Genomic Instability in Head and Neck Cancer

Scholes, Andrea G. M.; Field, John K.

doi:10.1007/978-3-642-80169-3_7

Cited by 7 publications

(2 citation statements)

References 67 publications

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“…The frequency of LOH at chromosome 3p ranges between 50% and almost 100%, depending on the location of the markers on 3p examined. In samples from this study and our previous one [13], a frequency of 57% was found by using ®ve markers that spanned the entire chromosome arm, and this result is concordant with previous published allelotypes [10,11]. The region that demonstrated the highest prevalence of LOH was 3p25, which contains the von Hippel-Lindau (VHL) tumor suppressor gene and hOGG1.…”

Section: Discussionsupporting

confidence: 91%

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Frequent allelic loss at chromosome 3p distinct from genetic alterations of the 8-oxoguanine DNA glycosylase 1 gene in head and neck cancer

Blons¹,

Radicella

Laccourreye

et al. 1999

Mol. Carcinog.

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Cigarette smoking is the major known risk factor for head and neck cancer. Tobacco promotes oxidative stress and enhances tissue levels of 8-hydroxyguanine (8-OH-G) in smokers. The presence of 8-OH-G does not impede replication but leads to an accumulation of G-->T transversions. Recently, the gene for human 8-oxoguanine DNA glycosylase 1 (hOGG1), an enzyme involved in the repair of 8-OH-G in humans, was cloned and mapped to chromosome 3p. In head and neck tumors, the hOGG1 gene locus is often targeted by loss of heterozygosity (LOH), and the spectrum of mutations in the p53 gene shows a bias in favor of G:C-->T:A transversions, as would be expected if HOGG1 repair functions were disabled. To test the involvement of hOGG1 in head and neck carcinogenesis, we had previously screened 56 tumors for LOH at 3p. From these tumors and two others, we selected 33 tumors demonstrating LOH for further mutational analysis of this gene. No somatic inactivating mutation was found in hOGG1. Polymorphisms involving intron 4 and exon 7 were present in 30% of the patients. A new polymorphism was identified in one patient in exon 6 and led to the amino-acid change G308E. Similar repair activities were found for the wild-type and exon 6-variant enzymes. Therefore, the involvement of hOGG1 in head and neck carcinogenesis is not strongly supported by this work.

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Section: Discussionsupporting

confidence: 91%

“…The hOGG1 gene maps to 3p25, one of the most commonly lost chromosome segments in HNSCC [10,11]. Moreover, the study of p53 mutations in HNSCC-related tumors showed a bias in favor of G:C 3 T:A transversions, as it would be expected if hOGG1 repair function were disabled [12].…”

Section: Introductionmentioning

confidence: 99%