权益分类	功能权益	普通用户	{{item.name}}会员
{{category.name}}	{{benefitItem.name}}

Clinical and Experimental Study of Production of Abnormal Prothrombin PIVKA-II in Hepatocellular Carcinoma.

肝细胞癌中凝血酶原 PIVKA-II 异常产生的临床和实验研究。

基本信息

批准号：
62570337
负责人：
OKUDA Hiroaki
金额：
$ 1.34万
依托单位：
Tokyo Women's Medical College
依托单位国家：
日本
项目类别：
Grant-in-Aid for General Scientific Research (C)
财政年份：
1987
资助国家：
日本
起止时间：
1987 至 1988
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-62570337/
关键词：
Hepatocellular carcinoma PIVKA-II Vit. K Hepatoma cell Prothrombin related antigen level F-II vit.K プロトロンビン前駆体プロトロンビン関連抗原

项目摘要

Fifty-nine percent of patients with hepatocellular carcinoma (HCC) had elevated plasma PIVKA-II levels. None of the cirrhotic patients had elevated pivka-ii levels. Thus PiVKA-II has a high specificity for HCC. There was no correlation between PICKA-II and AFP levels indicating that the combination of these 2 markers seems to be useful in the diagnosis of HCC. There was a correlation between tumor size and PIVKA-II levels in HCC. The half-life of PIVKA-II in HCC patients was 60 hr and was identical to that in vit. K deficiency patients, suggesting that PIVKA-II in HCC patients has the same vit. K sensitivity as that in vit. K deficiency patients. Thus it seems useful to follow HCC patients with PIVKA-II measurement after therapy for its half-life and reduction rate. PIVKA-II was detected in the cultures of 5 hepatoma cell lines and was not detected in non-hepatoma cell lines. There was a marked decrease of PIVKA-II with added vit.K.Thus PIVKA-II is produced by hepatoma cells and its production is dependent on the amount of vit. K available. Using hepatoma cell line huH-2, we found out that all 3 enzymes involved in the production of normal prothrombin, K-epoxide-reductase, K-reductase (vit. K cycle) and -glutamyl-carboxylase, functions in huH-2. The cancerous tissue of HCC patients positive for plasma PIVKA-II showed high PIVKA-II levels and the non-cancreous tissur showed low levels. Prothrombin related antigen levels F-II was higher in cancerous tissue than in non-cancerous tissue. The cancerous tissue of PIVKA-II positive HCC patients showed a more marked F-II staining than in PIVKA-II negative HCC patients. There was postitve PIVKA-II staining in the cancerous tissue of several HCC patients. Thus production of either PIVKA-II or F-II was suggested in hepatoma cell. Is was suggested that increased formation of F-II occurs in HCC, resulting in relative vit. K deficiency and appearance of PIVKA-II.

59%的肝细胞癌（HCC）患者血浆PIVKA-II水平升高。没有肝硬化患者出现pikv -ii水平升高。因此PiVKA-II对HCC具有高特异性。pica - ii和AFP水平之间没有相关性，这表明这两种标志物的结合在HCC的诊断中似乎是有用的。肝癌中PIVKA-II水平与肿瘤大小有相关性。PIVKA-II在HCC患者中的半衰期为60小时，与在肝细胞中的半衰期相同。提示PIVKA-II在HCC患者中具有相同的作用。K的灵敏度与vit的灵敏度相同。缺钾症患者。因此，在治疗后对HCC患者进行PIVKA-II测量以了解其半衰期和降低率似乎是有用的。PIVKA-II在5种肝癌细胞系中检测到，在非肝癌细胞系中未检测到。因此，PIVKA-II是由肝癌细胞产生的，其产生依赖于维生素k的量。K。利用肝癌细胞系hh -2，我们发现3种酶均参与正常凝血酶原、k -环氧化物还原酶、k -还原酶（vit）的生成。K循环)和-谷氨酰羧化酶，在huH-2中起作用。血浆PIVKA-II阳性的HCC患者癌组织PIVKA-II水平较高，非癌组织PIVKA-II水平较低。凝血酶原相关抗原F-II水平在癌组织中高于非癌组织。PIVKA-II阳性HCC患者癌组织的F-II染色比PIVKA-II阴性HCC患者更明显。几例HCC患者癌组织中可见PIVKA-II阳性染色。因此肝癌细胞中可能产生PIVKA-II或F-II。这表明，在HCC中，F-II的形成增加，导致相对的vit。钾缺乏和PIVKA-II的出现。