P1, N=12, Recruiting, Nantes University Hospital | Not yet recruiting --> Recruiting | Trial completion date: Jan 2028 --> Aug 2028 | Trial primary completion date: Jan 2028 --> Aug 2028

In this study, we investigated whether extracts from three Lepidium meyenii (maca) morphotypes, yellow (MY), red (MR), and black (MB), modulate doxorubicin (DOX) responses in 22Rv1 prostate cancer cells under mono-culture and co-culture conditions with human dermal fibroblasts (HDFa)...Additionally, maca extracts modulated PI3K, PSMA, FOXO1, FAP, and HAT1 in a morphotype-dependent manner. Overall, maca extracts acted primarily as context-dependent modulators of signaling and lipid metabolism markers rather than direct cytotoxic agents with their effects strongly dependent on both extract type and microenvironmental context.

Collectively, these findings provide a disease-oriented, cross-subtype systems-level view of the transcriptional changes associated with doxorubicin treatment in liposarcoma. This work is intended as a hypothesis-generating framework that may inform future functional studies and integrative approaches aimed at understanding therapeutic response and disease progression.

Functionally, MAGEC2 promoted malignant proliferation and induced resistance to adriamycin and bortezomib. MAGEC2 overexpression also exacerbated bone lesions in vivo. Collectively, these findings identify MAGEC2 as both a prognostic biomarker and a promising therapeutic target in MM, and highlight its role as a multifunctional regulator of the ubiquitin system.

These findings support further study of multi-parameter early monitoring and predictive modeling for risk stratification of accelerated cardiotoxic progression in animal models and, ultimately, in appropriately validated clinical cohorts.

The resistance of doxorubicin (DOX), the first-line chemotherapeutic drug for osteosarcoma (OS), stands as a pivotal obstacle in the effective treatment of OS. When ICCB280 and PD98059 are co-administered, the activation of GREM1 by C/EBPα and the inhibition of ERK phosphorylation are intensified. This suppresses OPA1 expression, promotes mitochondrial fission, and effectively counteracts chemotherapy resistance in osteosarcoma.

Despite radical-intent surgery followed by adjuvant carboplatin/etoposide, early recurrence developed with progression through multiple subsequent chemotherapy lines. Exploratory metabolomic profiling of tryptophan pathway metabolites in patient serum and PDO-culture media indicated tumor-associated metabolic alterations. We present clinical and translational efforts in difficult-to-treat NEC, illustrating both the translational challenges and the potential role of PDOs in advancing personalized treatment strategies for a cancer with very limited treatment options.

P=N/A, N=100, Completed, Centre Hospitalier Universitaire de Nice | Recruiting --> Completed | Trial completion date: Jan 2025 --> Jun 2026 | Trial primary completion date: Jan 2025 --> Oct 2025

In vitro cytotoxicity profile of compound 35 against MCF-7, HeLa and HCT-116 cells having IC50 values 1.21, 1.08, and 1.34 μM, respectively showing it is more potent than standard drug doxorubicin, especially in MCF-7 and HeLa cells. These outcomes paved a way for triazole-linked piperidinyl glyoxamide hybrids as promising lead candidates for further advancement in anticancer drug discovery.

In conclusion, we propose the iron-rifampicin complex as a potential candidate for nephroprotection against doxorubicin-induced nephrotoxicity, subject to further validation.

Doxorubicin was used to validate the utility of this model for drug screening...AZ-β microcarriers with a relative zein portion of 9:1 and an elastic modulus of 159.73 kPa were the optimal microcarrier for establishing the osteosarcoma model. This study presented a robust methodology for establishing 3D in vitro tumor models for developing therapeutic intervention.

Notably, HA and PEA-based LPNs significantly protected cardiomyocytes from DOXO toxicity, evidenced by decreased apoptosis, caspase activation, and LDH release, while upregulating protective proteins (Nrf2, SIRT1) and downregulating inflammatory mediators (NLRP3, MyD88, IL-1β, IL-6). These findings support the potential of HA and PEA-based LPNs as a targeted strategy to preserve anticancer efficacy while reducing DOXO-associated cardiotoxicity.