These transcriptional changes paralleled a transient inflammatory response, including early Tnf-α induction and female-specific Il-6 elevation. Collectively, these findings highlight sex-dependent modulation of hepatic ATO handling and drug metabolizing capacity, with important implications for risk assessment and individualized ATO containing regimens.

CCNJL has the potential to act as a valuable prognostic indicator and immunotherapy target in CHOL. Its expression pattern and associations with clinical outcomes, immune characteristics, and drug sensitivity highlight its potential for improving diagnostic and therapeutic approaches. Future research should focus on elucidating the underlying mechanisms and validating these findings in larger cohorts.

We present a case of a 66-year-old female with de novo metastatic NSCLC harboring an EGFR mutation, RET rearrangement, and ERBB2 amplification, who experienced transformation to SCLC while on osimertinib. Subsequently, she exhibited primary refractory disease to both first-line platinum doublet with immunotherapy and second-line lurbinectedin...The patient had minimal side effects and obtained a partial response with a progression-free survival (PFS) of 13.1 months, better than historically poor prognosis seen in transformed SCLC. This case underscores the potential role of human epidermal growth factor receptor 2 (HER-2) directed therapies, such as T-DXd, in transformed SCLC.

P2, N=30, Not yet recruiting, Sichuan University | Initiation date: Dec 2025 --> Oct 2026

The combination of elesclomol (a cuproptosis inducer) and selisistat (a SIRT1 inhibitor) effectively induced cuproptosis in CRC. Moreover, DLAT supplementation establishes a positive feedback loop that amplifies cuproptosis. These results underscore the critical role of nonhistone NAT10 lactylation in tumor cuproptosis and highlight the therapeutic potential of targeting this pathway for CRC treatment.

P2, N=53, Recruiting, National Cancer Institute (NCI) | Trial completion date: Dec 2028 --> Jun 2028

This resulted in intracellular Cu+ accumulation, triggering cuproptosis and excessive mitophagy, ultimately suppressing tumor growth. Therapeutically, the copper ionophore elesclomol potently inhibited tumor growth in a Thumpd1-knockout mouse model of LUAD.

Addressing this limitation, combination therapies integrating elesclomol with targeted agents such as ferroptosis inducers or chemotherapeutic drugs have demonstrated significant antitumor advantages. Future research must urgently leverage the selection of precise biomarkers and the development of novel intelligent nanodelivery systems to further advance the safe and efficient clinical translation of elesclomol.

We report a case of a 42-year-old patient with EVI1-positive AML harboring the MLL-AF6 fusion gene, who failed to achieve remission after undergoing standard "IA" induction therapy and was then treated with VAH (venetoclax, azacitidine, and homoharringtonine) consolidation chemotherapy. This case suggests that the combination of ATRA with the VAH regimen may demonstrate promising efficacy and an acceptable safety profile in patients with EVI1-positive AML who are refractory to conventional chemotherapy. However, further clinical studies are required to confirm its wider applicability.

P1/2, N=78, Recruiting, AB Science | Active, not recruiting --> Recruiting

P2, N=550, Recruiting, Synairgen Research Ltd. | - | Completed --> Recruiting

CuCl2 and elesclomol treatment induced cuproptosis, which was attenuated by SLC39A4 overexpression but potentiated by SLC39A4 knockdown, as confirmed through proliferation assays and cuproptosis marker analyses in cell cultures and xenograft models...Dual-luciferase assays demonstrated that mutation of the m6A site within SLC39A4's coding sequence abolished YTHDF1-mediated regulation. These findings establish SLC39A4 as a promoter of GC progression through cuproptosis suppression, modulated by YTHDF1 via m6A-dependent mRNA stabilization, revealing potential therapeutic targets for GC treatment.