生物谷报道：日前，第四军医大学西京医院普三科的研究人员在研究中发现，肝癌的发生与抑癌基因PTEN低表达有关，为今后进一步对PTEN在人肝癌细胞中的研究奠定了基础。
PTEN基因是定位于人体第10q23染色体上的肿瘤抑制基因。为了探讨PTEN表达与肝癌发生、发展的关系，西京医院普三科的研究人员应用免疫组织化学技术，检测PTEN蛋白在63例肝癌组织、14例肝硬化组织和8例正常肝组织中的表达情况，以观察该基因与肝癌转移和预后的关系。
研究发现，肝癌中PTEN表达阴性率为30.16％（19/63），显著高于正常肝组织0（0/8）和肝硬化组织7.15％（1/14）。随着恶性程度的增高，PTEN表达阴性率随之增加。PTEN表达阴性与是否转移及预后显著相关。结果表明，抑癌基因PTEN低表达多见于肝癌进展期，并与肝癌是否转移以及临床预后相关。
最新国外也有研究表明，SMAD4和PTEN两个基因在肝癌的起始中起决定性作用。刚刚出版的著名临床杂志JCI报道了这一信息。这一研究与中国国内的研究基本相似，这一研究为将来预防和治疗肝癌提供重要的理论依据。英文的信息如下：
Cholangiocellular carcinoma (CC) is the second most common type of primary liver cancer and is associated with a poor prognosis. It has been previously demonstrated that CCs possess alterations of a number of tumor-suppressor genes and oncogenes, however the key events that induce tumor formation have remained unclear. In a study appearing online in June in advance of print publication in the July issue of the Journal of Clinical Investigation, Chu-Xia Deng and colleagues from the NIH, generated a line of mice that develop CC by specifically disrupting expression of the tumor suppressor genes SMAD4 and PTEN in the livers of these mice. Tumors formed in the bile ducts of these animals by 4-7 months of age. The authors show that SMAD4 and PTEN regulate each others' activity in order to balance their expression and repress CC formation. The authors also examined human CC specimens and found that PTEN was inactivated in the majority of cases, and SMAD4 expression was lost in about half of the tumors examined. The results of this study help us understand the relationship between SMAD4 and PTEN and extend our understanding of CC formation.
TITLE: Induction of intrahepatic cholangiocellular carcinoma by liver-specific disruption of Smad4 and Pten mice
AUTHOR CONTACT:
Chu-Xia Deng
National Institutes of Health, Bethesda, Maryland, USA.
View the PDF of this article at: http://https://www.the-jci.org/article.php?id=27282
Contact: Brooke Grindlinger
Journal of Clinical Investigation
