Open AccessJournal Article
A high susceptibility of Fanconi's anemia to chromosome breakage by DNA cross-linking agents.
Masao S. Sasaki,Akira Tonomura +1 more
TLDR
Peripheral blood lymphocytes of patients with Fanconi9s anemia were tested for their susceptibility to chromosome breakage by caffeine, chloramphenicol, actinomycin D, methylmethanesulfonate, nitrogen mustard and mitomycin C, and the specifically increased susceptibility to these compounds is interpreted as an indication that the FA cells are defective in the repair mechanism to tolerate the cross-links produced in their DNA.Abstract:
Summary Peripheral blood lymphocytes of patients with Fanconi9s anemia (FA) were tested for their susceptibility to chromosome breakage by caffeine, chloramphenicol, actinomycin D, methylmethanesulfonate, nitrogen mustard, mitomycin C, decarbamoyl mitomycin C, N -methyl- N′ -nitro- N -nitrosoguanidine, 4-nitroquinoline 1-oxide, 8-methoxypsoralen, and 60 Co γ-ray and ultiviolet irradiations. A definitely abnormal response of the chromosomes of the FA cells was found when they were treated with nitrogen mustard and mitomycin C and after the irradiation with long-wavelength ultraviolet light in the presence of 8-methoxypsoralen. The specifically increased susceptibility to these compounds, which can introduce interstrand cross-links into DNA, is interpreted as an indication that the FA cells are defective in the repair mechanism to tolerate the cross-links produced in their DNA. The impairment of the capacity to tolerate the lesions produced in DNA may be implicated in the increased risk to develop malignant neoplasms in this hereditary disorder.read more
Citations
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Cloning of cDNAs for Fanconi's anaemia by functional complementation.
TL;DR: A functional complementation method is used to clone complementary DNAs that correct the defect of group C cells and represent a new gene involved in the cellular response to DNA damage in Fanconi's anaemia.
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The emerging genetic and molecular basis of Fanconi anaemia
Hans Joenje,Ketan J. Patel +1 more
TL;DR: The recent cloning of most of the FA-associated genes, and the characterization of their protein products, has provided tantalizing clues as to the molecular basis of this disease.
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Repair deficient human disorders and cancer
TL;DR: The analysis of the repair of damage to DNA in mammalian cells leads not only to a knowledge of which environmental agents are deleterious to living creatures, but also to an understanding of which reaction products in DNA are potentially carcinogenic and which tissues are the more sensitive.
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Molecular and genetic basis of furocoumarin reactions.
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Susceptibility of Fanconi's anaemia fibroblasts to chromosome damage by carcinogens
TL;DR: Experiments in which viable FA fibroblasts were exposed to a direct-acting mutagen or carcinogen for a period of 6 d, ensuring chronic exposure of the cells during one or more cell cycles, until increased cell density inhibited further cell division.
References
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Journal ArticleDOI
Discontinuities in the DNA synthesized in an Excision-defective strain of Escherichia coli following ultraviolet irradiation
W D Rupp,Paul Howard-Flanders +1 more
TL;DR: The amount of tritiated thymidine incorporated into the DNA of irradiated cells indicates that pyrimidine dimers in the DNA inhibit DNA synthesis but are not permanent blocks, and that the daughter-strand DNA synthesized after ultraviolet-irradiation contains gaps, or alkalilabile bonds.
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Evidence that xeroderma pigmentosum cells do not perform the first step in the repair of ultraviolet damage to their dna
TL;DR: Measurements of ultraviolet-induced pyrimidine dimers in cellular DNA show that normal diploid human skin fibroblasts excise up to 70 per cent of the dimer in 24 hours, but that fibro Blasts derived from the individual with XP excise less than 20 per cent in 48 hours.
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Base-Change Mutagenesis and Prophage Induction in Strains of ESCHERICHIA COLI with Different DNA Repair Capacities
TL;DR: Three types of repairless mutant strains of E. coli were tested for mutability by seven representative mutagens and one strain turned out more mutable than the wild type or nonmutable depending on the repair deficiency and the mutagen.
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Xeroderma pigmentosum: a human disease in which an initial stage of dna repair is defective
TL;DR: Homozygous xeroderma pigmentosum fibroblasts cannot repair damage to DNA bases, but can repair damage that involves chain breaks, and may be the result of somatic mutations caused by unrepaired damage.
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Repair replication of mammalian cell DNA: effects of compounds that inhibit DNA synthesis or dark repair.
TL;DR: From a comparison of the effects of acriflavine and caffeine on repair replication in HeLa cells and on the survival of UV-irradiated mouse L cells, it is concluded that repair replication is probably not the only form of replication.