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Microsatellite instability in ductal carcinomain situ of the breast

✍ Scribed by Walsh, Tom; Chappell, Stephen A.; Shaw, Jacqui A.; Walker, Rosemary A.

Publisher: John Wiley and Sons
Year: 1998
Tongue: English
Weight: 196 KB
Volume: 185
Category: Article
ISSN: 0022-3417
DOI: 10.1002/(sici)1096-9896(199805)185:1<18::aid-path41>3.0.co;2-g

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✦ Synopsis

Microsatellite instability (MI +

) is associated with defects in mismatch repair, resulting in a 'mutator' phenotype and the development and progression of cancer. MI + has been documented in invasive breast carcinomas. This study was undertaken to determine whether MI + is found in the early non-invasive form of breast cancer, ductal carcinoma in situ (DCIS). We examined microdissected ducts from 23 cases of DCIS with 11 markers comprising mono-, di-, and trinucleotide repeats from six chromosomal regions. Five tumours (22 per cent) displayed MI + at two or more loci, in all ducts examined. A further seven (30 per cent) tumours showed alterations at a single locus (the DM-1 trinucleotide), and for two of these, heterogeneity between ducts was observed. Alterations at microsatellite repeat motifs in the coding regions of four cancer-associated genes (TGF RII, IGFIIR, BAX, and E2F-4) were not observed. Immunohistochemistry revealed that there was no loss of reactivity for the mismatch repair proteins, MLH1, MSH2, and PMS2, in the DCIS cases. In general, MI + tumours and those with alterations at the DM-1 microsatellite were predominantly of higher nuclear grade and expressing c-erbB-2, suggesting that aberrations in DNA repair functions may lead to the acquisition of a more aggressive phenotype in breast cancer.

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