Cai YR, Gong L, Teng XY, Zhang HT, Wang CF, Wei GL, Guo L, Ding F, Liu ZH, Pan QJ, Su Q. Clonality and allelotype analyses of focal nodular hyperplasia compared with hepatocellular adenoma and carcinoma. World J Gastroenterol 2009; 15(37): 4695-4708 [PMID: 19787833 DOI: 10.3748/wjg.15.4695]
Corresponding Author of This Article
Qin Su, Professor, Department of Pathology, Cancer Institute and Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Panjiayuan Nanli 17, Beijing 100021, China. q.su@wjgnet.com
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World J Gastroenterol. Oct 7, 2009; 15(37): 4695-4708 Published online Oct 7, 2009. doi: 10.3748/wjg.15.4695
Clonality and allelotype analyses of focal nodular hyperplasia compared with hepatocellular adenoma and carcinoma
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
Yi-Ran Cai, Xiao-Ying Teng, Hong-Tu Zhang, Guo-Lian Wei, Lei Guo, Qin-Jing Pan, Qin Su, Department of Pathology, Cancer Institute and Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Panjiayuan Nanli 17, Beijing 100021, China
Li Gong, Department of Pathology, Tangdu Hospital, the Fourth Military Medical University, Xi’an 710038, Shaanxi Province, China
Cheng-Feng Wang, Department of Abdominal Surgery, Cancer Institute and Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100021, China
Fang Ding, Zhi-Hua Liu, State Key Laboratory of Molecular Oncology, Cancer Institute, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100021, China
Author contributions: Cai YR, Teng XY and Gong L performed the majority of experiments and participated in the manuscript preparation; Wei GL, Guo L and Ding F carried out some of the experiments; Wang CF, Liu ZH and Pan QJ provided valuable materials and performed data evaluation; Su Q designed the study and wrote the manuscript.
Supported by The National Natural Science Foundation of China (NSFC), Grants 30171052, 30572125 and 30772508 and the CAMS Cancer Hospital Clinical Research Project LC2007A21
Correspondence to: Qin Su, Professor, Department of Pathology, Cancer Institute and Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Panjiayuan Nanli 17, Beijing 100021, China. q.su@wjgnet.com
Telephone: +86-10-87787508 Fax: +86-10-67713359
Received: July 7, 2009 Revised: August 17, 2009 Accepted: August 24, 2009 Published online: October 7, 2009
Abstract
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 alterations.
RESULTS: 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%). Monoclonality 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.
