TP53 abnormalities and genetic instability in breast cancer

Jorunn E. Eyfjörd*, Steinunn Thorlacius, Rut Valgardsdottir, Solveig Gretarsdottir, Margret Steinarsdottir, Kesara Anamthawat-Jonsson

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

14 Citations (Scopus)

Abstract

TP53 abnormalities in breast carcinomas and inherited TP53 changes in breast cancer patients and in Li-Fraumeni-like families were looked for. Tumours were screened for mutations in the TP53 gene by means of the PCR-CDGE method followed by PCR and direct sequencing. Allelic loss was determined by polymorphic markers, by comparing normal and tumour DNA. Abnormal protein expression was examined by immunohistochemical staining. TP53 abnormalities in the tumours were examined in relation to genetic instability, clinical data and family history. Genetic instability was studied by detection of oncogene amplification, allelic loss, karyotype analysis and fluorescent in situ hybridization, FISH. Our studies showed that TP53 abnormalities were significantly associated with amplification of the erbB2 oncogene and allelic loss on chromosome 17. Chromosomal abnormalities were also significantly more common in tumours with TP53 abnormalities. Looking at clinical data we found significant association between TP53 abnormalities and poor prognosis.

Original languageEnglish
Pages (from-to)663-667
Number of pages5
JournalActa Oncologica
Volume34
Issue number5
DOIs
Publication statusPublished - 1995

Bibliographical note

Funding Information:
We thank Drs. Johannes Bjornsson, Jon Gunnlaugur Jonasson and staff of Departments of Pathology and Oncology, University Hospital Iceland, for supplying samples, clinical data and technical assistance. Thanks to the Agricultural Research Institute for molecular cytogenetics facilities, Drs. David Lane and Jiri Bartek for generous gifts of p53 antibodies, Prof. Anne-Lise Borresen for generous gift of probes and advice on CDGE and Laufey Tryggvadottir for assistance with statistical analysis. This work was supported by grants from The Icelandic Cancer Society Science Fund, The Nordic Cancer Union, The Icelandic Science Fund, The women’s branch of the Icelandic Red Cross and The National Hospital Science Fund.

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