An immunohistochemical and molecular analysis of papillary proliferation of the endometrium
Autor: | Colin J.R. Stewart, Susan M. Bigby, Tino Giardina, Benhur Amanuel, Fabienne Grieu-Iacopetta |
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Rok vydání: | 2018 |
Předmět: |
Adult
0301 basic medicine medicine.medical_specialty Pathology medicine.disease_cause Endometrium Pathology and Forensic Medicine Pathogenesis 03 medical and health sciences Polyps 0302 clinical medicine Biomarkers Tumor Endometrial Polyp Humans Medicine Atypical Endometrial Hyperplasia Aged business.industry Middle Aged medicine.disease Immunohistochemistry 030104 developmental biology medicine.anatomical_structure 030220 oncology & carcinogenesis Endometrial Hyperplasia Mutation Adenocarcinoma Female Histopathology KRAS business |
Zdroj: | Pathology. 50:286-292 |
ISSN: | 0031-3025 |
DOI: | 10.1016/j.pathol.2017.10.013 |
Popis: | Papillary proliferations of the endometrium (PPEs) are uncommon lesions that are often associated with endometrial polyps. PPEs occasionally precede or co-exist with atypical endometrial hyperplasia or adenocarcinoma, but their pathogenesis and relationship to endometrial neoplasia is uncertain. In the present study 11 PPEs, including eight benign papillary proliferations (BPPs) and three complex papillary hyperplasias (CPHs) were examined immunohistochemically for expression of PAX2, BAF250a, p16, β-catenin and DNA mismatch repair (MMR) proteins. Molecular analysis was also performed on the CPHs using targeted next generation sequencing (NGS). All PPEs demonstrated at least one immunohistochemical abnormality with altered expression of p16 and PAX2 in nine and seven cases, respectively, and β-catenin in one case. However, none of the cases showed loss of BAF250a or MMR protein staining. All CPHs showed KRAS mutations with additional mutations in AKT1 and FBXW7 in one case each, and both PIK3CA and CTNNB1 in the remaining case. Therefore, PPEs demonstrate immunophenotypical and molecular overlap with endometrial endometrioid neoplasia, although loss of BAF250a and MMR protein function do not appear to contribute significantly to these lesions. KRAS mutations may be important drivers in CPHs but this finding needs to be confirmed in larger studies. |
Databáze: | OpenAIRE |
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