title: Chromosomal amplifications, 3q gain and deletions of 2q33-q37 are the frequent genetic changes in cervical carcinoma.
abstract: BACKGROUND
  Carcinoma of uterine cervix is the second most common cancers among women worldwide. Combined radiation and chemotherapy is the choice of treatment for advanced stages of the disease. The prognosis is poor, with a five-year survival rate ranging from about 20-65%, depending on stage of the disease. Therefore, genetic characterization is essential for understanding the biology and clinical heterogeneity in cervical cancer (CC).
  
  
  METHODS
  We used a genome-wide screening method--comparative genomic hybridization (CGH) to identify DNA copy number changes in 77 patients with cervical cancer. We applied categorical and survival analyses to analyze whether chromosomal changes were related to clinico-pathologic characteristics and patients survival.
  
  
  RESULTS
  The CGH analysis revealed a loss of 2q33-q37 (57.1%), gain of 3q (54.5%) and chromosomal amplifications (20.77%) as frequent genetic changes. A total of 15 amplified chromosomal sites were detected in 16 cases that include 1p31, 2q32, 7q22, 8q21.2-q24, 9p22, 10q21, 10q24, 11q13, 11q21, 12q15, 14q12, 17p11.2, 17q22, 18p11.2, and 19q13.1. Recurrent amplified sites were noted at 11q13, 11q21, and 19q13.1. The genomic alterations were further evaluated for prognostic significance in CC patients, and we did not find any correlation with a number of clinical or histological parameters. The tumors harboring HPV18 exhibited higher genomic instability compared to tumors with HPV 16.
  
  
  CONCLUSIONS
  This study demonstrated that 2q33-q37 deletions, 3q gains and chromosomal amplifications as characteristic changes in invasive CC. These genetic alterations will aid in the identification of novel tumor suppressor gene(s) at 2q33-q37 and oncogenes at amplified chromosomal sites. Molecular characterization of these chromosomal changes utilizing the current genomic technologies will provide new insights into the biology and clinical behavior of CC.
authors.affiliation: Texas Children's Cancer Center, Baylor College of Medicine, Houston, TX, USA. prao@bcm.tmc.edu
authors.forename: Pulivarthi H
authors.initials: PH
authors.lastname: Rao
authors.forename: Hugo
authors.initials: H
authors.lastname: Arias-Pulido
authors.forename: Xin-Yan
authors.initials: XY
authors.lastname: Lu
authors.forename: Charles P
authors.initials: CP
authors.lastname: Harris
authors.forename: Hernan
authors.initials: H
authors.lastname: Vargas
authors.forename: Fang F
authors.initials: FF
authors.lastname: Zhang
authors.forename: Gopeshwar
authors.initials: G
authors.lastname: Narayan
authors.forename: Achim
authors.initials: A
authors.lastname: Schneider
authors.forename: Mary Beth
authors.initials: MB
authors.lastname: Terry
authors.forename: Vundavalli V V S
authors.initials: VV
authors.lastname: Murty
mesh_terms: D000230:Adenocarcinoma / Q000235:genetics*; D002294:Carcinoma, Squamous Cell / Q000235:genetics*; D002872:Chromosome Deletion; D002889:Chromosomes, Human, Pair 2; D002893:Chromosomes, Human, Pair 3; D005260:Female; D005784:Gene Amplification; D006801:Humans; D009693:Nucleic Acid Hybridization / Q000379:methods; D027383:Papillomaviridae / Q000302:isolation & purification; D002583:Uterine Cervical Neoplasms / Q000235:genetics* / Q000821:virology