[43] Subtype Classification of Hepatocellular Adenomas by Molecular Markers and Immunohistochemistry

Bioulac‐Sage, Paulette; Rebouissou, Sandra; Thomas, Cynthia L.; Blanc, Jean‐Frédéric; Saric, Jean; Jeannot, Emmanuelle; Cunha, A; Couchy, Gabrielle; Imbeaud, Sandrine; Balabaud, C.; Zucman–Rossi, Jessica

doi:10.1016/s0168-8278(07)61641-9

Cited by 2 publications

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“…Using a combination of β-catenin and glutamin synthetase staining, which increases the accuracy of this detection, prevalence of the activation in our patients was 16 out of 25 (64%). Not unexpectedly, it was higher in men (82%) than in women (25%) as β-catenin-activated HCAs are more prevalent in men than in women 15 16. This further explains the higher proportion of HCAs with malignant transformation that we have observed among men.…”

Section: Discussionmentioning

confidence: 55%

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Changing trends in malignant transformation of hepatocellular adenoma

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Dokmak

et al. 2010

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Prevalence of malignancy within HCA is 10 times more frequent in men than in women and management of HCA should primarily be based on gender. Whereas oral contraception is a classical cause of HCA in women but a marginal cause of HCC, the metabolic syndrome appears as an emerging condition associated with malignant transformation of HCA in men, and is the likely predisposing condition for HCC in this setting.

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Section: Discussionmentioning

confidence: 55%

“…A mutation of this gene is identified in 15–19% of normal HCA6 15 16 but higher figures have been reported in HCAs with malignant transformation. This was initially described in five of 11 patients with HCC arising in HCA or borderline lesions15 and subsequently in six out of six5 and three out of eight30 such patients.…”

Section: Discussionmentioning

confidence: 94%

Changing trends in malignant transformation of hepatocellular adenoma

Farges

Ferreira

Dokmak

et al. 2010

Gut

274

199

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“…Chen et al. [ 8 ], and later our group, identified a β-catenin-activating mutation in a few HCA cases [ 9 , 10 ]. We have not observed any HCA cases with both β-catenin mutations and biallelic inactivation of HNF1α, suggesting that these two tumourigenic pathways are mutually exclusive.…”

Section: Hcas Are Associated With Molecular Featuresmentioning

confidence: 99%

“…In these tumours, with specific pathological characteristics [ 4 , 12 ], the expression of members of the acute phase inflammatory response, serum amyloid protein (SAA) and C-reactive protein (CRP), was elevated at both the mRNA and protein levels [ 10 ]. Some inflammatory HCA also demonstrate β-catenin mutation.…”

Section: Hcas Are Associated With Molecular Featuresmentioning

confidence: 99%

“…Correlations with pathological and clinical data have shown that HNF1α mutations are mostly observed in a histologically homogeneous group of tumours, characterised by marked steatosis, no cytological abnormalities, no inflammatory infiltrates and a lack of LFABP expression in the tumour. Patients with germline HNF1α mutations were younger than those with somatic mutations, with or without clinical diabetes, and they frequently had a family history of liver adenomatosis [ 9 , 10 ].…”

Section: The Genotype Phenotype Classificationmentioning

confidence: 99%

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Hepatocellular adenoma: what is new in 2008

et al. 2008

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Patients (85%) with hepatocellular adenoma (HCA) are women taking oral contraceptives. They can be divided into four subgroups according to their genotype/ phenotype features. (1) Hepatocyte nuclear factor 1a (HNF1a) biallelic somatic mutations are observed in 35% of the HCA cases. It occurs in almost all cases in women. HNF1a-mutated HCA are most of the time, highly steatotic, with a lack of expression of liver fatty acid binding protein (LFABP) in immunohistochemistry analyses. Adenomatosis is frequently detected in this context. An HNF1a germline mutation is observed in less than 5% of HCA cases and can be associated with MODY 3 diabetes. (2) An activating b-catenin mutation was found in 10% of HCA. These b-catenin activated HCAs are observed in men and women, and specific risk factors, such as male hormone administration or glycogenosis, are associated with their development. Immunohistochemistry studies show that these HCAs overexpress b-catenin (nuclear and cytoplasmic) and glutamine synthetase. This group of tumours has a higher risk of malignant transformation into hepatocellular carcinoma. (3) Inflammatory HCAs are observed in 40% of the cases, and they are most frequent in women but are also found in men. Lesions are characterised by inflammatory infiltrates, dystrophic arteries, sinusoidal dilatation and ductular reaction. They express serum amyloid A and C-reactive protein. In this group, GGT is frequently elevated, with a biological inflammatory syndrome present. Also, there are more overweight patients in this group. An additional 10% of inflammatory HCAs express b-catenin, and are also at risk of malignant transformation. (4) Currently, less than 10% of HCAs are unclassified. It is hoped that in the near future it will be possible with clinical, biological and imaging data to predict in which of the 2 major groups (HNF1a-mutated HCA and inflammatory HCA) the patient belongs and to propose better guidelines in terms of surveillance and treatment.

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[43] Subtype Classification of Hepatocellular Adenomas by Molecular Markers and Immunohistochemistry

Cited by 2 publications

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Changing trends in malignant transformation of hepatocellular adenoma

Changing trends in malignant transformation of hepatocellular adenoma

Hepatocellular adenoma: what is new in 2008

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