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BMC Cancer. 2005 Jul 9;5:77.

Microarray comparative genomic hybridization detection of chromosomal imbalances in uterine cervix carcinoma.

Author information

1
Unidad de Investigación Médica en Enfermedades Oncológicas, Centro Médico Nacional Siglo XXI-IMSS, Mexico. ahidalgo@inmegen.org.mx

Abstract

BACKGROUND:

Chromosomal Comparative Genomic Hybridization (CGH) has been applied to all stages of cervical carcinoma progression, defining a specific pattern of chromosomal imbalances in this tumor. However, given its limited spatial resolution, chromosomal CGH has offered only general information regarding the possible genetic targets of DNA copy number changes.

METHODS:

In order to further define specific DNA copy number changes in cervical cancer, we analyzed 20 cervical samples (3 pre-malignant lesions, 10 invasive tumors, and 7 cell lines), using the GenoSensor microarray CGH system to define particular genetic targets that suffer copy number changes.

RESULTS:

The most common DNA gains detected by array CGH in the invasive samples were located at the RBP1-RBP2 (3q21-q22) genes, the sub-telomeric clone C84C11/T3 (5ptel), D5S23 (5p15.2) and the DAB2 gene (5p13) in 58.8% of the samples. The most common losses were found at the FHIT gene (3p14.2) in 47% of the samples, followed by deletions at D8S504 (8p23.3), CTDP1-SHGC- 145820 (18qtel), KIT (4q11-q12), D1S427-FAF1 (1p32.3), D9S325 (9qtel), EIF4E (eukaryotic translation initiation factor 4E, 4q24), RB1 (13q14), and DXS7132 (Xq12) present in 5/17 (29.4%) of the samples.

CONCLUSION:

Our results confirm the presence of a specific pattern of chromosomal imbalances in cervical carcinoma and define specific targets that are suffering DNA copy number changes in this neoplasm.

PMID:
16004614
PMCID:
PMC1186020
DOI:
10.1186/1471-2407-5-77
[Indexed for MEDLINE]
Free PMC Article

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