DNA damage and breast cancer risk

Tasha R. Smith, Mark S. Miller, Kurt K. Lohman, L. Douglas Case, Jennifer Hu

Research output: Contribution to journalArticle

118 Citations (Scopus)

Abstract

To evaluate whether deficient DNA repair contributes to elevated DNA damage and breast carcinogenesis, we used the comet assay (single-cell alkaline gel electrophoresis) to measure the levels of DNA damage in peripheral lymphocytes from 70 breast cancer cases and 70 controls. DNA damage, measured as the comet tail moment, was not influenced by age, family history (FH), age at menarche, age at first birth or parity. The results showed that cancer cases had significantly higher DNA damage compared with controls; the comet tail moments (mean ± SD) for cases and controls were: 10.78 ± 3.63 and 6.86 ± 2.76 (P < 0.001) for DNA damage at baseline (DB), 21.24 ± 4.88 and 14.97 ± 4.18 (P < 0.001) for DNA damage after exposure to 6 Gy of ionizing radiation (DIR), and 14.76 ± 5.35 and 9.75 ± 3.35 (P < 0.001) for DNA damage remaining after 10 min repair following exposure to 6 Gy of IR (DRP), respectively. Body mass index (BMI) affected DNA damage differently for cases and controls. Damage decreased with increasing BMI for controls, while damage increased with increasing BMI for cases. Above-median DNA damage was significantly associated with breast cancer risk; the age-adjusted odds ratio (OR) = 13.44 [95% confidence interval (CI) = 5.97-30.24] for DB, 13.65 (6.07-30.71) for DIR and 6.54 (3.11-13.79) for DRP, respectively, This association was stronger in women with above-median BMI. Our results, although based on a relatively small group of subjects, indicate that elevated DNA damage is significantly associated with breast cancer risk and warrant larger studies to further define the molecular mechanisms of DNA damage/repair in breast cancer susceptibility.

Original languageEnglish
Pages (from-to)883-889
Number of pages7
JournalCarcinogenesis
Volume24
Issue number5
DOIs
StatePublished - May 1 2003
Externally publishedYes

Fingerprint

DNA Damage
Breast Neoplasms
Body Mass Index
Comet Assay
DNA Repair-Deficiency Disorders
Radiation Dosage
Menarche
Birth Order
Ionizing Radiation
Parity
DNA Repair
Carcinogenesis
Breast
Odds Ratio
Lymphocytes
Confidence Intervals

ASJC Scopus subject areas

  • Cancer Research

Cite this

Smith, T. R., Miller, M. S., Lohman, K. K., Case, L. D., & Hu, J. (2003). DNA damage and breast cancer risk. Carcinogenesis, 24(5), 883-889. https://doi.org/10.1093/carcin/bgg037

DNA damage and breast cancer risk. / Smith, Tasha R.; Miller, Mark S.; Lohman, Kurt K.; Case, L. Douglas; Hu, Jennifer.

In: Carcinogenesis, Vol. 24, No. 5, 01.05.2003, p. 883-889.

Research output: Contribution to journalArticle

Smith, TR, Miller, MS, Lohman, KK, Case, LD & Hu, J 2003, 'DNA damage and breast cancer risk', Carcinogenesis, vol. 24, no. 5, pp. 883-889. https://doi.org/10.1093/carcin/bgg037
Smith TR, Miller MS, Lohman KK, Case LD, Hu J. DNA damage and breast cancer risk. Carcinogenesis. 2003 May 1;24(5):883-889. https://doi.org/10.1093/carcin/bgg037
Smith, Tasha R. ; Miller, Mark S. ; Lohman, Kurt K. ; Case, L. Douglas ; Hu, Jennifer. / DNA damage and breast cancer risk. In: Carcinogenesis. 2003 ; Vol. 24, No. 5. pp. 883-889.
@article{afbcd44c783e4f1faceeffa17bad92a7,
title = "DNA damage and breast cancer risk",
abstract = "To evaluate whether deficient DNA repair contributes to elevated DNA damage and breast carcinogenesis, we used the comet assay (single-cell alkaline gel electrophoresis) to measure the levels of DNA damage in peripheral lymphocytes from 70 breast cancer cases and 70 controls. DNA damage, measured as the comet tail moment, was not influenced by age, family history (FH), age at menarche, age at first birth or parity. The results showed that cancer cases had significantly higher DNA damage compared with controls; the comet tail moments (mean ± SD) for cases and controls were: 10.78 ± 3.63 and 6.86 ± 2.76 (P < 0.001) for DNA damage at baseline (DB), 21.24 ± 4.88 and 14.97 ± 4.18 (P < 0.001) for DNA damage after exposure to 6 Gy of ionizing radiation (DIR), and 14.76 ± 5.35 and 9.75 ± 3.35 (P < 0.001) for DNA damage remaining after 10 min repair following exposure to 6 Gy of IR (DRP), respectively. Body mass index (BMI) affected DNA damage differently for cases and controls. Damage decreased with increasing BMI for controls, while damage increased with increasing BMI for cases. Above-median DNA damage was significantly associated with breast cancer risk; the age-adjusted odds ratio (OR) = 13.44 [95{\%} confidence interval (CI) = 5.97-30.24] for DB, 13.65 (6.07-30.71) for DIR and 6.54 (3.11-13.79) for DRP, respectively, This association was stronger in women with above-median BMI. Our results, although based on a relatively small group of subjects, indicate that elevated DNA damage is significantly associated with breast cancer risk and warrant larger studies to further define the molecular mechanisms of DNA damage/repair in breast cancer susceptibility.",
author = "Smith, {Tasha R.} and Miller, {Mark S.} and Lohman, {Kurt K.} and Case, {L. Douglas} and Jennifer Hu",
year = "2003",
month = "5",
day = "1",
doi = "10.1093/carcin/bgg037",
language = "English",
volume = "24",
pages = "883--889",
journal = "Carcinogenesis",
issn = "0143-3334",
publisher = "Oxford University Press",
number = "5",

