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type=\u0022text\/css\u0022 rel=\u0022stylesheet\u0022 href=\u0022\/\/d282kpwvnogo5m.cloudfront.net\/sites\/default\/files\/advagg_css\/css__ce2QY63WIanKyr8eSq7eavr1XQRRmFD6ZSmwpyJi8lM__zXwFqpqmxrZOXXcd_TpBQpjuELbmIP9wBR5UuTDWAO4__YJWWMMdfCJuAFm5cUEp88OsodhO3ZA-2lzRfoBsSlk4.css\u0022 media=\u0022all\u0022 \/\u003E\n\u003Clink rel=\u0027stylesheet\u0027 type=\u0027text\/css\u0027 href=\u0027\/sites\/all\/modules\/contrib\/panels\/plugins\/layouts\/onecol\/onecol.css\u0027 \/\u003E\u003C\/head\u003E\u003Cbody\u003E\u003Cdiv class=\u0022panels-ajax-tab-panel panels-ajax-tab-panel-sageoa-tab-art\u0022\u003E\u003Cdiv class=\u0022panel-display panel-1col clearfix\u0022 \u003E\n  \u003Cdiv class=\u0022panel-panel panel-col\u0022\u003E\n    \u003Cdiv\u003E\u003Cdiv class=\u0022panel-pane pane-highwire-markup\u0022 \u003E\n  \n      \n  \n  \u003Cdiv class=\u0022pane-content\u0022\u003E\n    \u003Cdiv class=\u0022highwire-markup\u0022\u003E\u003Cdiv xmlns=\u0022http:\/\/www.w3.org\/1999\/xhtml\u0022 id=\u0022content-block-markup\u0022 xmlns:xhtml=\u0022http:\/\/www.w3.org\/1999\/xhtml\u0022\u003E\u003Cdiv class=\u0022article fulltext-view \u0022\u003E\u003Cspan class=\u0022highwire-journal-article-marker-start\u0022\u003E\u003C\/span\u003E\u003Cdiv class=\u0022section abstract\u0022 id=\u0022abstract-1\u0022\u003E\u003Ch2\u003ESummary\u003C\/h2\u003E\n            \u003Cp id=\u0022p-1\u0022\u003EBenign hepatocellular adenomas are not a uniform liver disease but include different types of tumors, which can be classified as hemangioma (nonepithelial), focal nodular hyperplasia, and hepatocellular adenoma, the latter 2 being epithelial tumors. This article discusses how insights from molecular biology have profoundly changed our clinical understanding of benign liver tumors and how using the genotype-phenotype classification of these tumors can identify new etiologies, as well as diagnostic and prognostic features of this disease.\u003C\/p\u003E\n         \u003C\/div\u003E\u003Cul class=\u0022kwd-group\u0022\u003E\u003Cli class=\u0022kwd\u0022\u003ELiver Conditions\u003C\/li\u003E\u003C\/ul\u003E\u003Cul class=\u0022kwd-group clinical-trial\u0022\u003E\u003Cli class=\u0022kwd\u0022\u003EHepatology\u003C\/li\u003E\u003Cli class=\u0022kwd\u0022\u003ELiver Conditions\u003C\/li\u003E\u003C\/ul\u003E\u003Cp id=\u0022p-2\u0022\u003EBenign hepatocellular adenomas are not a uniform liver disease but include different types of tumors, which can be classified as hemangioma (nonepithelial), focal nodular hyperplasia (FNH), and hepatocellular adenoma (HCA), the latter 2 being epithelial tumors. Prof Jessica Zucman-Rossi, Universit\u00e9 Paris Descartes, Paris, France, discussed how insights from molecular biology have profoundly changed our clinical understanding of benign liver tumors and how using the genotype-phenotype classification of these tumors can identify new etiologies, as well as diagnostic and prognostic features of this disease.\u003C\/p\u003E\u003Cp id=\u0022p-3\u0022\u003EOf the two main hepatocellular tumor types, 90% are classified as FNH and result in no complications. The remaining 10% of cases are HCAs, which are associated with bleeding (27%) and transformation to hepatocellular carcinoma (HCC, 4.2%). Patient management is based on 3 questions: (1) determine whether the patient has FNH, HCA, or HCC; (2) identify and prevent risk factors; and (3) evaluate the risk of malignant transformation and hemorrhages.