ArticleOncology letters2017
Distinct subcellular localization of E-cadherin between epithelioid angiomyolipoma and triphasic angiomyolipoma: A preliminary case-control study.
Article in Oncology letters, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- E-cadherin Interacts With Posttranslationally-Modified AGO2 to Enhance miRISC Activity.Frontiers in cell and developmental biology · 2021Article
- Allosteric and ATP-Competitive Inhibitors of mTOR Effectively Suppress Tumor Progression-Associated Epithelial-Mesenchymal Transition in the Kidneys of Tsc2Neoplasia (New York, N.Y.) · 2019Article
- Late local, peritoneal and systemic recurrence of renal angiomyolipoma: A case report.Molecular and clinical oncology · 2019Article
- Imaging appearance of renal epithelioid angiomyolipoma: A case report and literature review.Medicine · 2018Review
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epithelioid angiomyolipoma (EAML) is a rare variant of angiomyolipoma (AML). Previous studies have demonstrated that epithelial (E-)cadherin is expressed in two subtypes of AML, EAML and triphasic AML; however, the expression pattern of E-cadherin remains unclear. In the present study, a preliminary case-control study was conducted to determine the expression pattern of E-cadherin between EAML and triphasic AML, the control, focusing on the subcellular localization and expression category of E-cadherin. No significant difference was identified in the age, sex, history of tuberous sclerosis, smoking and alcohol consumption between the two groups (P>0.05). In EAML, 9 patients were categorized as exhibiting a low risk of malignant behavior and the other two were categorized as exhibiting an intermediate or high risk of malignant behavior. The proportion of cases expressing E-cadherin, human melanoma black-45 (HMB45), melanoma antigen recognized by T cells 1 (Mart1/Melan A), smooth muscle actin and progesterone receptor were 95.5 (21/22), 95.5 (21/22), 86.4 (19/22), 77.3 (17/22) and 86.4% (19/22), respectively. E-cadherin was identified to be localized, using staining techniques, in the cell membrane and/or cytoplasm. The subcellular localization of E-cadherin was significantly different between EAML and triphasic AML; the majority of EAML cases revealed membranous and cytoplasmic staining, whereas triphasic AML cases demonstrated cytoplasmic staining (P=0.0093). The expression of E-cadherin may be positively associated with HMB45 (P=0.0044) and Mart1/Melan A (P=0.0049). The results of the present study identified that the subcellular localization of E-cadherin may be different between EAML and the control group of triphasic AML. Additionally, E-cadherin and melanocytic markers may be co-expressed in distinct subtypes of AML. A follow-up study with a large sample size to validate the results of the present study, followed by a mechanistic study based on cell lines to determine any significance, are warranted.
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