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

doi:10.1186/1471-2407-5-77

BMC Cancer

Volume 5

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Hidalgo A
Baudis M
Petersen I
Arreola H
Piña P
Vázquez-Ortiz G
Hernández D
González J
Lazos M
López R
Pérez C
García J
Vázquez K
Alatorre B
Salcedo M

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Hidalgo A
Baudis M
Petersen I
Arreola H
Piña P
Vázquez-Ortiz G
Hernández D
González J
Lazos M
López R
Pérez C
García J
Vázquez K
Alatorre B
Salcedo M
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Research article

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

Alfredo Hidalgo¹^,8 , Michael Baudis² , Iver Petersen³ , Hugo Arreola¹ , Patricia Piña¹ , Guelaguetza Vázquez-Ortiz¹ , Dulce Hernández⁴ , José González⁵ , Minerva Lazos⁶ , Ricardo López¹ , Carlos Pérez¹ , José García⁷ , Karla Vázquez¹ , Brenda Alatorre¹ and Mauricio Salcedo¹

¹Laboratorio de Oncología Genómica, Unidad de Investigación Médica en Enfermedades Oncológicas, Centro Médico Nacional Siglo XXI-IMSS, México

²Division of Pediatric Haematology/Oncology, University of Florida, Gainesville, USA

³Institute of Pathology, University Hospital Charité, Berlin, Germany

⁴Servicio de Epidemiología, Hospital de Oncologia, Centro Médico Nacional Siglo XXI-IMSS, México

⁵Clínica de Displasias, Hospital de Gineco-Obstetrica No. 4, Luis Castelazo Ayala-IMSS, México

⁶Departamento de Patología, Facultad de Medicina UNAM-Hospital General de México, SS, México

⁷Laboratorio de Biología Teórica, Departamento de Investigación, Universidad La Salle, México

⁸Instituto Nacional de Medicina Genomica, Secretaria de Salud, Mexico

author email corresponding author email

BMC Cancer 2005, 5:77doi:10.1186/1471-2407-5-77


Published:	9 July 2005

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.