时间标签：数据日期 2026-10-31 · 生成时间 2026-11-01 05:30（Asia/Shanghai）｜ 检索窗口 PubMed edat 2026/10/28–2026/10/31 ｜ 情报发生日期 2026-10-31
研究问题
However, acquired resistance to bevacizumab remains a critical clinical challenge [].；However, the molecular mechanism by which ESM1 orchestrates lactate-mediated transcriptional regulation of downstream genes in the hypoxic OC microenvironment remains incompletely understood.
方法
Moreover, 34 patients received first-line systemic therapy combining bevacizumab (15 mg/kg, intravenous infusion, every 3 weeks) with chemotherapy following disease progression.；Tumor response was evaluated at baseline and every 6 weeks thereafter using computed tomography (CT) or magnetic resonance imaging (MRI) of the abdomen, pelvis, and chest, in accordance with the Response Evaluation Criteria in Solid Tumors (RECIST) version 1.1.；Overall survival (OS) was defined as the time from the date of surgery to the date of death from any cause (or censored at the last follow-up).；This study was approved by the Institutional Review Board of The Affiliated Zhuzhou Hospital of Xiangya Medical School (Zhuzhou, China; Approval No.
核心结论
ELISA analysis revealed significantly elevated lactate levels in recurrent OC tissues compared to treatment-sensitive cases (Fig.；A), suggesting enhanced glycolysis in bevacizumab-resistant tumors.；Comparative analysis further demonstrated significantly higher ESM1, pan-Kla, H4K8la and VE-cad (Endothelial marker) levels in bevacizumab resistant versus sensitive patients (Fig. ‖ 结论：In conclusion, our findings demonstrate that in OC cells treated with bevacizumab, ESM1-mediated histone H4K8 lactylation enhances ERBB2 transcription.
局限
We acknowledge there are limitations in this study.；Furthermore, this study has certain limitations.；Therefore, definitively determining whether platinum resistance is a key mediator of bevacizumab resistance warrants significant attention in future investigations.
对本项目的价值
★☆☆☆☆ 相关范围内，作为背景与横向对照收录。
全文来源
PMC JATS 全文（正文 45,595 字符，已过标题/DOI 逐字归属校验）
原文题录
- 英文标题：ESM1 drives H4K8 lactylation to promote vasculogenic mimicry and bevacizumab resistance in ovarian cancer.
- 期刊与标识：Cell Commun Signal · PMID 42947152 · DOI 10.1186/s12964-026-03071-z
A 级证据分级：A 级（同行评议人体研究）
本文属人体研究证据，但需注意：观察性或小样本干预的结论不等于已证实临床获益；效应量与长期安全性仍需更大规模、更长随访的试验验证。
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