etoposide IV

A2780ADR cells revealed cross‑resistance to multiple compounds, including anticancer drugs [cisplatin (CisPt) and etoposide (Eto)] and DNA repair/DNA damage response (DDR) inhibitors (olaparib, niraparib, entinostat, prexasertib and rabusertib). However, combination treatment with Doxo and Ver also increased the cytotoxic response of non‑malignant murine cardiomyocytes, murine embryonic stem cells and human induced pluripotent stem cells. Taken together, the present study suggested inhibition of MDR1‑mediated Doxo efflux by Ver a useful approach to overcome acquired drug resistance of A2780ADR cells by stimulating DDR‑related cytotoxicity, yet at the price of a potentially increased risk of normal tissue toxicity.

The research findings validate ETP-DNP as a promising nanocarrier system for ‎breast cancer. ‎.

He achieved complete remission following six cycles of R-CHOP chemotherapy (rituximab, cyclophosphamide, vindesine, liposomal doxorubicin, and dexamethasone)...He received four cycles of the histone deacetylase inhibitor (HDACi) chidamide combined with COEP chemotherapy (cyclophosphamide, vindesine, etoposide, and prednisone), resulting in a partial remission...Although the prognosis is generally poor, treatment combining HDAC inhibitors such as chidamide with chemotherapy may offer therapeutic potential. Further studies are needed to clarify the molecular mechanisms underlying such lymphoid evolution and to guide optimal management.

The patient was referred to a sarcoma center where he was started on systemic chemotherapy with a VAC/IE (vincristine, doxorubicin, cyclophosphamide/ifosfamide, etoposide) regimen. CONCLUSIONS This case highlights the diagnostic complexity of DSRCT, particularly in atypical liver-dominant presentations, and reinforces the importance of comprehensive tissue sampling and molecular confirmation to guide early, appropriate therapy. Continued research into targeted strategies is crucial to improve outcomes in this aggressive malignancy.

In particular, pharmacogenetic markers for the following drugs were analyzed: anthracyclines (doxorubicin, daunorubicin), vincristine, glucocorticoids (prednisone, dexamethasone), L-asparaginase, methotrexate, alkylating agents (cyclophosphamide, ifosfamide), 6-mercaptopurine, cytarabine, and etoposide. At present, only a few genes, TPMT and NUDT15, have well-established clinical utility, whereas the clinical relevance of pharmacogenetic markers for other drugs used in pediatric ALL therapy remains under investigation. The review also highlights the main knowledge gaps in current research and outlines promising directions for future studies aimed at integrating pharmacogenetic testing into clinical practice for personalized treatment of ALL.

ENETs are rare, aggressive tumors often diagnosed at an advanced stage. Combined adjuvant chemotherapy and radiotherapy were associated with improved outcomes. Molecular profiling may identify potential therapeutic targets.

Effective predictors of response to atezolizumab plus carboplatin/etoposide (CE) therapy in extensive-stage SCLC (ES-SCLC) remain limited. mOS and mPFS were not significantly different between SCLC subtypes but were numerically shorter in the SCLC-N group. CD8+ TIL density is a potential biomarker of clinical benefit in ES-SCLC and may facilitate patient selection for atezolizumab combination therapy.

P2, N=56, Not yet recruiting, Tianjin Medical University Cancer Institute and Hospital

P2, N=97, Active, not recruiting, National Cancer Institute (NCI) | Trial completion date: Jan 2026 --> Jan 2027

P3, N=94, Active, not recruiting, National Cancer Institute (NCI) | Trial completion date: Dec 2025 --> Dec 2026

Initial therapy with a decitabine-CAG (aclacinomycin, cytarabine, G-CSF)-venetoclax regimen failed to induce remission. Morphological complete remission was achieved after switching to a DAE (daunorubicin, cytarabine, etoposide) regimen...This case highlights the diagnostic and therapeutic complexities associated with the co-occurrence of AEL and HLH. Early identification of HLH as a potential complication in AEL is crucial, though outcomes remain dismal, emphasizing an urgent need for novel therapeutic strategies.

P1, N=12, Terminated, M.D. Anderson Cancer Center | Trial completion date: Dec 2027 --> Feb 2026 | Active, not recruiting --> Terminated | Trial primary completion date: Dec 2027 --> Feb 2026; <75% participation