lapatinib

Consistent with these subtype-specific features, CS1 tumors exhibited distinct sensitivities to dasatinib, lapatinib, paclitaxel, and cisplatin, indicating immune-state-associated therapeutic vulnerabilities. Together, these findings suggest a RUNX1-associated immunosuppressive tumor ecology in UVM and provide a conceptual framework for immune-state-guided therapeutic strategies.

In further support, lapatinib, an EGFR/HER2 tyrosine kinase inhibitor, attenuated mitochondrial respiration in NF639 murine mammary tumor epithelial cells. Together, this data highlights that the typical correlation between mitochondrial content and respiratory capacity may not apply to all tumor types and implicates HER2-linked activation of mitochondrial respiration supporting tumorigenesis in this model.

These results indicate a synergistic interaction between tras tuzumab and blood serum in both groups. We also found significant differences in CI values between healthy donors and breast cancer patients: blood serum samples from patients enhance the effect of trastuzumab to a greater extent.

All patients received anti-HER2 TKI therapy (including pyrotinib and lapatinib) in 28-day cycles. No unexpected toxic effects were reported. After progression following TKI therapy, T-DXd exhibited notable antitumor activity, although no significant efficacy differences were observed among ADC, mAb, and TKI groups.

P3, N=603, Completed, Institut National de la Santé Et de la Recherche Médicale, France | Active, not recruiting --> Completed

Low ASPG expression in HCC may drive aspartate metabolism and reprogramming of the TCA cycle, thereby influencing sensitivity to drug treatment.

These findings reveal that MUC16 promotes endometrial cancer progression through the ESR1/PI3K/AKT axis and highlight MUC16 as a potential prognostic biomarker and therapeutic target.

Collectively, these findings substantiate a mechanistic and quantitative synergy between HSAmediated HER inhibition and VGB3based VEGFR blockade. This dualtarget HSALapatinib/VGB3 system offers enhanced potency, reduced resistance, and a promising platform for precisionguided TNBC therapy.

P1/2, N=24, Terminated, Institut Paoli-Calmettes | N=106 --> 24 | Suspended --> Terminated; Drug development withdrawn

The HER2 inhibitors represent different mechanisms of actions, including trastuzumab, pertuzumab, tucatinib, and lapatinib, all of which are clinically approved, as well as PEPDG278D, a recombinant human protein which was previously shown to induce the degradation of HER2 and epidermal growth factor receptor (EGFR). Despite p95HER2 expression and resistance to current HER2 inhibitors, HER2-positive BC cells and tumors are highly vulnerable to PEPDG278D-induced degradation of HER2 and EGFR. By inducing HER2 degradation, PEPDG278D eliminates p95HER2 in HER2-positive BC cells and tumors.

In addition, there are significant differences in sensitivity to most drugs between high-risk and low-risk cohorts, with WIKI4 and Lapatinib negatively correlated with risk scores, while Doramapimod and Niraparib positively correlated with risk scores. The drug sensitivity results also provide drug guidance for the clinical application of this feature, all of which provide important clinical utility for the prognosis of LUAD. At the same time, the intercellular communication network was plotted based on the GRPS score, providing insights into the pathogenesis of LUAD and offering new ideas for developing targeted therapies and precision medicine methods.

The triple combination showed moderate tolerability and termination occurred after the first stage of Phase II due to insufficient efficacy. Our findings highlight challenges in translating organoid-derived drug combinations to clinical practice.