PMID- 8625240
OWN - NLM
STAT- MEDLINE
DCOM- 19960626
LR  - 20100324
IS  - 0008-543X (Print)
IS  - 0008-543X (Linking)
VI  - 77
IP  - 2
DP  - 1996 Jan 15
TI  - Evaluation of chromosome aneuploidy in tissue sections of preinvasive breast 
      carcinomas using interphase cytogenetics.
PG  - 315-20
AB  - 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.
FAU - Visscher, D W
AU  - Visscher DW
AD  - Department of Pathology, Harper Receiving Hospital, Wayne State University School 
      of Medicine, Detroit, Michigan 48201, USA.
FAU - Wallis, T L
AU  - Wallis TL
FAU - Crissman, J D
AU  - Crissman JD
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Cancer
JT  - Cancer
JID - 0374236
SB  - IM
MH  - Aneuploidy
MH  - Breast/cytology
MH  - Breast Neoplasms/*genetics
MH  - Carcinoma/*genetics
MH  - Carcinoma in Situ/*genetics
MH  - Carcinoma, Ductal, Breast/genetics
MH  - Carcinoma, Lobular/genetics
MH  - Chromosomes, Human, Pair 17
MH  - Chromosomes, Human, Pair 8
MH  - Humans
MH  - In Situ Hybridization, Fluorescence
MH  - Interphase
EDAT- 1996/01/15 00:00
MHDA- 2000/06/20 09:00
CRDT- 1996/01/15 00:00
PHST- 1996/01/15 00:00 [pubmed]
PHST- 2000/06/20 09:00 [medline]
PHST- 1996/01/15 00:00 [entrez]
AID - 10.1002/(SICI)1097-0142(19960115)77:2<315::AID-CNCR14>3.0.CO;2-4 [pii]
AID - 10.1002/(SICI)1097-0142(19960115)77:2<315::AID-CNCR14>3.0.CO;2-4 [doi]
PST - ppublish
SO  - Cancer. 1996 Jan 15;77(2):315-20. doi: 
      10.1002/(SICI)1097-0142(19960115)77:2<315::AID-CNCR14>3.0.CO;2-4.