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Genetic expression profiles and chromosomal alterations in sporadic breast cancer in Mexican women
Breast cancer is the second-leading cause of death among Mexican women >35 years of age. At the molecular level, changes in many genetic pathways have been reported to be associated with this neoplasm. To analyze these changes, we determined gene expression profiles and chromosomal structural alt...
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Published in: | Cancer genetics and cytogenetics 2006-10, Vol.170 (2), p.147-151 |
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Main Authors: | , , , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | Breast cancer is the second-leading cause of death among Mexican women >35 years of age. At the molecular level, changes in many genetic pathways have been reported to be associated with this neoplasm. To analyze these changes, we determined gene expression profiles and chromosomal structural alterations in tumors from Mexican women. We obtained mRNA to identify expression profiles with microarray technology, and DNA to determine amplifications and deletions, in 10 fresh sporadic breast tumor biopsies without treatment, as well as in 10 nonaffected breast tissues. Expression profiles were compared with genetic changes observed by comparative genomic hybridization (CGH). We compared the expression profiles against the structural alterations from the studied genes by means of microarrays; at least 17 of these genes correlated with DNA copy number alterations. We found that the following genes were overexpressed:
LAMC1,
PCTK3,
CCNC,
CCND1,
FGF3,
PCTK2,
L1CAM,
BGN, and
PLXNB3 (alias
PLEXR). Underexpressed genes included
CASP9,
FGR,
TP73,
HSPG2, and
ERCC1; genes turned off included
FRAP1,
EPHA2 (previously
ECK),
IL12A,
E2F5,
TNFRSF10B,
TNFRSF10A,
EFNB3, and
BCL2. The results will allow us, in the near future, to outline genes that could serve as diagnostic, prognostic, or target therapy markers for the Mexican population. |
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ISSN: | 0165-4608 1873-4456 |
DOI: | 10.1016/j.cancergencyto.2006.06.002 |