中文English
ISSN 1001-5256 (Print)
ISSN 2097-3497 (Online)
CN 22-1108/R
Issue 11
Nov.  2013
Turn off MathJax
Article Contents

Hepatocellular adenoma: new understandings of molecular pathology and novel model of clinical diagnosis and therapy

DOI: 10.3969/j.issn.1001-5256.2013.11.001
Research funding:

 

  • Received Date: 2013-07-30
  • Published Date: 2013-11-20
  • Hepatocellular adenoma ( HCA) is the most common benign hepatocellular tumor, and its causes remain unclear. In Western countries, HCA is usually seen in the women of reproductive age who have a history of long- term use of oral contraceptives ( OCs) . In the latest 2010 WHO Histological Classification of Hepatobiliary Tumors, which is mainly based on the research results in European countries, it is proposed that HCA is classified into four molecular subtypes, i. e., type I: HNF1α- inactivated HCA; type II: β- catenin- activated HCA; type III: inflammatory HCA; type IV: unclassified HCA. The research progress in the molecular pathology of HCA in foreign countries is reviewed. In addition, the main results of a recent study of 189 patients with HCA who underwent hepatectomy in our hospital are outlined. It was shown that 70% of HCA patients were middle- aged men, and 50% were overweight or obese; even female patients seldom had a history of long- term use of OCs. The gene sequencing showed that the mutational hotspots and frequency of HNF1α in this group of HCA patients were significantly different from those reported in European countries, and no β- catenin and gp130 mutations were found.Therefore, based on the above results, it is considered that the population and pathogenesis of HCA are different in China than in European countries. In light of the reports of malignant transformation of HCA in literature, a feasibility study is conducted to assess the risk of malignant transformation of HCA by detecting the microsatellite instability or loss of heterozygosity, which may provide a molecular pathological basis for developing individualized treatment strategies.

     

