Abstract |
Hepatocellular adenomas have recently been classified into four subtypes based on molecular findings: hepatocyte nuclear factor 1α (HNF1α) inactivated, inflammatory/telangiectatic, β- catenin activated, and unclassifiable. β- catenin-activated adenomas have the potential for malignant transformation and are thus important to recognize. Diffuse glutamine synthetase immunohistochemical positivity has been shown to be a reliable surrogate marker for β- catenin activation, though variations in staining patterns may be difficult to interpret. We report a case of a peliotic adenoma that was morphologically consistent with a β- catenin wild-type hepatocellular adenoma but harbored a β- catenin mutation by molecular analysis. The tumor lacked nuclear β- catenin positivity and demonstrated a hitherto undescribed pattern of glutamine synthetase overexpression restricted to areas of peliosis with mostly negative staining in non-peliotic areas. This pattern was initially interpreted as physiologic and may represent a potential pitfall in glutamine synthetase interpretation.
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Authors | Ryan S Berry, Rama R Gullapalli, Jin Wu, Katherine Morris, Joshua A Hanson |
Journal | Virchows Archiv : an international journal of pathology
(Virchows Arch)
Vol. 465
Issue 2
Pg. 241-5
(Aug 2014)
ISSN: 1432-2307 [Electronic] Germany |
PMID | 24997695
(Publication Type: Case Reports, Journal Article)
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Chemical References |
- Biomarkers, Tumor
- beta Catenin
- Glutamate-Ammonia Ligase
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Topics |
- Adenoma, Liver Cell
(diagnosis, epidemiology, metabolism)
- Biomarkers, Tumor
(metabolism)
- Comorbidity
- Female
- Gene Expression Regulation, Neoplastic
- Glutamate-Ammonia Ligase
(biosynthesis)
- Hepatectomy
- Humans
- Liver
(metabolism, pathology, surgery)
- Liver Neoplasms
(diagnosis, epidemiology, metabolism)
- Middle Aged
- Mutation
(genetics)
- Peliosis Hepatis
(epidemiology, metabolism)
- Up-Regulation
- beta Catenin
(genetics, metabolism)
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