克洛诺吉斯·辛内西斯 (Clonorchis sinensis) 感染通过增强血管新生促进肝细胞癌的进展
Caibiao Wei1, Junxian Chen1, Qiuhai Yu1
1Department of Clinical Laboratory, Guangxi Medical University Cancer Hospital, Nanning, China.
PLoS neglected tropical diseases
|November 11, 2024
概括
克洛诺基斯·辛内斯感染通过促进血管生成,使肝癌的结果变得更糟. 这种寄生虫感染增加了微血管密度,并在肝细胞癌 (HCC) 患者中提高了血管生成相关的生物标志物.
科学领域:
- 肝病学 肝病学是一种肝病学.
- 在瘤学瘤学.
- 寄生虫学的寄生虫学
背景情况:
- 昆虫Clonorchis sinensis (C. sinensis) 感染与肝癌发生有关.
- 在肝细胞癌 (HCC) 进展中C. sinensis的确切作用尚未完全理解.
- 这项研究调查了C. sinensis对HCC血管生成的贡献.
研究的目的:
- 为了确定C. sinensis感染是否在HCK中促进血管生成.
- 评估C. sinensis感染对HCC患者存活率和微血管密度的影响.
- 分析与血管生成相关的基因和生物标志物的表达在HCC患者和没有C. sinensis感染.
主要方法:
- 根据C. sinensis感染状况分层的947名HCC患者的临床分析.
- 卡普兰-梅尔生存分析和总生存率 (OS) 和无复发生存率 (RFS) 的日志等级测试.
- CD34免疫组织化学检测微血管密度 (MVD),生物化学检测生物标志物,以及基因表达的qRT-PCR (CD34,Ang1,Ang2,VEGF,PDGF).
主要成果:
- 菌感染与明显较差的OS (p=0.014) 和RFS (p<0.001) 相关.
- 在C. sinensis (+) HCC患者中观察到MVD增加 (p=0.041) 和循环血管生成生物标志物 (MONO,EOSO,C3,FIB,PLT,LDH,GLDH) 的升高.
- 在患有C. sinensis感染的患者的HCC组织中检测到血管生成相关基因的过度表达.
结论:
- 菌感染与HCC患者的治疗结果较差有关.
- 寄生虫通过增加MVD和相关生物标志物和基因表达来促进HCC中的血管生成.
- 菌感染可能通过炎症反应和代谢重编程增强HCC恶性病变.
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