长期饮酒引发食道癌的分子机制

Huai Yi Chen, Chia Rou Por, Yong Kai Hong, Eason Qi Zheng Kong, Vetriselvan Subramaniyan
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摘要

本文综述了酒精诱导食管癌发生的机制,包括DNA损伤、氧化应激和营养缺乏。酒精代谢主要涉及酒精脱氢酶(ADH)将乙醇转化为乙醛,这会导致DNA损伤,抑制修复机制,形成DNA加合物,从而抑制DNA复制。此外,它还深入研究了与酒精相关的食道癌相关的流行病学证据、遗传易感性、表观遗传修饰、生物标志物和预防策略。饮酒会增加胃食管反流病的风险,从而损害食管粘膜的完整性,因为IL-18、TNFA、GATA3、TLR4和CD68等细胞因子的失调会扩大上皮细胞的细胞间隙。遗传变异,如ADH1B rs1229984和ALDH2 rs671,显著影响酒精相关食管癌的易感性,这些变异影响乙醛代谢和癌症风险。了解这些因素对于早期发现、有效治疗和制定有针对性的预防策略至关重要。生物标记物,如miRNA和代谢物标记物,为早期检测提供了非侵入性方法,而先进的内窥镜技术提供了更好的诊断准确性。药物干预,如他汀类药物和质子泵抑制剂,也显示出在高危人群中减少癌症进展的潜力。尽管取得了进展,但晚期食管癌诊断仍然很常见,这突出了更好的筛查和预防的必要性。包括本研究在内的进一步研究应致力于改善早期发现,个性化预防,并探索新的治疗方法,以减少酒精相关食管癌的病例并提高预后。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

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Molecular mechanisms underlying oesophageal cancer development triggered by chronic alcohol consumption

This review explores the mechanisms underlying alcohol-induced oesophageal carcinogenesis, including DNA damage, oxidative stress, and nutritional deficiencies. Alcohol metabolism primarily involves alcohol dehydrogenase (ADH) converting ethanol to acetaldehyde, which can cause DNA damage, inhibit repair mechanisms, and form DNA adducts thus inhibiting DNA replication. Plus, it delves into the epidemiological evidence, genetic susceptibility, epigenetic modifications, biomarkers, and preventive strategies associated with alcohol-related oesophageal cancers. Consumption of alcohol increases the risk of gastroesophageal reflux disease thus compromising mucosal integrity of the oesophagus as dysregulation of cytokines such as IL-18, TNFA, GATA3, TLR4, and CD68 expands the intercellular spaces of epithelial cells. Genetic variants, such as ADH1B rs1229984 and ALDH2 rs671, significantly influence susceptibility to alcohol-related oesophageal cancers, with these variations affecting acetaldehyde metabolism and cancer risk. Understanding these factors is crucial for early detection, effective treatment, and the development of targeted prevention strategies. Biomarkers, such as miRNA and metabolite markers, offer non-invasive methods for early detection, while advanced endoscopic techniques provide better diagnostic accuracy. Pharmacological interventions, such as statins and proton pump inhibitors, also show potential for reducing cancer progression in high-risk individuals. Despite advances, late-stage oesophageal cancer diagnoses are still common, highlighting the need for better screening and prevention. Further research, including this study, should aim to improve early detection, personalise prevention, and explore new treatments to reduce cases and enhance outcomes in alcohol-related oesophageal cancers.

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