Afzal Hadiya, Shaukat Ayesha, Ul Haq Muhammad Zain, Khaliq Nawal, Zahid Maha, Shakeel Laiba, Wasay Zuberi Muhammad Abdul, Akilimali Aymar
Department of Internal Medicine, Dow University of Health Sciences, Karachi, Pakistan.
Department of Research, Medical Research Circle (MedReC), Goma, Democratic Republic of the Congo.
Ann Med Surg (Lond). 2024 Dec 19;87(2):583-597. doi: 10.1097/MS9.0000000000002977. eCollection 2025 Feb.
Chronic gastritis (CG), particularly when associated with () infection, is a significant precursor to gastric cancer (GC), a leading cause of cancer-related deaths worldwide. The persistent inflammation in CG, driven by factors such as , induces oxidative stress and DNA damage in gastric epithelial cells, which can lead to malignant transformation. Atrophic gastritis, a form of CG, can be categorized into autoimmune and -associated types, both of which increase the risk of GC development, particularly when compounded by external factors like smoking and dietary habits. This manuscript explores the pathophysiological mechanisms underlying CG and its progression to GC, highlighting the critical role of metabolomics in advancing our understanding of these processes. Metabolomics, the comprehensive study of metabolites, offers a novel approach to identifying biomarkers that could facilitate early detection and improve the accuracy of GC diagnosis and prognosis. The analysis of metabolic alterations, particularly in glucose, lipid, and amino acid metabolism, reveals distinct biochemical pathways associated with the progression from benign gastritis to malignancy. Integrating metabolomic profiling with traditional diagnostic methods can revolutionize GC management, enabling more personalized treatment strategies and improving clinical outcomes. However, significant challenges remain, including the need to validate biomarkers across diverse populations and standardize metabolomic techniques. Future research should address these challenges to fully realize the potential of metabolomics in early GC detection and treatment, ultimately aiming to reduce the global burden of this deadly disease.
慢性胃炎(CG),尤其是与()感染相关时,是胃癌(GC)的重要前驱病变,胃癌是全球癌症相关死亡的主要原因。CG中的持续性炎症由诸如等因素驱动,可诱导胃上皮细胞产生氧化应激和DNA损伤,进而导致恶性转化。萎缩性胃炎作为CG的一种形式,可分为自身免疫性和相关性类型,这两种类型都会增加GC发生的风险,尤其是当与吸烟和饮食习惯等外部因素共同作用时。本手稿探讨了CG及其向GC进展的病理生理机制,强调了代谢组学在推进我们对这些过程理解方面的关键作用。代谢组学是对代谢物的全面研究,它提供了一种新方法来识别生物标志物,这些生物标志物有助于早期检测并提高GC诊断和预后的准确性。对代谢改变的分析,特别是在葡萄糖、脂质和氨基酸代谢方面,揭示了与从良性胃炎进展到恶性肿瘤相关的独特生化途径。将代谢组学分析与传统诊断方法相结合可以彻底改变GC的管理,实现更个性化的治疗策略并改善临床结果。然而,重大挑战仍然存在,包括需要在不同人群中验证生物标志物以及使代谢组学技术标准化。未来的研究应应对这些挑战,以充分实现代谢组学在早期GC检测和治疗中的潜力,最终目标是减轻这种致命疾病的全球负担。