Comparison of ultraviolet irradiation-induced mutagenesis of the lacI gene in Escherichia coli and in human 293 cells

Hsia, Han Chao; Lebkowski, Jane; Leong, Phaik-Mooi; Calos, Michèle P.; Miller, Jeffrey H

doi:10.1016/0022-2836(89)90368-9

Cited by 66 publications

(11 citation statements)

References 23 publications

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“…As in our study, most (80%) of these mutations were localized at codon 61. However, in both studies the mutational spectrum (60% transversions and 40% transitions) is different from the predominant UV-induced G->A transitions reported for other systems (4,9,10 Conclusions. Although an increasing number of human tumors have been screened for the occurrence of rczs gene mutations (3), only a few cases are known in which a xenobiotic agent may have been involved in the actual induction of the mutation.…”

contrasting

confidence: 64%

“…This result showed a significant correlation (P < 0.001) between continuous sun exposure and r-as mutation, suggesting that UV irradiation was the mutagenic agent. The fact that we found no N-ras mutations at intermittently exposed sites does not exclude a role for UV irradiation in the development of these tumors (7) geted most frequently to dipyrimidine sites (4,9,10). In our study, the affected sequences opposite the codons of the N-ras oncogene all harbored pyrimidine doublets (TT or CC; Table 2).…”

mentioning

confidence: 69%

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N-ras mutations in human cutaneous melanoma from sun-exposed body sites.

Veer¹,

Burgering²,

Versteeg³

et al. 1989

Mol. Cell. Biol.

249

128

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In 7 of 37 patients with cutaneous melanoma, mutations in the N-ras gene were found. The primary tumors of these seven patients were exclusively localized on body sites continuously exposed to sunlight. Moreover, the ras mutations were all at or near dipyrimidine sites known to be targets of UV damage. Two primary tumors were biclonal with respect to ras mutation. An active role for UV irradiation in induction of the mutations is suggested.In animals, a wide range of xenobiotic agents are capable of inducing mutations in the r-as oncogene family (2). Little is known, however, about the involvement of mutagenic agents in the induction of ras mutations in humans. For human cutaneous melanoma, there is epidemiological evidence suggesting a role of UV irradiation in occurrence of the tumor (18).N-ras activated in melanoma. To investigate the role of UV irradiation in the activation of ras genes, we studied 63 tumor samples from 37 cutaneous melanoma patients (Table 1) for mutations in H-, K-, or N-r-as. These samples included 10 primary tumors, 40 metastases, and 13 cell lines, all of the non-lentigo maligna type. To analyze mutational activation of ras genes, polymerase chain reaction-amplified DNA samples were prepared aR described previously (17) either from DNA obtained from fresh tumor specimens and cell lines or from Formalin-fixed and paraffin-embedded material (16). All samples contained at least 50% tumor cells. In certain cases (e.g., primary tumors of patients 4 and 10), parts of paraffin sections that contained more than 90% tumor cells were chosen. The amplified DNA was spotted onto nylon membranes and hybridized to probes 20 nucleotides long as described elsewhere (21) (Fig.

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contrasting

confidence: 64%

mentioning

confidence: 69%

N-ras mutations in human cutaneous melanoma from sun-exposed body sites.

Veer¹,

Burgering²,

Versteeg³

et al. 1989

Mol. Cell. Biol.

249

128

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“…the known environmental differences in connection with high lung cancer mortality in some eastern countries (e.g. China and • AFB 1 is a potent mutagen and carcinogen in laboratory studies 100-102 • AFB 1 is enzymatically activated by human hepatocytes 103,104 and the 8,9-AFB 1 oxide binds to the third base (G) in codon 249 105 • AFB 1 exposure to human liver cells 57,58 in vitro produces codon 249 ser p53 mutations • 249 ser p53 expression inhibits apoptosis, 106 p53mediated transcription, 107 and enhances liver cell growth in vitro 108 • UV is a mutagen and carcinogen in laboratory studies 120 • Cyclobutane pyrimidine dimers and pyrimidine photoproducts are the two major adducts produced by UV-irradiation and induces C to T, at non-CpG sites, and CC to TT mutations 60,121 • Skin cancer in xeroderma pigmentosum patients, with defective nucleotide excision repair, contains a high frequency of CC to TT mutations 122 • UV exposure produces CC to TT mutations in studies using phage, bacteria, and mice 60,[123][124][125] indoor coal combustion in connection with high lung cancer incidence in women, [68][69][70], we have analysed the p53 database in western and eastern geographical areas of the world.…”

Section: P53 Mutations In Lung Cancers From Smokers and Former-smokersmentioning

confidence: 99%

Molecular epidemiology of human cancer risk: gene-environment interactions andp53 mutation spectrum in human lung cancer

et al. 1999

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“…The mutagenic potency of UV light has been clearly shown both in vitro and in vivo using a variety of experimental systems in mammalian cells as well as in bacteria (1)(2)(3). Numerous lesions are induced by UV light, usually implicating a doublet of adjacent pyrimidines, as in the pyrimidine dimers and the pyrimidine pyrimidones (4).…”

Section: Introductionmentioning

confidence: 99%

Mutagenicity of a unique thymine-thymine dimer or thymine-thymine pyrimidine pyrimidone (6-4) photoproduct in mammalian cells

Gentil

Page

Margot

et al. 1996

Nucleic Acids Research

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The mutagenic properties of UV-induced photoproducts, both the cis-syn thymine-thymine dimer (TT) and the thymine-thymine pyrimidine pyrimidone (6-4) photoproduct [T(6-4)T] were studied in mammalian cells using shuttle vectors. A shuttle vector able to replicate in both mammalian cells and bacteria was produced in its single-stranded DNA form. A unique photoproduct was inserted at a single restriction site and after recircularization of the single-stranded DNA vector, this latter was transfected into simian COS7 cells. After DNA replication the vector was extracted from cells and used to transform bacteria. Amplified DNA was finally analyzed without any selective screening, DNA from randomly picked bacterial colonies being directly sequenced. Our results show clearly that both lesions are mutagenic, but at different levels. Mutation frequencies of 2 and 60% respectively were observed with the TT dimer and the T(6-4)T. With the TT dimer the mutations were targeted on the 3'-T. With the T(6-4)T a large variety of mutations were observed. A majority of G-->T transversions were semi-targeted to the base before the 5'-T of the photoproduct. These kinds of mutations were not observed when the same plasmid was transfected directly into SOS-induced JM105 bacteria or when the T(6-4)T oligonucleotide inserted in a different plasmid was replicated in SOS-induced SMH10 Escherichia coil bacteria. These semi-targeted mutations are therefore the specific result of bypass of the T(6-4)T lesion in COS7 cells by one of the eukaryotic DNA polymerases.

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Comparison of ultraviolet irradiation-induced mutagenesis of the lacI gene in Escherichia coli and in human 293 cells

Cited by 66 publications

References 23 publications

N-ras mutations in human cutaneous melanoma from sun-exposed body sites.

N-ras mutations in human cutaneous melanoma from sun-exposed body sites.

Molecular epidemiology of human cancer risk: gene-environment interactions andp53 mutation spectrum in human lung cancer

Mutagenicity of a unique thymine-thymine dimer or thymine-thymine pyrimidine pyrimidone (6-4) photoproduct in mammalian cells

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