Exit Dose in Dermatologic Roentgen Therapy

Andrews, George C.

doi:10.1001/archderm.1944.01510180003001

Arch Dermatol

1944

DOI: 10.1001/archderm.1944.01510180003001

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Exit Dose in Dermatologic Roentgen Therapy

George C. Andrews¹

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1949

1984

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Cited by 6 publications

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“…The prior stimulation of DNA repair would serve as a prescreening mechanism to remove potentially miscoding lesions from DNA to ensure the fidelity of DNA synthesis (9,10). Alterations in this temporal sequence in human cells such that DNA would not be prescreened prior to replication would be expected to lead to increased rates of mutagenesis or oncogenesis (11,12).…”

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confidence: 99%

Altered temporal expression of DNA repair in hypermutable Bloom's syndrome cells.

Gupta¹,

Sirover²

1984

Proc. Natl. Acad. Sci. U.S.A.

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The temporal regulation of DNA repair during synchronous cell proliferation was examined in normal human skin fibroblasts and in Bloom's syndrome skin fibroblasts. Normal human cells regulated DNA repair in a defined temporal sequence prior to the induction of DNA replication. Nucleotide-excision repair was stimulated prior to the induction of base-excision repair, which itself was increased prior to the induction of DNA replication. This temporal sequence was observed (i) by quantitation of the induction of the base-excision repair enzyme uracil DNA glycosylase during cell proliferation in the absence of cellular insult and (it) by quantitation of nucleotide-excision repair after UV irradiation or base-excision repair after exposure to methylmethane sulfonate. In contrast, Bloom's syndrome cells were characterized by specific alterations in this temporal sequence of gene regulation, such that DNA repair was not enhanced prior to the induction of DNA replication. Nucleotide-excision repair, base-excision repair, and the uracil DNA glycosylase were induced in a temporal sequence identical to that observed for DNA polymerase and for DNA replication. The inability of Bloom's syndrome cells to enhance DNA repair prior to DNA replication suggests that miscoding lesions remain in DNA and are replicated during cell proliferation.Recent studies have examined the enzymatic mechanisms through which human cells recognize and correct perturbations in DNA structure. Two major excision-repair pathways have been identified: (i) nucleotide-excision repair, in which DNA adducts are removed within oligonucleotides, and (ii) base-excision repair, in which DNA adducts are removed as modified bases leaving an apurinic or apyrimidinic site in DNA (1-3). Recent results from this laboratory have suggested that human cells regulate these enzymatic pathways during cell proliferation in a defined and ordered temporal sequence with respect to DNA replication (4-8). In particular, nucleotide-excision repair and base-excision repair reached their peak activity several hours prior to DNA replication. The base-excision repair enzyme uracil DNA glyco-

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mentioning

confidence: 99%

Altered temporal expression of DNA repair in hypermutable Bloom's syndrome cells.

Gupta¹,

Sirover²

1984

Proc. Natl. Acad. Sci. U.S.A.

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Relation of Exit Dose and Other Dosage Factors to Roentgen Injuries

Shafer¹

1949

Arch Dermatol

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X-Ray, Radium and Ultraviolet Light Therapy in Dermatology: With Particular Reference to Safety Factors and Reduction of Depth and Gonad Doses

Brauer

1959

Medical Clinics of North America

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Exit Dose in Dermatologic Roentgen Therapy

Cited by 6 publications

References 5 publications

Altered temporal expression of DNA repair in hypermutable Bloom's syndrome cells.

Altered temporal expression of DNA repair in hypermutable Bloom's syndrome cells.

Relation of Exit Dose and Other Dosage Factors to Roentgen Injuries

X-Ray, Radium and Ultraviolet Light Therapy in Dermatology: With Particular Reference to Safety Factors and Reduction of Depth and Gonad Doses

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