\u003C\/p\u003E\u003Cp id=\u0022p-4\u0022\u003EUntil recently, it has been difficult to differentiate these tumors, but the advent of molecular classification of benign liver tumors has made it possible to better define the lesions and their molecular subtypes and to identify new biomarkers that can be used to better assess their pathology. FNH is more common in females (F:M = 8:1). Oral contraceptives play only a limited role in the development of FNH, and there is usually no bleeding or malignant transformation. FNH is defined by the accumulation of mature normal hepatocytes that are arranged in plates 1 to 2 cells thick and centered on a fibrous central scar with dystrophic arterial vessels that are located in the center of the lesion. There are also ductular reactions at the interface of the fibrous scar. FNH is a type of hyperplastic lesion composed of a reactive proliferation of hepatocytes that is due to a polyclonal proliferation of hepatocytes. The occurrence of FNH is related to a preexisting vascular malformation associated with an increased expression of angiopoietin 1 (proteins involved in angiogenesis) but also to an overexpression of transforming growth factor beta (TGF\u03b2) and platelet-derived growth factor (PDGF) at the central scar. WNT\/\u03b2-catenin is also activated and is involved in the benign hepatocyte proliferation and metabolic zonation in the liver. A typical maplike pattern of glutamine synthetase (GS) expression shows an altered zonation in FNH, and it is a good marker for easily identifying resected FNH from other hepatocellular nodules [Bioulac-Sage P et al. \u003Cem\u003ELiver Int.\u003C\/em\u003E 2008; Rebouissou S et al. \u003Cem\u003EJ Hepatol\u003C\/em\u003E. 2008].\u003C\/p\u003E\u003Cp id=\u0022p-5\u0022\u003EHCAs are rare benign monoclonal liver tumors mainly observed in young women after oral contraceptive use. They may be seen as solitary adenomas, multiple (2 to 4 nodules), or adenomatosis (\u0026gt; 10 nodules). Molecular subtypes include mutation-inactivating hepatocyte nuclear factor 1 alpha (HNF1A; 30% to 40% of tumors), inflammatory (40% to 50%), \u03b2-catenin activation (12% to 19%), and unclassified with nonspecific features (10%).\u003C\/p\u003E\u003Cp id=\u0022p-6\u0022\u003EHNF1A tumors are phenotypically characterized by marked homogeneous steatosis. Bi-allelic inactivation and heterozygous germline mutations of HNF1A are associated with familial hepatic adenomatosis and maturity-onset diabetes of the young (MODY) type 3 [Reznik Y et al. \u003Cem\u003EJ Clin Endocrinol Metab\u003C\/em\u003E. 2004]. Patients with liver adenomatosis should be tested for familial diabetes and HNF1A germline mutations.\u003C\/p\u003E\u003Cp id=\u0022p-7\u0022\u003EThe subgroup of tumors classified as inflammatory lesions are characterized by the presence of inflammatory infiltrates, sinusoidal dilatation, and dystrophic vessels [Zucman-Rossi J et al. \u003Cem\u003EHepatology\u003C\/em\u003E. 2006]. Inflammatory adenomas are defined by a STAT3 activation explained in 80% of the cases by activating mutations in either gp130, STAT3, FRK, JAK1, or GNAS genes. Rare unexplained inflammatory syndromes can be caused by inflammatory adenoma and cured by tumor resection. Risk factors of inflammatory-type tumors include obesity and excessive alcohol use. Glycogen storage disease is a rare hereditary metabolic disease resulting from deficiency of the glucose-6-phosphate complex, which can predispose an individual to inflammatory hepatocellular adenomas [Calderaro J et al. \u003Cem\u003EJ Hepatol\u003C\/em\u003E. 2013]. A positive serum amyloid protein is the immunohistochemistry (IHC) marker for inflammatory adenomas.