Esophageal Squamous Cell Carcinoma

Mechanistically, we demonstrated that DNA damage and elevated lactate levels induced PARP1 K654 lactylation, enhancing its enzymatic activity and augmenting poly(ADP-ribosyl)ation of downstream targets, potentially playing a pivotal role in chemotherapy resistance-associated pathways. This comprehensive tissue-level landscape of Kla dynamics in ESCC response to chemotherapy establishes Kla as a critical regulatory mechanism in treatment response, potentially offering novel therapeutic targets and predictive biomarkers for personalized treatment strategies.

P=N/A, N=208, Active, not recruiting, Bristol-Myers Squibb | Recruiting --> Active, not recruiting | N=500 --> 208

The CCT6A targeted by the traditional Chinese medicine component quercetin may inhibit PANoptosis by promoting the differentiation of Mono-CD14 cells into TAM-SPP1 macrophages. We constructed prognostic and diagnostic models using PANoptosis-related prognostic biomarkers, analyzed the differences and treatments between high-risk and low-risk groups, and revealed a new mechanism by which CCT6A may inhibit PANoptosis by promoting TAM-SPP1 differentiation, providing new targets and biomarkers for ESCA treatment.

However, PRDX4 overexpression showed opposite effects, which were partly reversed by the ferroptosis inhibitor, ferrostatin-1 and the inducer erastin. Most crucially, PRDX4 depletion-mediated inactivation of the phosphoinositide 3-kinase (PI3K)/AKT signaling pathway could be rescued by 740 Y-P (a PI3K activator), whereas PRDX4 overexpression triggered the activation of the PI3K/AKT signaling pathway, which could be reversed by the PI3K inhibitor LY294002. Collectively, the data suggest that PRXD4 suppresses ferroptosis in ESCC cells by activating the PI3K/AKT signaling pathway, suggesting that targeting PRDX4 may be a novel strategy for treating patients with ESCC.

The maximum tolerated dose was not reached with ifinatamab deruxtecan; however, one death due to treatment-related interstitial lung disease highlights the importance of prompt evaluation and careful management of patients who develop interstitial lung disease. Promising antitumour activity was observed across various solid tumours. These findings support further evaluation of ifinatamab deruxtecan in randomised controlled trials.

The mechanism may involve LPS-induced, non-degranulatory MC activation that modulates the desmoplastic microenvironment. Targeting this axis presents a promising strategy for ESCC treatment.

P=N/A, N=9, Recruiting, Fudan University | Trial completion date: Sep 2025 --> Dec 2026 | Trial primary completion date: Sep 2025 --> Dec 2026

P1, N=6, Active, not recruiting, West China Hospital | Recruiting --> Active, not recruiting | Trial completion date: Oct 2025 --> Feb 2027 | Trial primary completion date: Oct 2025 --> Jun 2025

Drugs like VX.702 and BMS.754807 were more effective in the high-risk group...ESCC tumor tissues exhibited markedly decreased AMN and ERICH5 expression but increased HRG compared to normal controls. This study identified prognostic signature genes associated with CRT and PS in ESCC and constructed a risk model that may predict patient survival, which could provide valuable insights for future research on ESCC diagnosis and treatment.

The MCCH system not only enhances curcumin's delivery efficiency but also synergizes with cisplatin to trigger ferroptosis through dual modulation of GPX4/ACSL4 pathways. This innovative approach represents a promising targeted therapy for ESCC with substantial clinical translational potential.

Pharmacologic inhibition of FTO restores miR-200b/a/429 cluster expression and partially rescues the oncogenic phenotype elicited by FTO overexpression. Collectively, our findings uncover a previously unrecognized FTO-m6A-miR-200b/a/429 axis that propels ESCC progression and highlight FTO as a promising therapeutic target for patients with ESCC.

Combination treatment with mebendazole and oxaliplatin significantly enhanced chemosensitivity in ESCC cells. Collectively, these findings establish the USP5-IMPDH2-guanine axis as a critical driver of ESCC progression and highlight its potential as a promising therapeutic target for ESCC.