Loss of heterozygosity at 9q33 and hypermethylation of the DBCCR1 gene in oral squamous cell carcinoma
Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt
Standard
Loss of heterozygosity at 9q33 and hypermethylation of the DBCCR1 gene in oral squamous cell carcinoma. / Gao, S; Worm, J; Guldberg, P; Eiberg, H; Krogdahl, A; Sørensen, J A; Liu, C-J; Reibel, J; Dabelsteen, Erik.
I: B J C, Bind 91, Nr. 4, 16.08.2004, s. 760-4.Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt
Harvard
APA
Vancouver
Author
Bibtex
}
RIS
TY - JOUR
T1 - Loss of heterozygosity at 9q33 and hypermethylation of the DBCCR1 gene in oral squamous cell carcinoma
AU - Gao, S
AU - Worm, J
AU - Guldberg, P
AU - Eiberg, H
AU - Krogdahl, A
AU - Sørensen, J A
AU - Liu, C-J
AU - Reibel, J
AU - Dabelsteen, Erik
PY - 2004/8/16
Y1 - 2004/8/16
N2 - The DBCCR1 gene at chromosome 9q33 has been identified as a candidate tumour suppressor, which is frequently targeted by promoter hypermethylation in bladder cancer. Here, we studied the possible involvement of DBCCR1 in the development of oral squamous cell carcinoma. DNA from 34 tumours was examined for loss of heterozygosity (LOH) at three markers surrounding DBCCR1 and for hypermethylation of the DBCCR1 promoter, using methylation-specific PCR and methylation-specific melting-curve analysis. LOH was found in 10 of 31 cases (32%), and DBCCR1 hypermethylation was present in 15 of 34 cases (44%). Hypermethylation of DBCCR1 was also present in three of seven epithelial tissues adjacent to the tumours, including two hyperplastic and one histologically normal epithelia. Furthermore, of four oral leukoplakias with dysplasia, one showed LOH at 9q33 and two showed DBCCR1 hypermethylation. These data suggest that LOH at 9q33 and hypermethylation of the DBCCR1 promoter are frequent and possibly early events in oral malignant development.
AB - The DBCCR1 gene at chromosome 9q33 has been identified as a candidate tumour suppressor, which is frequently targeted by promoter hypermethylation in bladder cancer. Here, we studied the possible involvement of DBCCR1 in the development of oral squamous cell carcinoma. DNA from 34 tumours was examined for loss of heterozygosity (LOH) at three markers surrounding DBCCR1 and for hypermethylation of the DBCCR1 promoter, using methylation-specific PCR and methylation-specific melting-curve analysis. LOH was found in 10 of 31 cases (32%), and DBCCR1 hypermethylation was present in 15 of 34 cases (44%). Hypermethylation of DBCCR1 was also present in three of seven epithelial tissues adjacent to the tumours, including two hyperplastic and one histologically normal epithelia. Furthermore, of four oral leukoplakias with dysplasia, one showed LOH at 9q33 and two showed DBCCR1 hypermethylation. These data suggest that LOH at 9q33 and hypermethylation of the DBCCR1 promoter are frequent and possibly early events in oral malignant development.
KW - Adult
KW - Aged
KW - Carcinoma, Squamous Cell
KW - Cell Transformation, Neoplastic
KW - Chromosomes, Human, Pair 9
KW - DNA Methylation
KW - Female
KW - Genes, Tumor Suppressor
KW - Humans
KW - Loss of Heterozygosity
KW - Male
KW - Middle Aged
KW - Mouth Neoplasms
KW - Precancerous Conditions
KW - Promoter Regions, Genetic
KW - Tumor Suppressor Proteins
U2 - 10.1038/sj.bjc.6601980
DO - 10.1038/sj.bjc.6601980
M3 - Journal article
C2 - 15226771
VL - 91
SP - 760
EP - 764
JO - The British journal of cancer. Supplement
JF - The British journal of cancer. Supplement
SN - 0007-0920
IS - 4
ER -
ID: 119538458