PMID- 15588854
OWN - NLM
STAT- MEDLINE
DCOM- 20050111
LR  - 20161025
IS  - 0165-4608 (Print)
IS  - 0165-4608 (Linking)
VI  - 156
IP  - 1
DP  - 2005 Jan 1
TI  - Molecular cytogenetic analysis of a human breast metastasis model: identification 
      of phenotype-specific chromosomal rearrangements.
PG  - 37-48
AB  - We have previously characterized an experimental system in which the role of 
      candidate metastasis-related genes can be screened and tested. Monoclonal cell 
      lines M4A4 and NM2C5 originated from the MDA-MB-435 breast tumor cell line but 
      have opposite metastatic capabilities in vivo. To investigate gross genetic 
      changes present in this model, we performed a detailed molecular cytogenetic 
      evaluation of the parental cell line, the M4A4 and NM2C5 cell lines, and related 
      clones of metastatic phenotype. Using a combination of spectral karyotyping 
      (SKY), G-banding, and fluorescence in situ hybridization (FISH), we were able to 
      resolve the identity of all common marker chromosomes present in MDA-MB-435 
      cells, and to define several chromosomal changes, which were specific to each 
      monoclonal cell line. Twenty identical structural and numerical chromosomal 
      aberrations, including trisomies of chromosomes 2 and 5 as well as t(1;7), 
      t(1;10), t(8;11), t(8;15), and t(20;21), were present in all cell lines. The 
      majority of translocations were relatively simple non-reciprocal rearrangements, 
      most frequently involving chromosomes 19, 1, 6, and 20. Chromosomal gains of 1, 
      7q, 8q, and 20q are common alterations in breast cancer. The metastatic M4A4 cell 
      line contained numerous unique chromosomal aberrations, of which an abnormal 
      banding region on chromosome 22, abr(22), was the best clone-specific identifier. 
      Conversely, the t(12;15)(q22;q26.1) was found exclusively in the non-metastatic 
      NM2C5 cell line. The integration of these karyotypic data with other cytogenetic 
      and genomic databases will enhance our ability to identify genes that play 
      critical roles in cancer development and progression.
FAU - Goodison, Steve
AU  - Goodison S
AD  - Department of Pathology, University of Florida, Shands Health Science Center, 655 
      West 8th Street, Jacksonville, FL 32209-6511, USA. steve.goodison@jax.ufl.edu
FAU - Viars, Carrie
AU  - Viars C
FAU - Urquidi, Virginia
AU  - Urquidi V
LA  - eng
GR  - R01 CA108597/CA/NCI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Cancer Genet Cytogenet
JT  - Cancer genetics and cytogenetics
JID - 7909240
SB  - IM
MH  - Breast Neoplasms/*genetics/pathology
MH  - Chromosome Aberrations
MH  - Chromosome Banding
MH  - Cytogenetic Analysis
MH  - Female
MH  - Humans
MH  - In Situ Hybridization, Fluorescence
MH  - Karyotyping
MH  - Neoplasm Metastasis/genetics
MH  - Phenotype
MH  - Spectral Karyotyping
MH  - Tumor Cells, Cultured
EDAT- 2004/12/14 09:00
MHDA- 2005/01/12 09:00
CRDT- 2004/12/14 09:00
PHST- 2004/01/20 00:00 [received]
PHST- 2004/04/02 00:00 [revised]
PHST- 2004/04/07 00:00 [accepted]
PHST- 2004/12/14 09:00 [pubmed]
PHST- 2005/01/12 09:00 [medline]
PHST- 2004/12/14 09:00 [entrez]
AID - S0165-4608(04)00173-6 [pii]
AID - 10.1016/j.cancergencyto.2004.04.005 [doi]
PST - ppublish
SO  - Cancer Genet Cytogenet. 2005 Jan 1;156(1):37-48. doi: 
      10.1016/j.cancergencyto.2004.04.005.