}

TY - JOUR

T1 - DNA damage and breast cancer risk

AU - Smith, Tasha R.

AU - Miller, Mark S.

AU - Lohman, Kurt K.

AU - Case, L. Douglas

AU - Hu, Jennifer

PY - 2003/5/1

Y1 - 2003/5/1

N2 - To evaluate whether deficient DNA repair contributes to elevated DNA damage and breast carcinogenesis, we used the comet assay (single-cell alkaline gel electrophoresis) to measure the levels of DNA damage in peripheral lymphocytes from 70 breast cancer cases and 70 controls. DNA damage, measured as the comet tail moment, was not influenced by age, family history (FH), age at menarche, age at first birth or parity. The results showed that cancer cases had significantly higher DNA damage compared with controls; the comet tail moments (mean ± SD) for cases and controls were: 10.78 ± 3.63 and 6.86 ± 2.76 (P < 0.001) for DNA damage at baseline (DB), 21.24 ± 4.88 and 14.97 ± 4.18 (P < 0.001) for DNA damage after exposure to 6 Gy of ionizing radiation (DIR), and 14.76 ± 5.35 and 9.75 ± 3.35 (P < 0.001) for DNA damage remaining after 10 min repair following exposure to 6 Gy of IR (DRP), respectively. Body mass index (BMI) affected DNA damage differently for cases and controls. Damage decreased with increasing BMI for controls, while damage increased with increasing BMI for cases. Above-median DNA damage was significantly associated with breast cancer risk; the age-adjusted odds ratio (OR) = 13.44 [95% confidence interval (CI) = 5.97-30.24] for DB, 13.65 (6.07-30.71) for DIR and 6.54 (3.11-13.79) for DRP, respectively, This association was stronger in women with above-median BMI. Our results, although based on a relatively small group of subjects, indicate that elevated DNA damage is significantly associated with breast cancer risk and warrant larger studies to further define the molecular mechanisms of DNA damage/repair in breast cancer susceptibility.

AB - To evaluate whether deficient DNA repair contributes to elevated DNA damage and breast carcinogenesis, we used the comet assay (single-cell alkaline gel electrophoresis) to measure the levels of DNA damage in peripheral lymphocytes from 70 breast cancer cases and 70 controls. DNA damage, measured as the comet tail moment, was not influenced by age, family history (FH), age at menarche, age at first birth or parity. The results showed that cancer cases had significantly higher DNA damage compared with controls; the comet tail moments (mean ± SD) for cases and controls were: 10.78 ± 3.63 and 6.86 ± 2.76 (P < 0.001) for DNA damage at baseline (DB), 21.24 ± 4.88 and 14.97 ± 4.18 (P < 0.001) for DNA damage after exposure to 6 Gy of ionizing radiation (DIR), and 14.76 ± 5.35 and 9.75 ± 3.35 (P < 0.001) for DNA damage remaining after 10 min repair following exposure to 6 Gy of IR (DRP), respectively. Body mass index (BMI) affected DNA damage differently for cases and controls. Damage decreased with increasing BMI for controls, while damage increased with increasing BMI for cases. Above-median DNA damage was significantly associated with breast cancer risk; the age-adjusted odds ratio (OR) = 13.44 [95% confidence interval (CI) = 5.97-30.24] for DB, 13.65 (6.07-30.71) for DIR and 6.54 (3.11-13.79) for DRP, respectively, This association was stronger in women with above-median BMI. Our results, although based on a relatively small group of subjects, indicate that elevated DNA damage is significantly associated with breast cancer risk and warrant larger studies to further define the molecular mechanisms of DNA damage/repair in breast cancer susceptibility.

UR - http://www.scopus.com/inward/record.url?scp=0037972270&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0037972270&partnerID=8YFLogxK

U2 - 10.1093/carcin/bgg037

DO - 10.1093/carcin/bgg037

M3 - Article

VL - 24

SP - 883

EP - 889

JO - Carcinogenesis

JF - Carcinogenesis

SN - 0143-3334

IS - 5

ER -