Hepatocellular adenoma classification: Difference between revisions
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* '''HNF-1 alpha inactivated hepatocellular adenoma (35-40%)''' | |||
** This group of hepatocellular adenomas is defined by the somatic inactivation of HNF1A (hepatocyte nuclear factor 1 A) gene, by a mutational mechanism in tumor cells. | |||
** HNF1A is a transcription factor controlling hepatocyte metabolism. | |||
** Most of these variants show macrovesicular steatosis of variable extent and no atypical hepatocytes and are associated to metabolic syndrome. | |||
** This type occurs mostly in women and is often associated with maturity onset diabetes of young (MODY3). | |||
** Expression of liver fatty acid binding protein (LFABP) involved in lipid trafficking, usually expressed in normal liver, is specifically downregulated in these cases as a consequence of HNF1A mutation. | |||
* '''Inflammatory hepatocellular adenoma (40-50%)''' | |||
** The most important feature of these tumors is activation of JAk/STAT pathway. | |||
** Inflammatory hepatocellular adenomas also exhibit over expression of serum amyloid alpha (SAA) and C-reactive protein (CRP) induced by STAT3. | |||
** They show greater morphological pleomorphism as they may show pseudo portal tracts, sinusoidal dilatation, dystrophic arteries, hemorrhage and inflammatory infiltrate. | |||
** Inflammatory syndrome, obesity and alcohol consumption are reported in these patients. | |||
** Five different molecular drivers, IL6 signal transducer, FRK, STAT3, GNAS and JAK1 have been reported. | |||
* '''Beta catenin mutated hepatocellular adenoma (10-15%)''' | |||
** These are frequently associated with exposure to male hormones, glycogenolysis and familial adenomatous polyposis. | |||
** This group has a higher risk of malignant potential. | |||
** Morphologically these tumors have cytoogical and architectural atypical features of tumoral hepatocytes and cholestasis as well. | |||
** On immunohistochemical staining, these adenomas tend to stain for glutamine synthetase rather than beta catenin, which stains patchily. | |||
* '''Unclassified hepatocellular adenoma (10%)''' | |||
** By definition, they lack characteristics of other subtypes and their identification rlies on a silent phenotype and by exclusion of criteria featuring other subtypes. | |||
** Until now their pathogenesis remains unidentified. | |||
** These adenomas do not stain for the C-reactive protein (CRP), beta catenin or glutamine synthetase. | |||
==References== | ==References== | ||
Revision as of 22:30, 11 December 2018
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Hepatocellular adenoma Microchapters |
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Hepatocellular adenoma classification On the Web |
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American Roentgen Ray Society Images of Hepatocellular adenoma classification |
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Risk calculators and risk factors for Hepatocellular adenoma classification |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Zahir Ali Shaikh, MD[2]
Overview
Classification
- In 2007, Bioulac-sage and associates from bordeaux classified the hepatocellular adenomas based on molecular patterns called phenotypic-genotypic classification. They classified heaptocellular adenomas into 04 main groups.[1][2]
| Hepatocellular Adenoma | |||||||||||||||||||||||||||||||||||||||||||
| HNF-1 alpha inactivated adenoma | Beta catenin activated adenoma | Inflammatory hepatic adenoma | Unclassified type adenoma | ||||||||||||||||||||||||||||||||||||||||
- HNF-1 alpha inactivated hepatocellular adenoma (35-40%)
- This group of hepatocellular adenomas is defined by the somatic inactivation of HNF1A (hepatocyte nuclear factor 1 A) gene, by a mutational mechanism in tumor cells.
- HNF1A is a transcription factor controlling hepatocyte metabolism.
- Most of these variants show macrovesicular steatosis of variable extent and no atypical hepatocytes and are associated to metabolic syndrome.
- This type occurs mostly in women and is often associated with maturity onset diabetes of young (MODY3).
- Expression of liver fatty acid binding protein (LFABP) involved in lipid trafficking, usually expressed in normal liver, is specifically downregulated in these cases as a consequence of HNF1A mutation.
- Inflammatory hepatocellular adenoma (40-50%)
- The most important feature of these tumors is activation of JAk/STAT pathway.
- Inflammatory hepatocellular adenomas also exhibit over expression of serum amyloid alpha (SAA) and C-reactive protein (CRP) induced by STAT3.
- They show greater morphological pleomorphism as they may show pseudo portal tracts, sinusoidal dilatation, dystrophic arteries, hemorrhage and inflammatory infiltrate.
- Inflammatory syndrome, obesity and alcohol consumption are reported in these patients.
- Five different molecular drivers, IL6 signal transducer, FRK, STAT3, GNAS and JAK1 have been reported.
- Beta catenin mutated hepatocellular adenoma (10-15%)
- These are frequently associated with exposure to male hormones, glycogenolysis and familial adenomatous polyposis.
- This group has a higher risk of malignant potential.
- Morphologically these tumors have cytoogical and architectural atypical features of tumoral hepatocytes and cholestasis as well.
- On immunohistochemical staining, these adenomas tend to stain for glutamine synthetase rather than beta catenin, which stains patchily.
- Unclassified hepatocellular adenoma (10%)
- By definition, they lack characteristics of other subtypes and their identification rlies on a silent phenotype and by exclusion of criteria featuring other subtypes.
- Until now their pathogenesis remains unidentified.
- These adenomas do not stain for the C-reactive protein (CRP), beta catenin or glutamine synthetase.
References
- ↑ Kun Jiang, Sameer Al-Diffhala & Barbara A. Centeno (2018). "Primary Liver Cancers-Part 1: Histopathology, Differential Diagnoses, and Risk Stratification". Cancer control : journal of the Moffitt Cancer Center. 25 (1): 1073274817744625. doi:10.1177/1073274817744625. PMID 29350068. Unknown parameter
|month=ignored (help) - ↑ H. Dharmana, S. Saravana-Bawan, S. Girgis & G. Low (2017). "Hepatocellular adenoma: imaging review of the various molecular subtypes". Clinical radiology. 72 (4): 276–285. doi:10.1016/j.crad.2016.12.020. PMID 28126185. Unknown parameter
|month=ignored (help)