Quantitative analysis using ELISA of vascular endothelial growth factor and basic fibroblast growth factor in human colorectal cancer,liver metastasis of colorectal cancer and hepatocellular carcinoma

TO THE EDITOR Angiogenesis consists of the sprouting of capillaries from pre-existing vessels . It is well-known that tumor growth is angiogenesis-dependent. Vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) stimulated vascular endothelial cell proliferation and are involved in the neoplastic angiogenesis of several types of tumors including those of the intestinal tract.Authors usually investigated VEGF and bFGF protein expressions using immunohistochemistry or Western blotting and VEGF and bFGF transcripts using reverse transcriptase polymerase chain reaction (RT-PCR). We recently reported in a previous issue of the World Journal of Gastroenterology that cirrhotic liver tissue levels of these two

VEGF in hepatocellular carcinoma and surrounding cirrhotic liver tissues

TO THE EDITORWe read with a great interest the recent work of Deli andcolleagues. in the World Journal of Gastroenterology reportingvascular endothelial growth factor (VEGF) expressionin hepatocellular carcinoma (HCC) and cirrhotic livertissues. This well-documented work shows that VEGFwas significantly higher in surrounding cirrhotic livertissues than in HCC. Authors assessed VEGF expressionusing immunohistochemistry.The

Prokineticin 2/Bv8 is expressed in Kupffer cells in liver and is down regulated in human hepatocellular carcinoma

AIM: To study the implication of prokineticin 1 (PK1/EG- VEGF) and prokineticin 2 (PK2/Bv8) in hepatocellular carcinoma angiogenesis. METHODS: The gene induction of PK1/EG-VEGF and PK2/Bv8 was investigated in 10 normal, 28 fibrotic and 28 tumoral livers by using real time PCR. Their expression was compared to the expression of VEGF (an angiogenesis marker), vWF (an endothelial cell marker) and to CD68 (a monocyte/macrophage marker). Furthermore, the mRNA levels of PK1/EG-VEGF, PK2/Bv8, prokineticin receptor 1 and 2 were evaluated by real time PCR in isolated liver cell populations. Finally, PK2/Bv8 protein was detected in normal liver paraffin sections and in isolated liver cells by immunohistochemistry and immunocytochemistry. RESULTS: PK2/Bv8 mRNA but not PK1/EG-VEGF was expressed in all types of normal liver samples examined. In the context of liver tumor development, we reported that PK2/Bv8 correlates only with CD68 and showed a significant decrease in expression as the pathology evolves towards cancer. Whereas, VEGF and vWF mRNA were significantly upregulated in both fibrosis and HCC,as expected. In addition, out of all isolated liver cells examined, only Kupffer cells (liver resident macrophages) express significant levels of PK2/Bv8 and its receptors, prokineticin receptor 1 and 2. CONCLUSION: In normal liver PK2/Bv8 and its receptors were specifically expressed by Kupffer cells. PK2/Bv8 expression decreased as the liver evolves towards cancer and did not correlate with HCC angiogenesis.

Platelet-activating factor in cirrhotic liver and hepatocellular carcinoma

瞄准：激活血小板的因素(PAF ) 是一个支持 inflammatory 和 angiogenic 类脂化合物调停人。这里，我们试图调查 PAF 的层次， lyso-PAF ( PAF 先锋)，磷脂酶 A ( 2 )( PLA ( 2 )，产生 lyso-PAF 的酶的活动)， acetylhydrolase 活动(啊哈， PAF 降级的酶)并且在硬变肝和肝细胞癌( HCC )的 PAF 受体( PAF-R )抄本。方法：有 HCC 的 29 个病人在这研究被注册。肝硬化在十四个病人是在场的，七没有肝疾病。织物 PAF 层次被血小板聚集试金调查。Lyso-PAF 在它的化学乙酰化作用以后被估计进 PAF。啊哈被降级决定[(3 ) H ]-PAF。PLA (2 ) 层次被 EIA 估计。PAF-R 抄本用 RT-PCR 被调查。结果：PAF 和 PAF-R 抄本的提高的数量(白血球类型) 1 作为与非肝脏硬化症的相比在肝脏硬化症的纸巾被发现。PAF 和 PAF-R 抄本的更高的数量(织物类型) 1 和 2 作为与非肿瘤纸巾相比在 HCC 纸巾被发现。PLA (2 ) ， lyso-PAF 和啊哈层次没在肝脏硬化症的纸巾和 HCC 被改变。结论：当 PAF 的角色在肝生理学当前是未知的时，这研究在在 HCC 期间在硬变肝并且在 angiogenic 反应发现的煽动性的网络建议它的潜在的参与。