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MYB oncogene amplification in hereditary BRCA1 breast cancer

Kauraniemi, P; Hedenfalk, Ingrid LU ; Persson, Karin; Duggan, D J; Tanner, Minna; Johannsson, Oskar; Olsson, Håkan LU ; Trent, J M; Isola, Jorma LU and Borg, Åke LU (2000) In Cancer Research 60(19). p.5323-5328
Abstract
Comparative genomic hybridization analysis has demonstrated that breast tumors from BRCA1 and BRCA2 germ-line mutation carriers contain a large number of chromosomal copy number gains and losses. A high regional copy number gain at 6q22-q24 was observed in one BRCA1 tumor, and fluorescence in situ hybridization analysis indicated a strong amplification of the MYB oncogene (15 copies of MYB compared with 1 copy of chromosome 6 centromere). Fluorescence in situ hybridization analysis revealed amplification of MYB in 5 (29%) of 17 BRCA1 breast tumors, whereas none of 8 BRCA2 tumors and 13 breast cancer cell lines, and only 2 of 100 sporadic breast tumors exhibited altered MYB copy numbers. Gene amplification resulted in mRNA overexpression as... (More)
Comparative genomic hybridization analysis has demonstrated that breast tumors from BRCA1 and BRCA2 germ-line mutation carriers contain a large number of chromosomal copy number gains and losses. A high regional copy number gain at 6q22-q24 was observed in one BRCA1 tumor, and fluorescence in situ hybridization analysis indicated a strong amplification of the MYB oncogene (15 copies of MYB compared with 1 copy of chromosome 6 centromere). Fluorescence in situ hybridization analysis revealed amplification of MYB in 5 (29%) of 17 BRCA1 breast tumors, whereas none of 8 BRCA2 tumors and 13 breast cancer cell lines, and only 2 of 100 sporadic breast tumors exhibited altered MYB copy numbers. Gene amplification resulted in mRNA overexpression as determined by Northern blot and cDNA microarray analysis, and protein overexpression by immunohistochemical staining. We conclude that MYB amplification is infrequent in sporadic breast cancer but common in breast tumors from BRCA1 mutation carriers, suggesting a role of this cell cycle regulator and transcription factor in the progression of some BRCA1 tumors. However, we cannot rule out the significance of other genes in the 6q22-q24 amplicon. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Cancer Research
volume
60
issue
19
pages
5323 - 5328
publisher
American Association for Cancer Research Inc.
external identifiers
  • pmid:11034064
  • scopus:0034307159
ISSN
1538-7445
language
English
LU publication?
yes
id
ed5f235d-9dc9-453b-9557-ed23548c838c (old id 1116597)
alternative location
http://cancerres.aacrjournals.org/cgi/content/full/60/19/5323
date added to LUP
2008-07-02 08:59:15
date last changed
2017-01-01 07:20:04
@article{ed5f235d-9dc9-453b-9557-ed23548c838c,
  abstract     = {Comparative genomic hybridization analysis has demonstrated that breast tumors from BRCA1 and BRCA2 germ-line mutation carriers contain a large number of chromosomal copy number gains and losses. A high regional copy number gain at 6q22-q24 was observed in one BRCA1 tumor, and fluorescence in situ hybridization analysis indicated a strong amplification of the MYB oncogene (15 copies of MYB compared with 1 copy of chromosome 6 centromere). Fluorescence in situ hybridization analysis revealed amplification of MYB in 5 (29%) of 17 BRCA1 breast tumors, whereas none of 8 BRCA2 tumors and 13 breast cancer cell lines, and only 2 of 100 sporadic breast tumors exhibited altered MYB copy numbers. Gene amplification resulted in mRNA overexpression as determined by Northern blot and cDNA microarray analysis, and protein overexpression by immunohistochemical staining. We conclude that MYB amplification is infrequent in sporadic breast cancer but common in breast tumors from BRCA1 mutation carriers, suggesting a role of this cell cycle regulator and transcription factor in the progression of some BRCA1 tumors. However, we cannot rule out the significance of other genes in the 6q22-q24 amplicon.},
  author       = {Kauraniemi, P and Hedenfalk, Ingrid and Persson, Karin and Duggan, D J and Tanner, Minna and Johannsson, Oskar and Olsson, Håkan and Trent, J M and Isola, Jorma and Borg, Åke},
  issn         = {1538-7445},
  language     = {eng},
  number       = {19},
  pages        = {5323--5328},
  publisher    = {American Association for Cancer Research Inc.},
  series       = {Cancer Research},
  title        = {MYB oncogene amplification in hereditary BRCA1 breast cancer},
  volume       = {60},
  year         = {2000},
}