risk of CRS.

ADCC was maintained upon exposure to specific ABL or JAK-inhibitors, in contrast to the multi-target TKI dasatinib impeding SYK-dependent ADCC. In conclusion, optimized ML-NK cell and CD19 antibody-based immunotherapy combined with carefully selected TKI demonstrates significant in vitro treatment efficacy in kinase-driven leukemia.

P2, N=40, Recruiting, Washington University School of Medicine | Trial completion date: May 2026 --> Jan 2026 | Trial primary completion date: May 2025 --> Jan 2026

In this case, a phototoxic rash that developed in a 78-year-old bcr-abl positive acute lymphoblastic leukemia patient is presented. This case supports that phototoxic reactions may occur with dasatinib and emphasizes that clinicians should be alert for this side effect.

Drug prediction indicated that dasatinib is a potential therapeutic agent. Our findings provide insights into the role of the senescence gene set in patient stratification and precision medicine.

P2, N=156, Completed, M.D. Anderson Cancer Center | Active, not recruiting --> Completed | Trial completion date: Nov 2024 --> Mar 2025 | Trial primary completion date: Nov 2024 --> Mar 2025

P2, N=174, Completed, University of Liverpool | Unknown status --> Completed

P2, N=130, Completed, Bristol-Myers Squibb | Active, not recruiting --> Completed | Trial completion date: Dec 2029 --> Jan 2025

The ALL/MRD2014 trial underscores the importance of MRD status and allo-HSCT in Ph+ ALL. Continuous dasatinib-based regimens offer favorable outcomes in MRD-negative patients.

P2, N=120, Recruiting, St. Jude Children's Research Hospital | N=60 --> 120

NGEF facilitates the infiltration of nerve and the growth of cancer cells in lung adenocarcinoma through the Ephrin-A3/EphA2 pathway, suggesting that NGEF is a promising target for disrupting interactions between nerves and tumors. Biomaterials that focus on NGEF are anticipated to be a potential treatment option for lung cancer.

This study suggests that intermittent DQ treatment is feasible and safe; data hint at potential functional benefits in older adults at risk of Alzheimer's disease. The observed reduction in TNF-α and its correlation with increases in MoCA scores suggests that DQ may improve cognition by modulating the SASP. However, there was not an appropriate control group. Data are preliminary and must be interpreted cautiously.

The accumulation of senescent LECs reduces regenerative capacity, disrupts lens homeostasis, and contributes to cataractogenesis. Emerging senotherapeutics, such as dasatinib, quercetin, and metformin, show promise in reducing the senescent cell burden and modulating the SASP to preserve lens transparency.

Drug sensitivity analysis revealed that patients with a poorer prognosis and lower MSMB/epithelial cell ratio showed increased sensitivity to cyclophosphamide, cisplatin, and dasatinib. The model developed in this study provides a robust and accurate tool for predicting PCa progression. It offers significant potential for enhancing risk stratification and informing personalized treatment strategies for PCa patients.

The scratch assay showed that this combination medication down-regulated the cell migration-regulating MMP2 gene. Both Das and Eda decreased AGS cell proliferation, suggesting treatment with Eda may prevent metastasis.

PS holds promise as a target antigen for CAR-T cell therapy, underscoring the need to address fratricide as a key challenge in the development of PS-targeting CAR-T cells.

Additionally, drug sensitivity analysis indicated that patients with a high PCDS may exhibit resistance to immunotherapy and standard adjuvant chemotherapy regimens; however, they may benefit from the FDA-approved drug Dasatinib. Overall, we confirmed that the PCDS is a prognostic risk factor and a valuable predictor of immunotherapy response in GC patients, which provides new evidence for the potential application of GC.

Notably, the S3 subtype demonstrated sensitivity to dasatinib but resistance to methotrexate. Finally, we developed a user-friendly Shiny-based website to facilitate the application of our prognostic and subtype classification models (https://jli-bioinfo.shinyapps.io/NCI_online/). This study establishes a critical prognostic marker and proposes a novel molecular classification framework grounded in miRNA-regulated gene expression profiles, advancing our understanding of the non-coding mechanisms driving OV heterogeneity.

Co-inhibition of AXL and SRC synergistically reduced KRAS activity and induced apoptosis in NSCLC.

P4, N=46, Not yet recruiting, Centro de Atencion e Investigacion Medica | Trial completion date: Jan 2024 --> Apr 2026 | Trial primary completion date: Dec 2023 --> Dec 2025

Moreover, the in vitro cytotoxicity study revealed decreased IC50 value in case of the dual drug-loaded NPs compared to all treated groups, with significant decrease in the expression levels of cyclin D1, COX-2, p-Src and FAK proteins, besides, increased caspase-3 level. The findings suggest that DAS/CXB-loaded BSA NPs could serve as a drug delivery platform with increased antitumor effectiveness.

Additionally, we illustrated that KM UCAR-T cells displayed anti-tumor activity in a xenograft murine model and verified the expansion and cytotoxicity of KM UCAR-T over traditional UCAR-T in the presence of allogeneic PBMCs when treated with dasatinib in vivo. These findings offer a novel strategy for UCAR-T cells to resist host immune rejection and achieve sustained expansion.

P2, N=97, Active, not recruiting, National Cancer Institute (NCI) | Trial completion date: Jan 2025 --> Jan 2026

Targeted dasatinib-loaded lipopolyplexes exhibited superior cell proliferation and migration inhibition and cellular uptake than dasatinib, polyplexes and non-targeted lipopolyplexes. Moreover, in comparison with non-targeted lipopolyplexes and polyplexes, targeted lipopolyplexes significantly transfected MDA-MB-231 cells and downregulated Notch-1 mRNA.