\u003C\/p\u003E\u003Cp id=\u0022p-8\u0022\u003ETumors defined by \u03b2-catenin activation have frequent cytological abnormalities, pseudoglandular formation, and cholestasis. CTNNB1 (cadherin-associated protein) encodes \u03b2-catenin, and somatic mutations at exon 3 result in high \u03b2-catenin activity, whereas those at exon 7 and exon 8 result in low \u03b2-catenin levels. GS and positive \u03b2-catenin are IHC markers for inflammatory lesions. A high percentage (38%) of this subtype occurs in males. Androgen therapy and anabolic intake are risk factors for the development of \u03b2-catenin adenomas. Although androgens should be stopped when possible, there is a risk of malignant transformation even after stoppage.\u003C\/p\u003E\u003Cp id=\u0022p-9\u0022\u003EPrior to the identification of these different subtypes, imaging features of HCAs were nonspecific. Now, it is well established that the different molecular features correspond to distinct phenotypical features that can be validated by magnetic resonance imaging (MRI). For instance, diffuse signal dropout on T1-weighted chemical shift sequence is a specific MRI feature of HNF1A-inactivated adenoma.\u003C\/p\u003E\u003Cp id=\u0022p-10\u0022\u003EAs mentioned, hemorrhage at diagnosis is associated with HCA in about 27% of cases and is more frequent in large (\u0026gt; 5 cm) HCA adenomas [van Aalten SM et al. \u003Cem\u003EBr J Surg\u003C\/em\u003E. 2012]. Malignant transformation of HCAs into hepatocellular carcinomas, although rare, occurs in 4.2% of cases, almost all in tumors exceeding 5 cm in size [Stoot JH et al. \u003Cem\u003EHPB (Oxford)\u003C\/em\u003E. 2010]. High activation of the WNT\/\u03b2-catenin pathway (through the CTNNB1 exon 3 mutation), the earliest event, is associated with a high risk of malignant transformation, whereas low activity of WNT\/\u03b2-catenin signaling (through CTNNB1 exon 7 and 8 mutations) is associated with no increased risk of transformation. Exome sequencing identified mutations that induce constitutive kinase activity, STAT3 activation, and telomerase activation by telomerase reverse transcriptase promoter [Pilati C et al. \u003Cem\u003ECancer Cell\u003C\/em\u003E. 2014]. Telomerase activation was seen as crucial for malignancy.\u003C\/p\u003E\u003Cp id=\u0022p-11\u0022\u003EFuture developments in this area might include a better understanding of the role of estrogen exposure in HCA development, as well as more clarity regarding the mechanism of the occurrence of multiple adenomas. New markers to predict hemorrhages and an evaluation of molecular classification in routine clinical care are needed.\u003C\/p\u003E\u003Cp id=\u0022p-12\u0022\u003EHCA molecular classification can help in diagnoses at imaging and histological levels.