title: PML protein expression in hereditary and sporadic breast cancer.
abstract: The PML protein is concentrated in the PML nuclear bodies. Downregulation of the PML protein has been described in various types of cancer and is in accordance with the fact that dysqualification of tumor suppressive functions of the PML protein might promote cancer development. Various differences have been described between sporadic breast cancer and that associated with BRCA1 and BRCA2 gene mutations. Expression of the PML protein has not been studied yet. The aim of this study was to determine if there is any difference in PML protein expression in breast cancer of BRCA1 and BRCA2 gene mutation carriers compared to sporadic breast cancer and if the PML protein can be used as a prognostic marker. There were 47 breast cancer samples included, 14 and 10 from BRCA1 and BRCA2 germline mutation carriers, respectively, and 23 from patients without a BRCA1/BRCA2 germline mutation. Immunofluorescence staining was used. Downregulation of PML protein expression was found in 2 of 14 (14%), 3 of 10 (30%) and 15 of 47 (31%) cases of breast cancer samples from BRCA1, BRCA2 and no BRCA1/BRCA2 mutation carriers, respectively (p(BRCA1) = 0.019; p(BRCA2) = 0.111). There was no correlation between PML protein expression and age, histological types, estrogen and progesterone receptor, c-erbB-2 and PCNA expression, TNM classification, disease-free and overall survival. In conclusion, the PML protein is downregulated in approximately 30% of breast cancers cases. Downregulation of PML protein expression was significantly less frequent in BRCA1 mutation carriers compared to sporadic cases. No correlation was found between PML protein expression and any of the other clinical and laboratory characteristics.
authors.affiliation: Institute of Pathology and Laboratory of Molecular Pathology, Medical Faculty of the Palacký University, Olomouc, Czech Republic. pavlina.plevova@volny.cz
authors.forename: P
authors.initials: P
authors.lastname: Plevová
authors.forename: J
authors.initials: J
authors.lastname: Bouchal
authors.forename: M
authors.initials: M
authors.lastname: Fiurásková
authors.forename: L
authors.initials: L
authors.lastname: Foretová
authors.forename: M
authors.initials: M
authors.lastname: Navrátilová
authors.forename: J
authors.initials: J
authors.lastname: Zapletalová
authors.forename: R
authors.initials: R
authors.lastname: Curík
authors.forename: O
authors.initials: O
authors.lastname: Kubala
authors.forename: J
authors.initials: J
authors.lastname: Prokop
authors.forename: Z
authors.initials: Z
authors.lastname: Kolár
mesh_terms: D002288:Adenocarcinoma, Mucinous / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D019313:BRCA1 Protein / Q000235:genetics; D024682:BRCA2 Protein / Q000235:genetics; D001943:Breast Neoplasms / Q000235:genetics* / Q000378:metabolism* / Q000473:pathology; D018270:Carcinoma, Ductal, Breast / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D018275:Carcinoma, Lobular / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D002467:Cell Nucleus / Q000378:metabolism / Q000473:pathology; D005260:Female; D019084:Fluorescent Antibody Technique, Indirect; D018095:Germ-Line Mutation / Q000235:genetics*; D006579:Heterozygote; D006801:Humans; D009363:Neoplasm Proteins / Q000378:metabolism*; D009687:Nuclear Proteins / Q000378:metabolism*; D000071156:Promyelocytic Leukemia Protein; D011960:Receptors, Estrogen / Q000378:metabolism; D011980:Receptors, Progesterone / Q000378:metabolism; D014157:Transcription Factors / Q000378:metabolism*; D025521:Tumor Suppressor Proteins / Q000378:metabolism*; D016335:Zinc Fingers