PMID- 9665480
OWN - NLM
STAT- MEDLINE
DCOM- 19980723
LR  - 20181113
IS  - 0002-9440 (Print)
IS  - 1525-2191 (Electronic)
IS  - 0002-9440 (Linking)
VI  - 153
IP  - 1
DP  - 1998 Jul
TI  - Genetic aberrations in hypodiploid breast cancer: frequent loss of chromosome 4 
      and amplification of cyclin D1 oncogene.
PG  - 191-9
AB  - The evolution of somatic genetic aberrations in breast cancer has remained poorly 
      understood. The most common chromosomal abnormality is hyperdiploidy, which is 
      thought to arise via a transient hypodiploid state. However, hypodiploidy 
      persists in 1 to 2% of breast tumors, which are characterized by a poor 
      prognosis. We studied the genetic aberrations in 15 flow cytometrically 
      hypodiploid breast cancers by comparative genomic hybridization (CGH) and 
      fluorescence in situ hybridization (FISH). Surprisingly, numerous copy number 
      gains were detected in addition to the copy number losses. The number of gains 
      per tumor was 4.3 +/- 3.2 and that of losses was 4.5 +/- 3.3 (mean +/- SD), which 
      is similar to that previously observed in hyperdiploid breast cancers. Gains at 
      chromosomes or chromosomal regions at 11q13, 1q, 19, and 16p and losses of 2q, 4, 
      6q, 9p, 13, and 18 were most commonly observed. Compared with unselected breast 
      carcinomas, hypodiploid tumors showed certain differences. Loss of chromosome 4 
      (53%) and gain of 11q13 (60%) were significantly more common in hypodiploid 
      tumors. The gain at 11q13 was found by FISH to harbor amplification of the Cyclin 
      D1 oncogene, which is therefore three to four times more common in hypodiploid 
      than in unselected breast cancers (15 to 20%). Structural chromosomal aberrations 
      (such as Cyclin D1 amplification) were present both in diploid and hypodiploid 
      tumor cell populations, as assessed by FISH and CGH after flow cytometric 
      sorting. Together these results indicate that hypodiploid tumors form a distinct 
      genetic entity of invasive breast cancer, although they probably share a common 
      genetic evolution pathway where structural chromosomal aberrations precede gross 
      DNA ploidy changes.
FAU - Tanner, M M
AU  - Tanner MM
AD  - Laboratory of Cancer Genetics, University and University Hospital of Tampere, 
      Finland.
FAU - Karhu, R A
AU  - Karhu RA
FAU - Nupponen, N N
AU  - Nupponen NN
FAU - Borg, A
AU  - Borg A
FAU - Baldetorp, B
AU  - Baldetorp B
FAU - Pejovic, T
AU  - Pejovic T
FAU - Ferno, M
AU  - Ferno M
FAU - Killander, D
AU  - Killander D
FAU - Isola, J J
AU  - Isola JJ
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Am J Pathol
JT  - The American journal of pathology
JID - 0370502
RN  - 136601-57-5 (Cyclin D1)
SB  - IM
MH  - Adult
MH  - Aged
MH  - Aged, 80 and over
MH  - Breast Neoplasms/*genetics
MH  - *Chromosome Aberrations
MH  - Chromosomes, Human, Pair 11
MH  - *Chromosomes, Human, Pair 4
MH  - Cyclin D1/*genetics
MH  - Diploidy
MH  - Female
MH  - Flow Cytometry
MH  - Gene Amplification
MH  - Humans
MH  - In Situ Hybridization, Fluorescence
MH  - Middle Aged
MH  - Nucleic Acid Hybridization
PMC - PMC1852954
EDAT- 1998/07/17 00:00
MHDA- 1998/07/17 00:01
PMCR- 1999/01/01
CRDT- 1998/07/17 00:00
PHST- 1998/07/17 00:00 [pubmed]
PHST- 1998/07/17 00:01 [medline]
PHST- 1998/07/17 00:00 [entrez]
PHST- 1999/01/01 00:00 [pmc-release]
AID - S0002-9440(10)65560-5 [pii]
AID - 1335 [pii]
AID - 10.1016/S0002-9440(10)65560-5 [doi]
PST - ppublish
SO  - Am J Pathol. 1998 Jul;153(1):191-9. doi: 10.1016/S0002-9440(10)65560-5.