Esophageal Squamous Cell Carcinoma

P3, N=172, Not yet recruiting, Asan Medical Center | Initiation date: Jun 2025 --> Jan 2026

P1/2, N=45, Recruiting, West China Hospital | Not yet recruiting --> Recruiting | Trial completion date: Apr 2028 --> Sep 2028 | Initiation date: Apr 2025 --> Sep 2025 | Trial primary completion date: Apr 2027 --> Sep 2027

P1, N=31, Terminated, Shanghai Junshi Bioscience Co., Ltd. | N=198 --> 31 | Recruiting --> Terminated; The trial was stopped early on the initiative of the sponsor on the basis of a change in the research and development strategy without safety concerns

These findings provide critical insights into early tumorigenesis, highlighting the potential of precursor cells as biomarkers for early detection and therapeutic targets of esophageal squamous cell cancer. By elucidating the cellular dynamics underlying esophageal preneoplasia, this research lays the foundation for strategies to prevent malignant progression, offering broader implications for improving cancer diagnostics and treatment approaches.

While the correlation between treatment effects on PFS and OS was weak in ESCC, it was moderate in PD-L1-low GEA, and good in PD-L1-high GEA. Therefore, PFS is an adequate co-primary endpoint in future trials investigating novel ICIs-based regimens in GEA, especially if the analyses are pre-planned in PD-L1-high subgroups.

E2F7 promotes ESCC progression and cisplatin resistance by transcriptionally activating DVL3 and activating the Wnt signaling pathway. Targeting the E2F7-DVL3 axis may provide a promising therapeutic strategy for ESCC treatment.

Our findings suggest that IL-15 levels could serve as a biomarker for identifying ESCC patients who are likely to benefit from RT and IM. These results also provide a rationale for targeting IL-15 as a novel therapeutic strategy to enhance treatment outcomes for ESCC patients.

These results suggest that LCR functions as an independent prognostic parameter for postoperative ESCC, and that the combined nomogram model incorporating LCR and TNM staging may offer a refined tool for individualized clinical survival evaluation. The observed association between reduced LCR levels and both tumor progression and systemic inflammation implies potential therapeutic implications.

This study is the first to investigate postoperative survival and chemotherapy resistance based on genomic panel testing using PleSSision-160 for resectable ESCC. The findings suggested that high CNA status was a risk factor for long-term survival. Compared to previous genomic sequencing studies in ESCC, further investigation using PleSSision-160 appears to be a promising approach.

In conclusion, this study demonstrated that myxoid stroma in the invasive front of ESCC is closely associated with the density of CD3+ and CD8+ positive lymphocytes.

The combined use of palbociclib and PIK75 synergistically inhibited the expression of the cell cycle proteins CCNE1, CDC6, and CDC25A, as well as the abnormal activation of PIK3CA and AKT phosphorylation. The combination of these two drugs synergistically inhibited tumor cell cycle progression and promoted apoptosis in vitro and in vivo, which provides a promising idea for the treatment of ESCC in the future.

Intriguingly, administration of the histone deacetylase inhibitor trichostatin A resulted in the upregulation of CYP3A5 expression...Because ESCC develops, CYP3A5 suppression promotes tumor metastasis and invasion. CYP3A5 is a potential biomarker and therapeutic target for ESCC.