DNA double-strand break repair in two radiation-sensitive mouse mammary carcinoma cell lines

Raymond L. Warters; Louis R. Barrows; David J. Chen

doi:10.1016/0921-8777(94)00036-6

DNA double-strand break repair in two radiation-sensitive mouse mammary carcinoma cell lines

Raymond L. Warters, Louis R. Barrows, David J. Chen

Research output: Contribution to journal › Article › peer-review

12 Scopus citations

Abstract

The capacity of two radiation-sensitive clones (SX9 and SX10) of the mouse mammary carcinoma cell line SR1 to rejoin radiation-induced DNA double-strand breaks (DSBs) was determined by pulsed-field agarose gel electrophoresis. DSBs were produced with equivalent efficiency in all three cell lines. Both the SX9 and SX10 cell lines demonstrated a significantly diminished capacity to rejoin radiation-induced DSBs. The fraction of the original DNA DSB damage remaining in the DNA of 20 Gy-exposed SR1, SX9 and SX10 cells after 6 h of 37°C incubation was estimated to be 14, 82 and 54%, respectively. In addition the SX10 cell line exhibited enhanced cytotoxicity when exposed to the DNA topoisomerase II poison mitoxantrone. The results indicate that both the SX9 and SX10 cell lines are DNA DSB repair mutants.

Original language	English (US)
Pages (from-to)	1-7
Number of pages	7
Journal	Mutation Research-DNA Repair
Volume	336
Issue number	1
DOIs	https://doi.org/10.1016/0921-8777(94)00036-6
State	Published - Jan 1995

Keywords

DNA double-strand break repair
Mouse mammary carcinoma
X-irradiation

ASJC Scopus subject areas

Molecular Biology
Toxicology
Genetics

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10.1016/0921-8777(94)00036-6

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title = "DNA double-strand break repair in two radiation-sensitive mouse mammary carcinoma cell lines",

abstract = "The capacity of two radiation-sensitive clones (SX9 and SX10) of the mouse mammary carcinoma cell line SR1 to rejoin radiation-induced DNA double-strand breaks (DSBs) was determined by pulsed-field agarose gel electrophoresis. DSBs were produced with equivalent efficiency in all three cell lines. Both the SX9 and SX10 cell lines demonstrated a significantly diminished capacity to rejoin radiation-induced DSBs. The fraction of the original DNA DSB damage remaining in the DNA of 20 Gy-exposed SR1, SX9 and SX10 cells after 6 h of 37°C incubation was estimated to be 14, 82 and 54%, respectively. In addition the SX10 cell line exhibited enhanced cytotoxicity when exposed to the DNA topoisomerase II poison mitoxantrone. The results indicate that both the SX9 and SX10 cell lines are DNA DSB repair mutants.",

keywords = "DNA double-strand break repair, Mouse mammary carcinoma, X-irradiation",

author = "Warters, {Raymond L.} and Barrows, {Louis R.} and Chen, {David J.}",

note = "Funding Information: We wish to thank Dr. Graydon Harker of the Departmento f Internal Medicine, University of Utah for the gift of mitoxantrone,a nd Bradley W. Lyons and Glenn S. Eldredge for assistancein some of the experiments.T his work was supported by NC1 Grant CA25957 (R.L.W.), DOE ContractK PO400-00518(1D .J.C.) and the University of Utah {\textquoteleft}Drug Testing Facility{\textquoteright} (L.R.B).",

year = "1995",

month = jan,

doi = "10.1016/0921-8777(94)00036-6",

language = "English (US)",

volume = "336",

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journal = "Mutation Research-DNA Repair",

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T1 - DNA double-strand break repair in two radiation-sensitive mouse mammary carcinoma cell lines

AU - Warters, Raymond L.

AU - Barrows, Louis R.

AU - Chen, David J.

N1 - Funding Information: We wish to thank Dr. Graydon Harker of the Departmento f Internal Medicine, University of Utah for the gift of mitoxantrone,a nd Bradley W. Lyons and Glenn S. Eldredge for assistancein some of the experiments.T his work was supported by NC1 Grant CA25957 (R.L.W.), DOE ContractK PO400-00518(1D .J.C.) and the University of Utah ‘Drug Testing Facility’ (L.R.B).

PY - 1995/1

Y1 - 1995/1

N2 - The capacity of two radiation-sensitive clones (SX9 and SX10) of the mouse mammary carcinoma cell line SR1 to rejoin radiation-induced DNA double-strand breaks (DSBs) was determined by pulsed-field agarose gel electrophoresis. DSBs were produced with equivalent efficiency in all three cell lines. Both the SX9 and SX10 cell lines demonstrated a significantly diminished capacity to rejoin radiation-induced DSBs. The fraction of the original DNA DSB damage remaining in the DNA of 20 Gy-exposed SR1, SX9 and SX10 cells after 6 h of 37°C incubation was estimated to be 14, 82 and 54%, respectively. In addition the SX10 cell line exhibited enhanced cytotoxicity when exposed to the DNA topoisomerase II poison mitoxantrone. The results indicate that both the SX9 and SX10 cell lines are DNA DSB repair mutants.

AB - The capacity of two radiation-sensitive clones (SX9 and SX10) of the mouse mammary carcinoma cell line SR1 to rejoin radiation-induced DNA double-strand breaks (DSBs) was determined by pulsed-field agarose gel electrophoresis. DSBs were produced with equivalent efficiency in all three cell lines. Both the SX9 and SX10 cell lines demonstrated a significantly diminished capacity to rejoin radiation-induced DSBs. The fraction of the original DNA DSB damage remaining in the DNA of 20 Gy-exposed SR1, SX9 and SX10 cells after 6 h of 37°C incubation was estimated to be 14, 82 and 54%, respectively. In addition the SX10 cell line exhibited enhanced cytotoxicity when exposed to the DNA topoisomerase II poison mitoxantrone. The results indicate that both the SX9 and SX10 cell lines are DNA DSB repair mutants.

KW - DNA double-strand break repair

KW - Mouse mammary carcinoma

KW - X-irradiation

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DNA double-strand break repair in two radiation-sensitive mouse mammary carcinoma cell lines

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