PMID- 10685634
OWN - NLM
STAT- MEDLINE
DCOM- 20000303
LR  - 20190722
IS  - 0046-8177 (Print)
IS  - 0046-8177 (Linking)
VI  - 31
IP  - 2
DP  - 2000 Feb
TI  - Histopathologic analysis of chromosome aneuploidy in ductal carcinoma in situ.
PG  - 201-7
AB  - Formalin-fixed, paraffin-embedded sections from 28 cases of ductal carcinoma in 
      situ (DCIS; 12 with coexisting invasive neoplasm) were analyzed for numerical 
      alterations of chromosomes 7, 8, 16, and 17 by performing fluorescence in situ 
      hybridization (FISH) using centromeric (alpha-satellite) probes. Based on signal 
      counts in 200 to 300 nuclei, each hybridization was classified as disomic (copy 
      loss in <40%, copy gain in < 10%), monosomic (copy loss in at least 50% of 
      nuclei, partial if 40% to 49%) or trisomic/polysomic (copy gain in at least 20% 
      of nuclei, partial if 10% to 19%). Grade I lesions were characterized by complete 
      lack of significant chromosome gain, but 29% showed partial (focal) monosomy. 
      Grade III lesions, in contrast, showed partial or complete trisomy/polysomy in 
      88% of hybridizations versus monosomy in only 4%. Grade II DCIS exhibited a mixed 
      pattern of chromosome aneuploidy: 38% hybridizations were disomic, 36% 
      trisomic/polysomic, and 26% monosomic (8 of 10 hybridizations showing complete 
      monosomy occurred in grade II lesions). Disomic hybridizations exhibiting rare 
      cells (5% to 10%) with copy gain were more frequent in tumors with coexisting 
      invasive neoplasm (5 of 17 v 2 of 33, P = .02). In morphologically heterogeneous 
      lesions, higher-grade foci were characterized by chromosome copy gain relative to 
      corresponding lower-grade areas in 17 of 22 (77%) hybridizations. These results 
      show the presence of multiple (at least 3) distinct chromosome aneuploidy 
      patterns in DCIS, in keeping with divergent mechanisms of genetic alteration. 
      Degree of chromosomal instability, moreover, may correlate with progression of 
      DCIS to invasive growth, implying that genetic instability is a parameter that 
      impacts the likelihood of early breast carcinoma progression.
FAU - Visscher, D
AU  - Visscher D
AD  - Department of Pathology, Harper Hospital, Detroit, MI 48201, USA.
FAU - Jimenez, R E
AU  - Jimenez RE
FAU - Grayson, M 3rd
AU  - Grayson M 3rd
FAU - Mendelin, J
AU  - Mendelin J
FAU - Wallis, T
AU  - Wallis T
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Hum Pathol
JT  - Human pathology
JID - 9421547
SB  - IM
MH  - *Aneuploidy
MH  - Breast Neoplasms/*genetics/pathology
MH  - Carcinoma in Situ/*genetics/pathology
MH  - Carcinoma, Ductal, Breast/*genetics/pathology
MH  - Chromosomes, Human, Pair 16
MH  - Chromosomes, Human, Pair 17
MH  - Chromosomes, Human, Pair 7
MH  - Chromosomes, Human, Pair 8
MH  - Female
MH  - Humans
MH  - In Situ Hybridization, Fluorescence
MH  - Monosomy
MH  - Trisomy
EDAT- 2000/02/24 09:00
MHDA- 2000/03/11 09:00
CRDT- 2000/02/24 09:00
PHST- 2000/02/24 09:00 [pubmed]
PHST- 2000/03/11 09:00 [medline]
PHST- 2000/02/24 09:00 [entrez]
AID - S0046-8177(00)80220-8 [pii]
AID - 10.1016/s0046-8177(00)80220-8 [doi]
PST - ppublish
SO  - Hum Pathol. 2000 Feb;31(2):201-7. doi: 10.1016/s0046-8177(00)80220-8.