P1, N=14, Not yet recruiting, National Institute of Allergy and Infectious Diseases (NIAID)

The MBRG-based model effectively predicts BLCA prognosis, integrates mechanisms of basement membrane remodeling, EMT, and immune suppression, and identifies DDR2 and SERPINF1 in CAFs as potential targets for personalized therapy.

P2, N=80, Recruiting, National Institute of Allergy and Infectious Diseases (NIAID) | Not yet recruiting --> Recruiting

Following dasatinib therapy, the enlarged nodes regressed. Despite the patient's advanced age, no significant adverse events have been observed during the course of treatment.

Low-dose dasatinib is effective and tolerable in imatinib-resistant CML-CP, with nearly two-thirds achieving DMRs. Predictive biomarkers (T315I mutation, high ELTS risk, high baseline BCR-ABL1) can guide dose optimization.

Inhibiting the Src pathway with dasatinib reversed this pro-migratory effect, markedly reducing their migration persistence. These insights refine our understanding of GBM infiltration and highlight Src inhibition as a promising strategy in EGFRvIII-positive tumors.

In patients with CBF-AML, the addition of dasatinib to intensive chemotherapy failed to improve survival outcomes. The addition of dasatinib was associated with an increase in toxicity. This trial was registered at www.

Under oxidative (H2O2) and genotoxic (etoposide) stress, myc-δC2 expression sensitized cells differently in the two cell lines: MCF-7 cells showed consistent sensitization, whereas in MDA-MB-468 cells, sensitization was observed only at higher stress levels or after dasatinib pretreatment. These results indicate a cell line-dependent pro-death role for the isolated PKC-δ C2 domain, highlighting that modulation of this domain, or its use as an autonomous pro-apoptotic agent, may offer new therapeutic avenues in breast cancer.

Thus, dasatinib could be used to minimize potential CAR123 toxicity toward endothelial cells without compromising its anti-leukemic effects. However, a higher dose could be used to completely inhibit CAR-T cell functionality in the event of toxicity.

Furthermore, treatment with the senolytic combination dasatinib and quercetin (D + Q) selectively eliminates senescent CAR cells and BMAds, effectively preventing chemotherapy-induced bone loss. Given that nearly all chemotherapy treated patients experience bone loss and associated fracture risk, our findings offer a promising therapeutic avenue to preserve bone integrity and improve quality of life for cancer patients.

Moreover, the combination of dasatinib with an anti-programmed cell death protein-1 (PD-1) antibody represents a potential therapeutic strategy. These findings highlight dasatinib as a potential therapeutic option for metastatic TNBC and suggest that selecting patients with high ETS1 expression may optimize treatment response.

In cell cultures, the 30%-70% of human senescent preadipocytes or human umbilical vein endothelial cells (HUVECs) that are senolytic-resistant (to Dasatinib or Quercetin, respectively) had increased p16INK4a, p21CIP1, senescence-associated β-galactosidase (SAβgal), γH2AX, and proliferative arrest similarly to the total SC population (comprising senolytic-sensitive plus-resistant SCs). Transplanting senolytic-resistant SCs intraperitoneally into younger mice caused less physical dysfunction than transplanting the total SC population. Because Ruxolitinib attenuates SC release of proapoptotic SASP factors, while pathogen-associated molecular pattern factors (PAMPs) can amplify the release of these factors rapidly (acting as "senosensitizers"), senolytic-resistant and senolytic-sensitive SCs appear to be interconvertible.