Clonality and allelotype analyses of focal nodular hyperplasia compared with hepatocellular adenoma and carcinoma

作     者：Yi-Ran Cai Li Gong Xiao-Ying Teng Hong-Tu Zhang Cheng-Feng Wang Guo-Lian Wei Lei Guo Fang Ding Zhi-Hua Liu Qin-Jing Pan Qin Su 

作者机构：Department of PathologyCancer Institute and Cancer Hospital Chinese Academy ofMedical Sciences and Peking Union Medical College PanjiayuanNanli 17 Beijing 100021 China Department of Pathology Tangdu Hospital the FourthMilitary Medical University Xi'an 710038 Shaanxi ProvinceChina Department of Abdominal Surgery CancerInstitute and Cancer Hospital Chinese Academy of MedicalSciences and Peking Union Medical College Beijing 100021China State Key Laboratory of Molecular Oncology Cancer Institute Chinese Academy of MedicalSciences and Peking Union Medical College Beijing 100021China 

出 版 物：《World Journal of Gastroenterology》 (世界胃肠病学杂志（英文版）)

年 卷 期：2009年第15卷第37期

页      面：4695-4708页

核心收录：

学科分类：0710[理学-生物学] 090603[农学-临床兽医学] 1002[医学-临床医学] 07[理学] 08[工学] 09[农学] 0906[农学-兽医学] 071007[理学-遗传学] 0901[农学-作物学] 0836[工学-生物工程] 090102[农学-作物遗传育种] 

基　　金：Supported by The National Natural Science Foundation of China (NSFC), Grants 30171052, 30572125 and 30772508 the CAMS Cancer Hospital Clinical Research Project LC2007A21 

主　　题：Clonality analysis Focal nodular hyperplasia Hepatocellular adenoma Liver tumorigenesis Loss of heterozygosity Nodules of altered hepatocytes 

摘      要：AIM： To identify clonality and genetic alterations in focal nodular hyperplasia （FNH） and the nodules derived from it. METHODS： Twelve FNH lesions were examined. Twelve hepatocellular adenomas （HCAs） and 22 hepatocellular carcinomas （HCCs） were used as references. Nodules of different types were identified and isolated from FNH by microdissection. An X-chromosome inactivation assay was employed to describe their clonality status. Loss of heterozygosity （LOH） was detected, using 57 markers, for genetic ***： Nodules of altered hepatocytes （NAH）, the putative precursors of HCA and HCC, were found in all the FNH lesions. Polyclonality was revealed in 10 FNH lesions from female patients, and LOH was not detected in any of the six FNH lesions examined, the results apparently showing their polyclonal nature. In contrast, monoclonality was demonstrated in all the eight HCAs and in four of the HCCs from females, and allelic imbalances were found in the HCAs （9/9） and HCCs （15/18）, with chromosomal arms 11p, 13q and 17p affected in the former, and 6q, 8p, 11p, 16q and 17p affected in the latter lesions in high frequencies （≥ 30%）. Monodonality was revealed in 21 （40%） of the 52 microdissected NAH, but was not found in any of the five ordinary nodules. LOH was found in all of the 13 NAH tested, being highly frequent at six loci on 8p, 11p, 13q and 17p. CONCLUSION： FNH, as a whole, is polyclonal, but some of the NAH lesions derived from it are already neoplastic and harbor similar allelic imbalances as HCAs.