Sequencing of double-stranded polymerase chain reaction products for mutation analysis

Anderson, R. David; Bao, C.-Y.; Minnick, Dana T.; Baxter, Jeff; Veigl, Martina L.; Sedwick, W. David

doi:10.1016/0027-5107(93)90219-6

Mutation Research/Fundamental and Molecular Mechanisms of Mutag

1993

DOI: 10.1016/0027-5107(93)90219-6

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Sequencing of double-stranded polymerase chain reaction products for mutation analysis

R. David Anderson

C.-Y. Bao

Dana T. Minnick

et al.

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Cited by 7 publications

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A high prevalence of p53 mutations in pre-malignant oral erythroplakia

Qin¹,

Park²,

Chen³

et al. 1999

Int. J. Cancer

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Oral squamous‐cell carcinoma is thought to be preceded by a number of precursor stages which induce morphological changes in cells of the oral mucosa resulting in clinically detectable pre‐malignant lesions such as erythroplakia or leukoplakia. To better understand the etiology of oral erythroplakia, we have examined the p53 tumor‐suppressor gene (exons 5–9) for mutations in 24 oral erythroplakia lesions of varying dysplastic phenotypes by PCR/single‐strand conformational polymorphism and direct DNA‐sequencing analyses. A total of 12 p53 mutations were detected in 11 of 24 (46%) erythroplakia specimens (one specimen contained two different p53 mutations); 25% were single‐base‐pair deletions and 33% were either G:C→T:A transversions or G:C→A:T transitions. A high prevalence of p53 mutation was observed in all categories of erythroplakia lesions: 33% for mildly dysplastic lesions, 50% for lesions exhibiting moderate to severe dysplasia and 50% for lesions that were carcinoma in situ. Although the combined prevalence of p53 mutations observed in erythroplakia was significantly higher (p = 0.02) than that observed earlier for leukoplakia, the prevalence of p53 mutations was similar in erythroplakia and leukoplakia specimens from smokers. The prevalence and spectrum of p53 mutations observed in this series of erythroplakia lesions are similar to those observed for oral squamous‐cell carcinoma. These results indicate that mutations of the p53 gene may be linked to the high malignant potential of erythroplakia and provide further evidence that p53 mutation may be an early event in the genesis of oral squamous‐cell carcinoma. Int. J. Cancer 80:345–348, 1999. © 1999 Wiley‐Liss, Inc.

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A high prevalence of p53 mutations in pre-malignant oral erythroplakia

Qin¹,

Park²,

Chen³

et al. 1999

Int. J. Cancer

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A low incidence of p53 mutations in pre‐malignant lesions of the oral cavity from non‐tobacco users

Lazarus

Sciubba

et al. 1995

Intl Journal of Cancer

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To determine the incidence of p53 mutations in pre-malignant lesions of the oral cavity from individuals without prior history of tobacco use, we have analyzed the conserved regions of the p53 gene (exons 5-9) in archival oral cavity lesion specimens obtained from patients with varied tobacco use histories, by polymerase chain reaction/single strand conformational polymorphism (PCR/SSCP) and DNA sequencing analysis. Twenty-six lesions were analyzed from 14 patients, with multiple lesions obtained from 8 patients. Six of these patients used tobacco, (3 being cigarette smokers, 1 ex-cigarette smoker, 1 moderate cigar smoker and 1 snuff chewer). The remaining 8 patients had no prior history of tobacco use. Thirteen of the pre-malignant lesions exhibited severe dysplasia, 9 exhibited moderate dysplasia and 4 exhibited mild dysplasia. Four of the 26 lesions exhibited p53 mutations, each being from a tobacco user. None of the 13 lesions from never-tobacco users exhibited p53 mutations. There was a significantly higher p53 mutation incidence in pre-malignant lesions from tobacco users (including ex-smokers) than in non-tobacco users as well as in cigarette smokers plus snuff chewers than in non-tobacco users. Two of the mutations were observed in lesions exhibiting severe dysplasia: 1 in a lesion exhibiting moderate dysplasia and 1 in a lesion exhibiting mild dysplasia. These data suggest that p53 mutation may be a very early event in oral cavity tumor progression and demonstrate that pre-malignant lesions obtained from non-tobacco users do not exhibit p53 mutations.

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Correlation of doxorubicin footprints with deletion endpoints in lacO of E. coli

Sedwick

Anderson

Baxter

et al. 1995

Mutation Research/Fundamental and Molecular Mechanisms of Mutag

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Sequencing of double-stranded polymerase chain reaction products for mutation analysis

Cited by 7 publications

References 13 publications

A high prevalence of p53 mutations in pre-malignant oral erythroplakia

A high prevalence of p53 mutations in pre-malignant oral erythroplakia

A low incidence of p53 mutations in pre‐malignant lesions of the oral cavity from non‐tobacco users

Correlation of doxorubicin footprints with deletion endpoints in lacO of E. coli

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