Absence of microsatellite instability in breast carcinomas with both p53 and c-erbB-2 alterations

• Published in: The Journal of pathology Vol. 187; no. 4; pp. 424 - 427
• Main Authors: Formantici, Cristina, Orlandi, Rosaria, Ronchini, Chiara, Pilotti, Silvana, Ranzani, Guglielmina N., Colnaghi, Maria I., Ménard, Sylvie
• Format: Journal Article
• Language: English
• Published: Chichester, UK John Wiley & Sons, Ltd 01.03.1999; Wiley
• Subjects: Adult; Biological and medical sciences; Biomarkers, Tumor - metabolism; breast carcinoma; Breast Neoplasms - genetics; Breast Neoplasms - metabolism; Breast Neoplasms - pathology; c-erbB-2; Female; Gynecology. Andrology. Obstetrics; Humans; Mammary gland diseases; Medical sciences; microsatellite instability; Microsatellite Repeats; Middle Aged; Neoplasm Proteins - metabolism; p53; PCR; Polymerase Chain Reaction; Receptor, ErbB-2 - metabolism; Tumor Suppressor Protein p53 - metabolism; Tumors; Human; Immunohistochemistry; Carcinoma; Malignant tumor; Carcinogenesis; Polymerase chain reaction; Pathology; Mammary gland diseases; TP53 Gene; Microsatellite DNA; C-Onc gene; Instability; Mammary gland; Mutation; Molecular biology; Protooncogene; Tumor suppressor gene
• ISSN: 0022-3417; 1096-9896
• DOI: 10.1002/(SICI)1096-9896(199903)187:4<424::AID-PATH259>3.0.CO;2-0

Based on a previous finding that amplification of the c‐erbB‐2 oncogene and alteration of p53 are strongly associated in most aggressive breast tumours, the present study investigated whether microsatellite instability (MI) might also be associated with this tumour phenotype. Nine polymorphic microsatellite markers, including six dinucleotide, one trinucleotide, and two tetranucleotide repeats, were amplified from paired normal and tumour DNA samples of 15 breast tumours that overexpressed both c‐erbB‐2 and p53 and of 15 control breast tumours that overexpressed neither protein. All 30 breast tumours analysed exhibited a replication error‐negative phenotype, with only one sample showing MI in one of the nine loci. This suggests that the genetic events underlying MI, which are critical in colorectal and gastric tumours, are not involved in the pathogenesis of c‐erbB‐2/p53 double‐altered breast tumours and do not play a central role in breast tumour formation. Copyright © 1999 John Wiley & Sons, Ltd.