lapatinib

In vivo, lapatinib suppressed tumor growth and downregulated SLC1A5/GPX4, effects that were reversible by DFO. This study reveals a novel mechanism by which lapatinib inhibits OS via the SLC1A5-GPX4 axis to induce ferroptosis, providing a preclinical rationale for further evaluation of lapatinib repurposing in osteosarcoma.

A significant negative correlation between RiskScore and the IC50 of XMD8-85, lapatinib, roscovitine, salubrinal, bexarotene, LFM-A13, FTI-277, and TGX221 chemotherapeutic agents was further noticed. In this study, we computationally identified genes associated with both disease progression and macrophage/monocyte-related characteristics in UVM and constructed a prognostic risk model with predicted immune infiltration patterns. These findings generate testable hypotheses that may inform future experimental studies on the immune mechanisms underlying UVM.

Two epidermal growth factor receptor inhibitors (EGFRi) commonly used in cancer therapy and known to cause GI side effects, erlotinib and lapatinib, emerged as strong inducers of EEC differentiation, dramatically increasing chromogranin A (CHGA) expression compared to controls, while maintaining ISC function and organoid growth. These findings provide important insight into EEC differentiation that could inform treatment strategies for EAD, metabolic diseases, and GI diseases. Inhibition of EGFR signaling promotes human ISC-to-EEC differentiation through activation of STAT1 signaling.

We previously demonstrated that lapatinib resistance in triple-negative breast cancer (TNBC) cells is associated with AnxA6 upregulation and accumulation of cholesterol in late endosomes...Finally, blocking extracellular AnxA6 with neutralizing antibodies reduced the viability of AnxA6-low TNBC cells but had little effect on AnxA6-high cells. These findings suggest that extracellular AnxA6 is critical for the survival of highly proliferative AnxA6-low basal-like breast cancer cells and that AnxA6 influences TNBC progression by facilitating the secretion of pro-inflammatory cytokines and cholesterol-enriched exosomes.

Treatment of HER2+ mBC with and without BMs in Saudi Arabia largely aligned with international recommendations identified in our literature analysis, although access to lapatinib, tucatinib and neratinib can be limited and may lead to use of alternative regimens. The tucatinib-combination may be considered the standard of care for adult patients with HER2+ locally advanced or mBC who have received at least two prior anti-HER2+ treatment regimens, including patients with BMs. Ensuring access to innovative HER2+ mBC therapies across Saudi Arabia is crucial to supporting best practice.

Patients in the high‑risk group showed improved responses to lapatinib, BI‑2536, OSI‑027, and SB505124, whereas those in the low‑risk subgroup had better sensitivity to axitinib, epirubicin, fulvestrant, and olaparib. Additionally, CD24 overexpression in BC cell lines promoted proliferation and migration, and inhibited apoptosis. These findings contribute to personalized treatment strategies and help elucidate the tumor microenvironment characteristics of BC patients.

In the context of the Chinese health system, none of the three alternative regimens-pyrotinib plus capecitabine, T-DM1, and T-DXd-demonstrated cost-effectiveness relative to lapatinib plus capecitabine at the current WTP threshold.

Among the tested analogs, 6e, 6f, and 6 g exerted promising cytotoxicity toward HS 578 T cells where compound 6f exhibited significant antiproliferative activity with an IC50 of 3.06 µM, exceeding that of Lapatinib by 7.6 fold...The findings illustrated that analog 6f exerted the most potent CDK-2 inhibition with an IC50 equal to 0.277 µM, which is approximately threefold the activity of Roscovitine (0.833 µM). As well, compound 6f arrested HS 578 T cell cycle at both S and G2/M phases and stimulated apoptosis by increasing Bax and Caspase-3 expression with a concurrent decline in the expression of Bcl-2. Additionally, ADMET prediction and the binding interaction of the most active derivatives with CDK-2 have been studied in silico to evaluate their potential as important antitumor agents.

Therapeutic limitations of current targeted therapies include resistance, toxicity, and the modest efficacy of monotherapies. As such, future investigations must refine endpoints (e.g., hearing stabilization vs. tumor regression), optimize dosing strategies, and personalize therapy based on age, tumor biology, and clinical trajectory. This review highlights the translational challenges and opportunities that lie ahead in delivering clinically efficacious therapies specific to each patient.

VS biology reflects integrated genetic and epigenomic dysregulation. Advancing care will require multi-omic classification, biomarker-driven trials, and combination therapies targeting both signaling and epigenetic vulnerabilities. Future management is expected to shift toward personalized, mechanism-based strategies aimed at durable tumor control while preserving hearing and quality of life.

P1, N=23, Active, not recruiting, National Cancer Institute (NCI) | Trial completion date: Jun 2026 --> May 2027

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.