\u003C\/p\u003E\u003Cp id=\u0022p-13\u0022\u003EKnowing the risk factors of malignant transformation (male, size \u0026gt; 5 cm, \u03b2-catenin activation) can modify treatment. A complicated but specific composite algorithm for the diagnosis and treatment of HCA has been proposed by Nault JC et al. [\u003Ca id=\u0022xref-fig-1-1\u0022 class=\u0022xref-fig\u0022 href=\u0022#F1\u0022\u003EFigure 1\u003C\/a\u003E; \u003Cem\u003EGastroenterology\u003C\/em\u003E. 2013]\u003C\/p\u003E\u003Cdiv id=\u0022F1\u0022 class=\u0022fig pos-float  odd\u0022\u003E\u003Cdiv class=\u0022highwire-figure\u0022\u003E\u003Cdiv class=\u0022fig-inline-img-wrapper\u0022\u003E\u003Cdiv class=\u0022fig-inline-img\u0022\u003E\u003Ca href=\u0022http:\/\/d282kpwvnogo5m.cloudfront.net\/content\/spmdc\/14\/48\/6\/F1.large.jpg?width=800\u0026amp;height=600\u0026amp;carousel=1\u0022 title=\u0022Algorithm for the Diagnoses and Treatment of Hepatocellular Adenoma\u0022 class=\u0022fragment-images colorbox-load\u0022 rel=\u0022gallery-fragment-images-749922893\u0022 data-figure-caption=\u0022Algorithm for the Diagnoses and Treatment of Hepatocellular Adenoma\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003E\u003Cimg class=\u0022fragment-image\u0022 alt=\u0022Figure 1.\u0022 src=\u0022http:\/\/d282kpwvnogo5m.cloudfront.net\/content\/spmdc\/14\/48\/6\/F1.medium.gif\u0022\/\u003E\u003C\/a\u003E\u003C\/div\u003E\u003C\/div\u003E\u003Cul class=\u0022highwire-figure-links inline\u0022\u003E\u003Cli class=\u00220 first\u0022\u003E\u003Ca href=\u0022http:\/\/d282kpwvnogo5m.cloudfront.net\/content\/spmdc\/14\/48\/6\/F1.large.jpg?download=true\u0022 class=\u0022highwire-figure-link highwire-figure-link-download\u0022 title=\u0022Download Figure 1.\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EDownload figure\u003C\/a\u003E\u003C\/li\u003E\u003Cli class=\u00221\u0022\u003E\u003Ca href=\u0022http:\/\/d282kpwvnogo5m.cloudfront.net\/content\/spmdc\/14\/48\/6\/F1.large.jpg\u0022 class=\u0022highwire-figure-link highwire-figure-link-newtab\u0022 target=\u0022_blank\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EOpen in new tab\u003C\/a\u003E\u003C\/li\u003E\u003Cli class=\u00222 last\u0022\u003E\u003Ca href=\u0022\/highwire\/powerpoint\/15584\u0022 class=\u0022highwire-figure-link highwire-figure-link-ppt\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EDownload powerpoint\u003C\/a\u003E\u003C\/li\u003E\u003C\/ul\u003E\u003C\/div\u003E\u003Cdiv class=\u0022fig-caption attrib\u0022\u003E\u003Cspan class=\u0022fig-label\u0022\u003EFigure 1.\u003C\/span\u003E \n            \u003Cp id=\u0022p-14\u0022 class=\u0022first-child\u0022\u003EAlgorithm for the Diagnoses and Treatment of Hepatocellular Adenoma\u003C\/p\u003E\n         \u003Cq class=\u0022attrib\u0022 id=\u0022attrib-1\u0022\u003ECRP, C-reactive protein; GS, glutamine synthetase; HCA, hepatocellular adenoma; HCC, hepatocellular carcinoma; HNF1A, hepatocyte nuclear factor 1 alpha; IHC, immunohistochemistry; LFABP, liver-type fatty acid-binding protein; MRI, magnetic resonance imaging; OC, oral contraception; SAA, serum amyloid A.\u003C\/q\u003E\u003Cq class=\u0022attrib\u0022 id=\u0022attrib-2\u0022\u003EAdapted with permission of AGA Institute, from Nault JC et al. Hepatocellular Benign Tumors\u2014From Molecular Classification to Personalized Clinical Care. \u003Cem\u003EGastroenterology\u003C\/em\u003E. 2013;144:888\u2013902. Copyright \u00a9 2013. Permission conveyed through Copyright Clearance Center, Inc.\u003C\/q\u003E\u003Cdiv class=\u0022sb-div caption-clear\u0022\u003E\u003C\/div\u003E\u003C\/div\u003E\u003C\/div\u003E\u003Cp id=\u0022p-15\u0022\u003EDr Zucman-Rossi concluded by saying that \u201cmolecular biology has profoundly changed our knowledge of the benign liver tumors.