This study uses Raman and fluorescence imaging to investigate the in vitro cytotoxic effects of two TKIs, imatinib and dasatinib, on human aortic endothelial cells (HAECs). The predominant mechanism appears to involve oxidative stress-mediated inflammation, as evidenced by increased lipid content in treated cells and ICAM-1 staining. This cytotoxicity may contribute to the cardiotoxic effects observed during TKI therapy.

Dasatinib also suppressed the expression of Nanog-1 and OCT-3 in SD292 attached on mesenchymal fibroblasts. This study may provide a base for targeted therapy against GCSCs/GCs progression in future preclinical/clinical settings.

The study highlights the prognostic significance of cuproptosis-related genes and provides new insights into developing pharmacological therapeutic strategies targeting cuproptosis for the prevention and treatment of ovarian cancer.

Depletion of CD8 cells compromised the durability of EPN responses and reduced overall survival. These data indicate that dasatinib has the potential to be an effective therapy for ST-EPN-ZFTA molecular subgroup of EPN and support further investigation of dasatinib in clinical trials.

Furthermore, elevated HNRNPA2B1 levels conferred resistance to multiple chemotherapeutics, including Dasatinib. Functional studies demonstrated that HNRNPA2B1 enhances lung cancer cell proliferation and migration by upregulating TARDBP and cell cycle-related genes, with m6A modification serving as a critical regulatory mechanism. Collectively, these findings establish HNRNPA2B1 as an oncogenic factor across multiple cancer types, underscoring its value as a prognostic marker and a promising therapeutic target, particularly in lung cancer, offering new insights for targeted therapeutic strategies.

To avoid fratricide of CD45 CAR T cells, genomic disruption of the CD45 gene was performed on human CD45 CAR T cells in combination with the signaling kinase inhibitor dasatinib...Similarly, CD45Δ CAR45 natural killer (NK) cells exhibited potent cytotoxicity toward tumor cell lines and human hematopoietic cells in vitro. Thus, we provide the proof of concept for the generation and preclinical efficacy of fratricide-resistant CAR45 T and NK cells directed against CD45-expressing tumors and hematopoietic cells.

P1/2, N=20, Enrolling by invitation, Mayo Clinic | Trial completion date: Dec 2024 --> Jun 2026 | Trial primary completion date: Dec 2024 --> Jun 2026

The analysis reveals that preclinical cytotoxic inhibition is highly predictive of clinical efficacy and shows that cancer regression can only be achieved when the drug-target is an essential oncogenic driver in a monodriver cancer. The analysis highlights dasatinib's potential in achieving stable disease in solid tumors, supporting its use in combination therapies.

In GBM, drug sensitivity analysis revealed significant associations between CTF1 expression and responsiveness to gemcitabine, dasatinib, and other agents. It acts as a predictive indicator and is associated with immune cell infiltration in GBM. These findings provide a foundation for further research into the molecular function of CTF1 and offer new insights for exploring the underlying mechanisms and developing treatments for glioma.

Inhibitory drugs dexamethasone, dasatinib, and sotrastaurin prevented NK cell transition to an activated state and suppressed the expression of IFN-γ by NK cells, thus preventing IFN-γ mediated target cell transcriptomic response. In conclusion, we discovered that SMAC mimetics sensitize cancer cells to NK cell mediated killing, with potential clinical applications especially in patients with advanced phase CML.

Chemotherapy with tyrosine kinase inhibitors such as Imatinib, Dasatinib, Sorafenib and follow- up depend upon risk category. All belonged to high risk category of GISTs. Any abdomino-pelvic mass detected on ultrasonography and with unusual presentation presenting at primary health centre the possibility of non-gynecological tumors especially GISTs should be kept in mind and should be referred to higher centres for further investigation and proper management.

Imatinib mesylate (IM) is a first-line therapy for chronic myeloid leukemia (CML) and exhibits good therapeutic effects, but not in all patients with CML owing to drug resistance. Importantly, PF also improved the sensitivity of CML cells to bosutinib and dasatinib via inhibition of Cyr61 production. In conclusion, we report for the first time that PF may effectively improve the sensitivity of IM-resistant CML cells to IM, bosutinib, and dasatinib, at least in part, by subsequently downregulating Cyr61.

Furthermore, these modified cells are more susceptible to dasatinib and ketoconazole. Additionally, this altered expression signature has led to the identification of new compounds with antiproliferative and pro-apoptotic effects on granulosa tumor cells. Our findings demonstrate the potential of CRISPR technology for the specific targeting and elimination of a mutation causing GCTs, highlighting its therapeutic promise for treating this rare ovarian cancer.

Dasatinib and quercetin eliminated senescent cells in MASLD, attenuated fat deposition, and suppressed fibrosis gene expression. The results indicate that dasatinib and quercetin as senolytic drugs are novel therapeutic agents that reduce MASLD.

Epstein-Barr virus (EBV)-associated lymphoproliferative disorders (EBV-LPD) occur in immunocompromised patients, such as those receiving methotrexate or other immunosuppressive drugs or after allogenic transplantation. EBV-LPD is also reported to be a rare side effect in patients receiving long-term dasatinib or imatinib...The subsequently removed splenic mass was largely composed of non-neoplastic cytotoxic T cells resulting from a reaction to EBV-infected B cells. EBV-LPD should be included in the differential diagnosis of patients who develop lymphadenopathy during dasatinib treatment, regardless of its duration.