Home LiteratureArticle Details
PMID: 9331099 Published · ppublish English Comparative Study Journal Article Research Support, Non-U.S. Gov't

Mapping of DNA amplifications at 15 chromosomal localizations in 1875 breast tumors: definition of phenotypic groups.

Cancer research ·Vol. 57 ·No. 19 ·1997-10-01 ·Pages 4360-7

Courjal F, Cuny M, Simony-Lafontaine J, Louason G, Speiser P, Zeillinger R, Rodriguez C, Theillet C

Abstract

DNA amplification is frequent in breast cancer and has been associated with specific clinicopathological parameters and/or worsened course of the disease. In the present work, we were interested in further defining the association linking the occurrence of DNA amplification to the emergence of specific breast tumor phenotype. To this aim, we studied by Southern blotting a total of 1875 breast tumor DNAs with 26 probes mapping at 15 distinct chromosomal localizations. Of the 26 loci tested, 11 loci showed elevated levels of amplification, 9 loci showed occasional and/or low level of DNA copy number increase, and 6 loci showed very rare or no variation. This allowed us to define six amplified domains mapping at 8p12, 8q24, 11q13, 12q13, 17q12, and 20q13.2, respectively. Over 60% of the tumors analyzed presented at least one amplification at one of these localizations. Amplifications often covered large regions of DNA and bore complex patterns involving coamplification of several colocalized markers. Statistical analysis revealed correlations associating DNA amplification with breast tumor phenotype, as well as sets of preferential coamplifications. Based on these correlations, we defined three subsets of breast cancer according to their patterns of DNA amplification. The first subset (group A) was organized around the amplifications at 11q13 and/or 8p12 and was predominantly composed of estrogen receptor-positive tumors and presented a large proportion of lobular cancers. The second subset (group B) was organized around the amplifications of ERBB2 and/or MYC. These tumors were mostly estrogen receptor-negative and of the ductal invasive type. The third subset (group C) corresponded to tumors in which no amplification was detected in the present screen. Tumors in this group were largely diploid and of low histopathological grading.

MeSH Terms
Adult Aged Blotting, Southern Breast Neoplasms/classification,genetics,pathology Carcinoma, Ductal, Breast/genetics,pathology Carcinoma, Lobular/genetics,pathology Chromosome Mapping Chromosomes, Human/genetics,ultrastructure DNA Probes DNA, Neoplasm/genetics Estrogens Female Gene Amplification Genes, myc Genetic Markers Humans Middle Aged Neoplasm Invasiveness Neoplasms, Hormone-Dependent/genetics,pathology Phenotype Receptor, ErbB-2/genetics
Chemicals
DNA Probes DNA, Neoplasm Estrogens Genetic Markers Receptor, ErbB-2
Authors & Affiliations
8 authors, click to expand affiliations / ORCID
Courjal F
Institut de Génétique Moléculaire de Montpellier, UMR 5535, CNRS, France.
Cuny M
Simony-Lafontaine J
Louason G
Speiser P
Zeillinger R
Rodriguez C
Theillet C
Article Info
Journal
Cancer research
Abbr.
Cancer Res
ISSN
0008-5472
Published
1997-10-01
Pages
4360-7
Language
English
Region
United States
NLM ID
2984705R
Subset
IM
Analysis Services
Analysis Services

Contact

No. 2 Wenbo Road, Zhangqiu District, Jinan, Shandong

Qilu Normal University · Genelibs Bioinformatics Lab

750 Shunhua Rd, Jinan

2F, Bldg F, University Science Park

Tel: 0531-88819269

WeChat Official Account

Follow our WeChat subscription account for real-time updates and the latest in medical and biological research.


Business Email

E-mail: product@genelibs.com