  • loading
  • [1]BIOLAC-SAGE P, BALABAUD C, WANLESS I.Focal nodular hyperplasia and hepatocellular adenoma[M]//BOSMAN FT, CARNEIRO F, HRUBAN RH, et al.World Health Organization classification of tumours of the digestive system.Lyon:IARC Press, 2010:198-204.[2]ROOKS JB, ORY HW, ISHAK KG, et al.Epidemiology of hepatocellular adenoma.The role of oral contraceptive use[J].JAMA, 1979, 242 (7) :644-648.[3]van AALTEN SM, TERKIVATAN T, de MAN RA, et al.Diagnosis and treatment of hepatocellular adenoma in the Netherlands:similarities and differences[J].Dig Surg, 2010, 27 (1) :61-67.[4]LIN H, van den ESSCHERT J, LIU C, et al.Systematic review of hepatocellular adenoma in China and other regions[J].J Gastroenterol Hepatol, 2011, 26 (1) :28-35.[5]CONG WM.Hepatocellular adenocarcinoma[M]//CONG WM, ZHU SN.Diagnostic surgical pathology of hepatobiliary tumors.Shanghai:Shanghai Scientific Technological Education Publishing House, 2011:79-87. (in Chinese) 丛文铭.肝细胞腺瘤[M]//丛文铭, 朱世能.肝胆肿瘤诊断外科病理学.上海:上海科技教育出版社, 2001:79-87.[6]BIOULAC-SAGE P, REBOUISSOU S, THOMAS C, et al.Hepatocellular adenoma subtype classification using molecular markers and immunohistochemistry[J].Hepatology, 2007, 46 (3) :740-748.[7]JEANNOT E, POGRIBNY IP, BELAND FA, et al.Chronic administration of ethanol leads to an increased incidence of hepatocellular adenoma by promoting H-ras-mutated cells[J].Cancer Lett, 2011, 301 (2) :161-167.[8]JEANNOT E, MELLOTTEE L, BIOULAC-SAGE P, et al.Spectrum of HNF1A somatic mutations in hepatocellular adenoma differs from that in patients with MODY3 and suggests genotoxic damage[J].Diabetes, 2010, 59 (7) :1836-1844.[9]REZNIK Y.Hepatocyte nuclear factor-1 gene inactivation:cosegregation between liver adenomatosis and diabetes phenotypes in two maturity-onset diabetes of the young (MODY) 3 families[J].J Clin Endocrinol Metab, 2004, 89 (3) :1476-1480.[10]KISHNANI PS, CHUANG TP, BALI D, et al.Chromosomal and genetic alterations in human hepatocellular adenomas associated with type Ia glycogen storage disease[J].Hum Mol Genet, 2009, 18 (24) :4781-4790.[11]BIOULAC-SAGE P, TAOUJI S, POSSENTI L, et al.Hepatocellular adenoma subtypes:the impact of overweight and obesity[J].Liver Int, 2012, 32 (8) :1217-1221.[12]CHANG CY, HERNANDEZ-PRERA JC, ROAYAIE S, et al.Changing epidemiology of hepatocellular adenoma in the United States:review of the literature[J].Int J Hepatol, 2013, 2013:604860.[13]BUNCHORNTAVAKUL C, BAHIRWANI R, DRAZEK D, et al.Clinical features and natural history of hepatocellular adenomas:the impact of obesity[J].Aliment Pharmacol Ther, 2011, 34 (6) :664-674.[14]PARADIS V, CHAMPAULT A, RONOT M, et al.Telangiectatic adenoma:an entity associated with increased body mass index and inflammation[J].Hepatology, 2007, 46 (1) :140-146.[15]STARLEY BQ, CALCAGNO CJ, HARRISON SA.Nonalcoholic fatty liver disease and hepatocellular carcinoma:a weighty connection[J].Hepatology, 2010, 51 (5) :1820-1832.[16]WAKE DJ, STRAND M, RASK E, et al.Intra-adipose sex steroid metabolism and body fat distribution in idiopathic human obesity[J].Clin Endocrinol (Oxf) , 2007, 66 (3) :440-446.[17]SASAKI M, YONEDA N, KITAMURA S, et al.Characterization of hepatocellular adenoma based on the phenotypic classification:The Kanazawa experience[J].Hepatol Res, 2011, 41 (10) :982-988.[18]ZUCMAN-ROSSI J, JEANNOT E, NHIEU JT, et al.Genotypephenotype correlation in hepatocellular adenoma:new classification and relationship with HCC[J].Hepatology, 2006, 43 (3) :515-524.[19]BIOULAC-SAGE P, BALABAUD C, ZUCMAN-ROSSI J.Subtype classification of hepatocellular adenoma[J].Dig Surg, 2010, 27 (1) :39-45.[20]MICCHELLI ST, VIVEKANANDAN P, BOITNOTT JK, et al.Malignant transformation of hepatic adenomas[J].Mod Pathol, 2008, 21 (4) :491-497.[21]REBOUISSOU S, AMESSOU M, COUCHY G, et al.Frequent inframe somatic deletions activate gp130 in inflammatory hepatocellular tumours[J].Nature, 2009, 457 (7226) :200-204.[22]PAN J, CONG WM.Analysis on loss of heterozygosity of four tumor suppressor genes in hepatocellular adenoma[J].J Clin Exp Pathol, 2003, 19 (5) :481-483. (in Chinese) 潘晶, 丛文铭.肝细胞腺瘤肿瘤抑制基因杂合性缺失分析[J].临床与实验病理学杂志, 2003, 19 (5) :481-483.[23]NAULT JC, BIOULAC-SAGE P, ZUCMAN-ROSSI J.Hepatocellular benign tumors-from molecular classification to personalized clinical care[J].Gastroenterology, 2013, 144 (5) :888-902.
  • 加载中

Catalog

    通讯作者: 陈斌, bchen63@163.com
    • 1. 

      沈阳化工大学材料科学与工程学院 沈阳 110142

    1. 本站搜索
    2. 百度学术搜索
    3. 万方数据库搜索
    4. CNKI搜索

    Article Metrics

    Article views (233) PDF downloads(120) Cited by()
    Proportional views
    Related

    /

    DownLoad:  Full-Size Img  PowerPoint
    Return
    Return