PMID- 21734802
OWN - NLM
STAT- MEDLINE
DCOM- 20111027
LR  - 20211020
IS  - 2219-2840 (Electronic)
IS  - 1007-9327 (Print)
IS  - 1007-9327 (Linking)
VI  - 17
IP  - 24
DP  - 2011 Jun 28
TI  - Genomic imbalances in esophageal carcinoma cell lines involve Wnt pathway genes.
PG  - 2909-23
LID - 10.3748/wjg.v17.i24.2909 [doi]
AB  - AIM: To identify molecular markers shared across South African esophageal 
      squamous cell carcinoma (ESCC) cell lines using cytogenetics, fluorescence in 
      situ hybridization (FISH) and single nucleotide polymorphism (SNP) array copy 
      number analysis. METHODS: We used conventional cytogenetics, FISH, and multicolor 
      FISH to characterize the chromosomal rearrangements of five ESCC cell lines 
      established in South Africa. The whole genome copy number profile was established 
      from 250K SNP arrays, and data was analyzed with the CNAT 4.0 and GISTIC 
      software. RESULTS: We detected common translocation breakpoints involving 
      chromosomes 1p11-12 and 3p11.2, the latter correlated with the deletion, or 
      interruption of the EPHA3 gene. The most significant amplifications involved the 
      following chromosomal regions and genes: 11q13.3 (CCND1, FGF3, FGF4, FGF19, 
      MYEOV), 8q24.21(C-MYC, FAM84B), 11q22.1-q22.3 (BIRC2, BIRC3), 5p15.2 (CTNND2), 
      3q11.2-q12.2 (MINA) and 18p11.32 (TYMS, YES1). The significant deletions included 
      1p31.2-p31.1 (CTH, GADD45alpha, DIRAS3), 2q22.1 (LRP1B), 3p12.1-p14.2 (FHIT), 
      4q22.1-q32.1 (CASP6, SMAD1), 8p23.2-q11.1 (BNIP3L) and 18q21.1-q21.2 (SMAD4, 
      DCC). The 3p11.2 translocation breakpoint was shared across four cell lines, 
      supporting a role for genes involved at this site, in particular, the EPHA3 gene 
      which has previously been reported to be deleted in ESCC. CONCLUSION: The finding 
      that a significant number of genes that were amplified (FGF3, FGF4, FGF19, CCND1 
      and C-MYC) or deleted (SFRP2 gene) are involved in the Wnt and fibroblast growth 
      factor signaling pathways, suggests that these pathways may be activated in these 
      cell lines.
FAU - Brown, Jacqueline
AU  - Brown J
AD  - National Health Laboratory Services and University of the Witwatersrand, York Rd, 
      Parktown Johannesburg 2193, South Africa. jacqueline.brown@nhls.ac.za
FAU - Bothma, Hannelie
AU  - Bothma H
FAU - Veale, Robin
AU  - Veale R
FAU - Willem, Pascale
AU  - Willem P
LA  - eng
GR  - Medical Research Council/United Kingdom
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - World J Gastroenterol
JT  - World journal of gastroenterology
JID - 100883448
RN  - 0 (Biomarkers, Tumor)
RN  - 0 (Wnt Proteins)
RN  - 62031-54-3 (Fibroblast Growth Factors)
SB  - IM
MH  - Biomarkers, Tumor/genetics
MH  - Carcinoma, Squamous Cell/*genetics
MH  - Cell Line, Tumor
MH  - Chromosome Aberrations
MH  - Chromosomes, Human, Pair 1/genetics
MH  - Chromosomes, Human, Pair 3/genetics
MH  - Cytogenetic Analysis
MH  - Esophageal Neoplasms/*genetics
MH  - Fibroblast Growth Factors/genetics
MH  - Humans
MH  - In Situ Hybridization, Fluorescence
MH  - Karyotyping
MH  - Polymorphism, Single Nucleotide
MH  - Signal Transduction/*genetics
MH  - Wnt Proteins/*genetics
PMC - PMC3129505
OTO - NOTNLM
OT  - Cancer
OT  - Esophagus
OT  - Fluorescent in situ hybridization
OT  - Single nucleotide polymorphism arrays
EDAT- 2011/07/08 06:00
MHDA- 2011/10/28 06:00
PMCR- 2011/06/28
CRDT- 2011/07/08 06:00
PHST- 2010/10/07 00:00 [received]
PHST- 2010/10/30 00:00 [revised]
PHST- 2010/11/06 00:00 [accepted]
PHST- 2011/07/08 06:00 [entrez]
PHST- 2011/07/08 06:00 [pubmed]
PHST- 2011/10/28 06:00 [medline]
PHST- 2011/06/28 00:00 [pmc-release]
AID - 10.3748/wjg.v17.i24.2909 [doi]
PST - ppublish
SO  - World J Gastroenterol. 2011 Jun 28;17(24):2909-23. doi: 10.3748/wjg.v17.i24.2909.