\u201d Using the genotype-phenotype HCA classification, as shown in \u003Ca id=\u0022xref-fig-2-1\u0022 class=\u0022xref-fig\u0022 href=\u0022#F2\u0022\u003EFigure 2\u003C\/a\u003E [Nault JC et al. \u003Cem\u003EGastroenterology\u003C\/em\u003E. 2013], can identify new etiologies and diagnostic and prognostic features of the disease, leading to more personalized medicine.\u003C\/p\u003E\u003Cdiv id=\u0022F2\u0022 class=\u0022fig pos-float  odd\u0022\u003E\u003Cdiv class=\u0022highwire-figure\u0022\u003E\u003Cdiv class=\u0022fig-inline-img-wrapper\u0022\u003E\u003Cdiv class=\u0022fig-inline-img\u0022\u003E\u003Ca href=\u0022http:\/\/d282kpwvnogo5m.cloudfront.net\/content\/spmdc\/14\/48\/6\/F2.large.jpg?width=800\u0026amp;height=600\u0026amp;carousel=1\u0022 title=\u0022Using the Genotype-Phenotype Hepatocellular Adenoma Classification for Personalized Treatment\u0022 class=\u0022fragment-images colorbox-load\u0022 rel=\u0022gallery-fragment-images-749922893\u0022 data-figure-caption=\u0022Using the Genotype-Phenotype Hepatocellular Adenoma Classification for Personalized Treatment\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003E\u003Cimg class=\u0022fragment-image\u0022 alt=\u0022Figure 2.\u0022 src=\u0022http:\/\/d282kpwvnogo5m.cloudfront.net\/content\/spmdc\/14\/48\/6\/F2.medium.gif\u0022\/\u003E\u003C\/a\u003E\u003C\/div\u003E\u003C\/div\u003E\u003Cul class=\u0022highwire-figure-links inline\u0022\u003E\u003Cli class=\u00220 first\u0022\u003E\u003Ca href=\u0022http:\/\/d282kpwvnogo5m.cloudfront.net\/content\/spmdc\/14\/48\/6\/F2.large.jpg?download=true\u0022 class=\u0022highwire-figure-link highwire-figure-link-download\u0022 title=\u0022Download Figure 2.\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EDownload figure\u003C\/a\u003E\u003C\/li\u003E\u003Cli class=\u00221\u0022\u003E\u003Ca href=\u0022http:\/\/d282kpwvnogo5m.cloudfront.net\/content\/spmdc\/14\/48\/6\/F2.large.jpg\u0022 class=\u0022highwire-figure-link highwire-figure-link-newtab\u0022 target=\u0022_blank\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EOpen in new tab\u003C\/a\u003E\u003C\/li\u003E\u003Cli class=\u00222 last\u0022\u003E\u003Ca href=\u0022\/highwire\/powerpoint\/15585\u0022 class=\u0022highwire-figure-link highwire-figure-link-ppt\u0022 data-icon-position=\u0022\u0022 data-hide-link-title=\u00220\u0022\u003EDownload powerpoint\u003C\/a\u003E\u003C\/li\u003E\u003C\/ul\u003E\u003C\/div\u003E\u003Cdiv class=\u0022fig-caption attrib\u0022\u003E\u003Cspan class=\u0022fig-label\u0022\u003EFigure 2.\u003C\/span\u003E \n            \u003Cp id=\u0022p-16\u0022 class=\u0022first-child\u0022\u003EUsing the Genotype-Phenotype Hepatocellular Adenoma Classification for Personalized Treatment\u003C\/p\u003E\n         \u003Cq class=\u0022attrib\u0022 id=\u0022attrib-3\u0022\u003ECRP, C-reactive protein; HCA, hepatocellular adenoma; HCC, hepatocellular carcinoma; HNF1A, hepatocyte nuclear factor 1 alpha; LFABP, liver-type fatty acid-binding protein 1; MODY3, maturity-onset diabetes of the young type 3; NT, normal tissue; SAA, serum amyloid A; T2W, T2-weighted.\u003C\/q\u003E\u003Cq class=\u0022attrib\u0022 id=\u0022attrib-4\u0022\u003EAdapted with permission of AGA Institute, from Nault JC et al. Hepatocellular Benign Tumors\u2014From Molecular Classification to Personalized Clinical Care. \u003Cem\u003EGastroenterology\u003C\/em\u003E. 2013;144:888\u2013113; 902. Copyright \u00a9 2013. 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