寄生虫感染和致癌:分子机制,免疫调节和新兴治疗策略
Marta Pawłowska1, Dorian Jarek2, Jan Milanowski2
1Department of Medical Biology and Biochemistry, Faculty of Medicine, Ludwik Rydygier Collegium Medicum in Bydgoszcz, Nicolaus Copernicus University in Toruń, 24 Karłowicza St., Bydgoszcz, 85-092, Poland.
Oncology research
|January 30, 2026
概括
慢性寄生虫感染通过引起炎症和改变瘤环境,导致癌症. 本综述探讨了感染相关癌症的机制和新疗法.
科学领域:
- 整合了寄生虫学,分子瘤学,免疫学和微生物组研究.
- 专注于与感染相关的恶性瘤和瘤发生.
背景情况:
- 寄生虫感染越来越多地与癌症的发展有关.
- 致癌机制尚未完全理解,但涉及慢性炎症,免疫调节和寄生虫外体.
- 选择的寄生虫包括 * Schistosoma haematobium * * Opisthorchis viverrini * * Toxoplasma gondii * * Plasmodium falciparum * * 和 * Leishmania * spp.
研究的目的:
- 综合当前关于寄生虫如何导致癌症发展的知识.
- 突出新兴的治疗和诊断机会.
- 整合寄生虫学和癌症生物学,以了解感染相关的恶性瘤.
主要方法:
- 在PubMed,Scopus和Web of Science索引的文献的叙事综述,截至2025年7月.
- 检查寄生虫在慢性炎症,免疫调节和瘤微环境中的作用.
- 探索寄生虫诱导的免疫抑制,共感染,以及它们对癌症风险的影响.
主要成果:
- 寄生虫通过持续的炎症,放松调节的途径,基因组不稳定性和外体驱动瘤发生.
- 寄生虫调节免疫反应,与与瘤相关的免疫细胞相互作用.
- 新的治疗方法包括途径抑制剂,表观遗传药物,微生物组调制和工程寄生虫.
结论:
- 了解寄生虫与癌症的联系需要将寄生虫学和瘤学整合起来.
- 未来的研究应该专注于基于寄生虫的免疫疗法,表观遗传效应和人工智能驱动的多组学.
- 进展为生物标志物,向疗法和感染诱导的瘤发生机制提供了新的见解.
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