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. 1996 Jan 15;77(2):315-20.
doi: 10.1002/(SICI)1097-0142(19960115)77:2<315::AID-CNCR14>3.0.CO;2-4.

Evaluation of chromosome aneuploidy in tissue sections of preinvasive breast carcinomas using interphase cytogenetics

D W Visscher  1 , T L Wallis, J D Crissman
Affiliations

Evaluation of chromosome aneuploidy in tissue sections of preinvasive breast carcinomas using interphase cytogenetics

D W Visscher et al. Cancer. .

Abstract

Background: Little is known about cellular level genetic alterations in preinvasive breast lesions, particularly lobular carcinoma in situ.

Methods: We employed fluorescence in situ hybridization (FISH) using pericentromeric (alpha satellite) probes to assess numerical alterations of chromosomes 1, 7, 8, 16, 17, and X in deparaffinized archival tissue sections of 9 lobular carcinomas in situ (LCIS), 10 ductal carcinomas in situ (DCIS), and a spectrum of proliferative lesions (including 3 ductal hyperplasias, 1 adenosis, 1 radial scar, and 2 atypical hyperplasias). Three of the LCIS lesions and five of the DCIS lesions were from patients who had a concurrent invasive neoplasm as a component of the tumor.

Results: None of the proliferative lesions exhibited detectable chromosome gains, and only 1 showed evidence of signal loss consistent with monosomy (chromosome 7 in the adenosis lesion). Six LCIS patients (67%) displayed evidence of monosomy, with involvement of chromosome 17 in 6 of 6 patients, chromosome 8 in 2 of 6 patients, and chromosome 7 in 2 of 6 patients. Two LCIS patients, each of whom had a concurrent invasive neoplasm, exhibited signal gains consistent with trisomy for chromosomes 1 and 8 (1 patient each). Chromosome aneuploidies were observed in 7 of 10 (70%) DCIS patients, including 2 of 5 patients (40%) without concurrent invasive neoplasm and 5 of 5 patients (100%) with concurrent invasive neoplasm. The pattern of numerical chromosome alteration in DCIS included two patients with losses only, 2 patients with gains only, and 3 patients with both gains and losses (i.e., involving different chromosomes). Chromosome 17 aneuploidy was observed in all DCIS and all LCIS patients who exhibited abnormalities; however, DCIS patients showed more frequent aneuploidies for chromosomes X and 16 (0 LCIS patients vs. 4 DCIS patients with each).

Conclusions: Distinctive pathologic subsets of preinvasive breast neoplasia have divergent patterns of genetic instability. Foci of residual in situ neoplasia that accompany invasive disease may have a greater degree of genetic instability than neoplasms that lack progression to invasive phenotype.

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