PMID- 18506748
OWN - NLM
STAT- MEDLINE
DCOM- 20081031
LR  - 20220321
IS  - 1098-2264 (Electronic)
IS  - 1045-2257 (Linking)
VI  - 47
IP  - 9
DP  - 2008 Sep
TI  - Identification of copy number gain and overexpressed genes on chromosome arm 20q 
      by an integrative genomic approach in cervical cancer: potential role in 
      progression.
PG  - 755-65
LID - 10.1002/gcc.20577 [doi]
AB  - Recurrent karyotypic abnormalities are a characteristic feature of cervical 
      cancer (CC) cells, which may result in deregulated expression of important genes 
      that contribute to tumor initiation and progression. To examine the role of gain 
      of the long arm of chromosome 20 (20q), one of the common chromosomal gains in 
      CC, we evaluated CC at various stages of progression using single nucleotide 
      polymorphism (SNP) array, gene expression profiling, and fluorescence in situ 
      hybridization (FISH) analyses. This analysis revealed copy number increase (CNI) 
      of 20q in >50% of invasive CC and identified two focal amplicons at 20q11.2 and 
      20q13.13 in a subset of tumors. We further demonstrate that the acquisition of 
      20q gain occurs at an early stage in CC development and the high-grade squamous 
      intraepithelial lesions (HSIL) that exhibit 20q CNI are associated (P = 0.05) 
      with persistence or progression to invasive cancer. We identified a total of 26 
      overexpressed genes as consequence of 20q gain (N = 14), as targets of amplicon 1 
      (N = 9; two genes also commonly expressed with 20q gain) and amplicon 2 (N = 6; 
      one gene also commonly expressed with 20q gain). These include a number of 
      functionally important genes in cell cycle regulation (E2F1, TPX2, KIF3B, PIGT, 
      and B4GALT5), nuclear function (CSEL1), viral replication (PSMA7 and LAMA5), 
      methylation and chromatin remodeling (ASXL1, AHCY, and C20orf20), and 
      transcription regulation (TCEA2). Our findings implicate a role for these genes 
      in CC tumorigenesis, represent an important step toward the development of 
      clinically significant biomarkers, and form a framework for testing as molecular 
      therapeutic targets.
CI  - 2008 Wiley-Liss, Inc.
FAU - Scotto, Luigi
AU  - Scotto L
AD  - Department of Pathology, Columbia University Medical Center, New York, NY 10032, 
      USA.
FAU - Narayan, Gopeshwar
AU  - Narayan G
FAU - Nandula, Subhadra V
AU  - Nandula SV
FAU - Arias-Pulido, Hugo
AU  - Arias-Pulido H
FAU - Subramaniyam, Shivakumar
AU  - Subramaniyam S
FAU - Schneider, Achim
AU  - Schneider A
FAU - Kaufmann, Andreas M
AU  - Kaufmann AM
FAU - Wright, Jason D
AU  - Wright JD
FAU - Pothuri, Bhavana
AU  - Pothuri B
FAU - Mansukhani, Mahesh
AU  - Mansukhani M
FAU - Murty, Vundavalli V
AU  - Murty VV
LA  - eng
GR  - CA095647/CA/NCI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PL  - United States
TA  - Genes Chromosomes Cancer
JT  - Genes, chromosomes & cancer
JID - 9007329
SB  - IM
MH  - *Chromosomes, Human, Pair 20
MH  - Disease Progression
MH  - Female
MH  - *Gene Amplification
MH  - *Gene Dosage
MH  - Gene Expression Profiling
MH  - Genome
MH  - Genomics
MH  - Humans
MH  - In Situ Hybridization, Fluorescence
MH  - Polymorphism, Single Nucleotide
MH  - Uterine Cervical Neoplasms/*genetics/pathology
EDAT- 2008/05/29 09:00
MHDA- 2008/11/01 09:00
CRDT- 2008/05/29 09:00
PHST- 2008/05/29 09:00 [pubmed]
PHST- 2008/11/01 09:00 [medline]
PHST- 2008/05/29 09:00 [entrez]
AID - 10.1002/gcc.20577 [doi]
PST - ppublish
SO  - Genes Chromosomes Cancer. 2008 Sep;47(9):755-65. doi: 10.1002/gcc.20577.