We aimed to qualitatively and quantitatively analyze, through a systematic review and meta-analysis, the current evidence on the differential expression of the hallmarks of cancer in oral lichen planus (OLP) samples, in order to know the earliest molecular mechanisms that could be involved in the malignant transformation of this oral potentially malignant disorder. We searched MEDLINE/PubMed, Embase, Web of Science, and Scopus for studies published before November 2023. We evaluated the methodological quality of studies and carried out meta-analyses to fulfill our objectives. Inclusion criteria were met by 110 primary-level studies, with 7065 OLP samples, in which the expression of 104 biomarkers were analyzed through immunohistochemistry. Most OLP samples showed sustained cell proliferation signaling (65.48%, 95%CI = 51.87–78.02), anti-apoptotic pathways (55.93%, 95%CI = 35.99–75.0), genome instability (48.44%, 95%CI = 13.54–84.19), and tumor-promoting inflammation events (83.10%, 95%CI = 73.93–90.74). Concurrently, OLP samples also harbored tumor growth suppressor mechanisms (64.00%, 95%CI = 53.27–74.12). In conclusion, current evidence indicates that molecular mechanisms promoting hyperproliferative signaling, an antiapoptotic state with genomic instability, and an escape of epithelial cells from immune destruction, are developed in LP-affected oral mucosa. It is plausible that these events are due to the actions exerted by the chronic inflammatory infiltrate. Malignant transformation appears to be prevented by tumor suppressor genes, which showed consistent upregulation in OLP samples.
本研究旨在通过系统综述和荟萃分析，对口腔扁平苔藓（OLP）样本中癌症标志物差异表达的现有证据进行定性和定量分析，以探究这一口腔潜在恶性病变发生恶变可能涉及的最早期分子机制。我们检索了截至2023年11月前发表于MEDLINE/PubMed、Embase、Web of Science和Scopus数据库的相关研究，评估了研究方法学质量，并通过荟萃分析实现研究目标。最终纳入110项原始研究，共涉及7065例OLP样本，通过免疫组化技术分析了104种生物标志物的表达情况。结果显示：多数OLP样本存在持续细胞增殖信号（65.48%，95%CI=51.87–78.02）、抗凋亡通路（55.93%，95%CI=35.99–75.0）、基因组不稳定性（48.44%，95%CI=13.54–84.19）及促瘤炎症事件（83.10%，95%CI=73.93–90.74）。同时，OLP样本中也存在肿瘤生长抑制机制（64.00%，95%CI=53.27–74.12）。结论表明，现有证据提示在受累口腔黏膜中已形成促进过度增殖信号、伴随基因组不稳定的抗凋亡状态以及上皮细胞逃避免疫破坏的分子机制，这些事件很可能源于慢性炎症浸润的作用。而抑癌基因在OLP样本中持续上调表达，可能对恶变过程起到抑制作用。
肿瘤(癌症)患者之家