Esophageal Squamous Cell Carcinoma

LINC00092 exerts tumor-suppressive effects in ESCC cells by inhibiting cancer progression through the LINC00092/MAZ/NFE2L2 axis and promoting ferroptosis. Therefore, LINC00092 may serve as a potential therapeutic target for ESCC.

The prognostic analysis revealed that lower NK cell counts before treatment were correlated with longer disease-free survival. In patients with advanced ESCC, specific lymphocyte subsets in peripheral blood before treatment are closely associated with ICI efficacy and patient prognosis, and thus could potentially guide treatment decisions.

This study elucidates the critical role and molecular mechanism through which KLF11 drives radiotherapy resistance in ESCC by regulating the MDM2/E2F1 axis and enhancing HR repair, thereby providing a solid theoretical foundation and potential target for the development of KLF11-targeted radiosensitization therapies for ESCC.

The clarification and materials provided by the authors upon request did not address the concerns. Accordingly, the article is retracted as the editors have lost confidence in the integrity and accuracy of the whole body of data presented in the article and consider its conclusions invalid.

This review emphasizes the crucial roles of the TRAP complex and its subunits (SSR1-SSR4) in various diseases, highlighting their potential as therapeutic targets and biomarkers. Future research should focus on understanding the mechanisms through integrated experimental and multi-omics approaches, defining subunit interactions, and exploring structure-based drug design for clinical applications.

Chemotherapy (chemo) combined with an immune checkpoint inhibitor (ICI) or dual ICI therapy with nivolumab and ipilimumab (nivo + ipi) is the standard first-line treatment for patients with advanced esophageal squamous cell carcinoma (ESCC). First-line immunotherapy is effective and safe for the treatment of patients with ESCC. Rapid and deep tumor shrinkage may serve as an early predictive biomarker for longer survival.

P=N/A, N=1197, Completed, Fudan University | Active, not recruiting --> Completed | N=600 --> 1197 | Trial completion date: Dec 2024 --> Dec 2025

In conclusions, FRA inhibited ESCC cell growth and immune evasion by inactivating HIF-1α/STAT3/PD-L1 signaling in vitro and vivo. This study suggested that FRA may serve as a potential therapeutic agent for ESCC treatment.

Notably, CDK inhibitors markedly inhibit ESCC cell proliferation. This research delineates the potential cellular origins of ESCC and their key regulons, thereby pioneering a single-cell-derived therapeutic strategy that exposes vulnerabilities in tumor-initiating cells.

Despite these developments, the clinical translation of multi-omics findings remains limited due to the lack of standardized analytical pipelines, insufficient multi-center validation, and the high cost and technical complexity of integrating multi-omics data into routine clinical workflows. Future research integrating artificial intelligence with multi-omics data holds promise for enhancing diagnostic accuracy and enabling more precise therapeutic decision-making in ESCC.