title: Expression of p16, p53, CD24, EpCAM and calretinin in serous borderline tumors of the ovary.
abstract: OBJECTIVE
  According to the widely accepted pathway, a serous borderline tumor becomes invasive either by progressing into a noninvasive micropapillary tumor or directly through microinvasion. Our objective was to investigate the role of serous borderline tumors and their accompanying extraovarian lesions in pathogenesis of serous ovarian cancer using immunohistochemistry as a tool.
  
  
  METHODS
  An immunohistochemical panel of p16, p53, CD24, EpCAM and calretinin was applied to cutting edge matrix assembly-like tissue arrays of 46 cases consisting of typical, focal micropapillary, micropapillary, microinvasive, cystadenoma, and low-grade carcinoma cases. These tissue arrays are better choices than conventional tissue arrays to examine thin walled and heterogenous neoplasia like serous borderline tumors as they facilitate the analysis with linear sections rather than a core.
  
  
  RESULTS
  For two tumor supressor gene markers; no diffuse and strong expression of p53, and strong and patchy/heterogenous expression of p16 were detected in all cases. Focal and strong calretinin expression was detected in micropapillary tumors while expression of EpCAM was lost in the same areas. Strong cytoplasmic CD24 expression was detected in cases with peritoneal implants, favoring the theory that change of expression localization of cell adhesion molecules is in accordance with phenotypical changes and tumor progresssion. Furthermore, circumfrential membranous and cytoplasmic expression of CD24 and EpCAM was detected in neoplastic cells in lymph nodes and microinvasion areas.
  
  
  CONCLUSIONS
  Our results show that different levels of serous ovarian tumor progression are accompanied by changes in the immunohistochemical expression pattern of EpCAM, CD24, and calretinin.
authors.affiliation: Department of Pathology, Hacettepe University, Faculty of Medicine, Ankara, Turkey.
authors.forename: Işıl Yildiz
authors.initials: IY
authors.lastname: Aktaş
authors.forename: Meral
authors.initials: M
authors.lastname: Buğdayci
authors.forename: Alp
authors.initials: A
authors.lastname: Usubütün
mesh_terms: D000951:Antigens, Neoplasm / Q000032:analysis / Q000096:biosynthesis; D014408:Biomarkers, Tumor / Q000032:analysis*; D051927:CD24 Antigen / Q000032:analysis / Q000096:biosynthesis; D064032:Calbindin 2; D015815:Cell Adhesion Molecules / Q000032:analysis / Q000096:biosynthesis; D019941:Cyclin-Dependent Kinase Inhibitor p16 / Q000032:analysis / Q000096:biosynthesis; D018284:Cystadenocarcinoma, Serous / Q000378:metabolism* / Q000473:pathology; D018450:Disease Progression; D000071858:Epithelial Cell Adhesion Molecule; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D010051:Ovarian Neoplasms / Q000378:metabolism* / Q000473:pathology; D064030:S100 Calcium Binding Protein G / Q000032:analysis / Q000096:biosynthesis; D046888:Tissue Array Analysis; D016159:Tumor Suppressor Protein p53 / Q000032:analysis / Q000096:biosynthesis
chemical_list: D000951:Antigens, Neoplasm; D014408:Biomarkers, Tumor; C576764:CALB2 protein, human; D051927:CD24 Antigen; D064032:Calbindin 2; D015815:Cell Adhesion Molecules; D019941:Cyclin-Dependent Kinase Inhibitor p16; C499379:EPCAM protein, human; D000071858:Epithelial Cell Adhesion Molecule; D064030:S100 Calcium Binding Protein G; D016159:Tumor Suppressor Protein p53