Background/Objectives: Oral leukoplakia (OL) is a prevalent oral potentially malignant disorder. Despite its clinical relevance, the molecular basis of its progression to malignancy is not yet fully elucidated. This scoping review of systematic reviews and meta-analyses aimed to synthesize current knowledge and evidence gaps regarding the implications of hallmarks of cancer expression in OL malignant transformation. Methods: A systematic search was conducted in MEDLINE, Embase, DARE, and the Cochrane Library to identify systematic reviews (with or without meta-analysis) published up to April-2025. Results: Twenty-two systematic reviews were included. The most frequently explored hallmark was activation of invasion and metastasis (n = 12; 32.40%), followed by tumor-promoting inflammation (n = 10; 27.03%), evasion of growth suppressors (n = 8; 21.60%), sustained proliferative signaling (n = 3; 8.10%), energy metabolism reprogramming (n = 2; 5.40%), replicative immortality (n = 1; 2.70%), and resistance to cell death (n = 1; 2.70%). No evidence was found for angiogenesis or immune evasion in OL. Conclusions: Available evidence indicates that OL may develop oncogenic mechanisms in early stages of oral oncogenesis, especially those related to sustained proliferation, evasion of growth suppressor signals, and cellular migration and invasion. Chronic inflammation also may facilitate the acquisition of other hallmarks throughout the multistep process of oral carcinogenesis. These findings also reveal evidence gaps in underexplored hallmarks of cancer, which highlights the need to expand future primary- and secondary-level investigations to better define the molecular mechanisms underlying OL malignant transformation.
背景/目的：口腔白斑是一种常见的口腔潜在恶性疾病。尽管其具有临床相关性，但其向恶性转化的分子基础尚未完全阐明。本范围综述旨在综合当前关于癌症标志物在口腔白斑恶性转化中作用的知识体系与证据缺口。方法：系统检索了MEDLINE、Embase、DARE和Cochrane图书馆数据库，纳入截至2025年4月发表的系统评价（含或不含荟萃分析）。结果：共纳入22篇系统评价。最常研究的癌症标志是侵袭与转移激活（12篇，占32.40%），其次是促瘤性炎症（10篇，27.03%）、生长抑制逃逸（8篇，21.60%）、持续增殖信号传导（3篇，8.10%）、能量代谢重编程（2篇，5.40%）、复制永生性（1篇，2.70%）和细胞死亡抵抗（1篇，2.70%）。未发现口腔白斑中存在血管生成或免疫逃逸的证据。结论：现有证据表明，口腔白斑可能在口腔癌发生的早期阶段就发展出致癌机制，特别是与持续增殖、生长抑制信号逃逸以及细胞迁移和侵袭相关的机制。慢性炎症也可能在口腔癌发生的多步骤过程中促进其他癌症标志的获得。这些发现同时揭示了在尚未充分研究的癌症标志领域存在证据缺口，凸显了未来需要加强基础研究与二次研究，以更明确地界定口腔白斑恶性转化的分子机制。
肿瘤(癌症)患者之家