TY - JOUR
T1 - Immunohistochemical analysis of oxidative stress and DNA repair proteins in normal mammary and breast cancer tissues
AU - Curtis, Carol D.
AU - Thorngren, Daniel L.
AU - Nardulli, Ann M.
N1 - We are indebted to Carle Foundation Hospital Surgery Center, M. Faith and the surgical team, and B. Hall for assistance in procuring the human mammary tissue. We thank G. Freund for helpful suggestions in the preparation of this manuscript. This work was supported by NIH grants R01 DK53884 and R56 DK 53884 (to AMN).
PY - 2010/1/11
Y1 - 2010/1/11
N2 - Background: During the course of normal cellular metabolism, oxygen is consumed and reactive oxygen species (ROS) are produced. If not effectively dissipated, ROS can accumulate and damage resident proteins, lipids, and DNA. Enzymes involved in redox regulation and DNA repair dissipate ROS and repair the resulting damage in order to preserve a functional cellular environment. Because increased ROS accumulation and/or unrepaired DNA damage can lead to initiation and progression of cancer and we had identified a number of oxidative stress and DNA repair proteins that influence estrogen responsiveness of MCF-7 breast cancer cells, it seemed possible that these proteins might be differentially expressed in normal mammary tissue, benign hyperplasia (BH), ductal carcinoma in situ (DCIS) and invasive breast cancer (IBC).Methods: Immunohistochemistry was used to examine the expression of a number of oxidative stress proteins, DNA repair proteins, and damage markers in 60 human mammary tissues which were classified as BH, DCIS or IBC. The relative mean intensity was determined for each tissue section and ANOVA was used to detect statistical differences in the relative expression of BH, DCIS and IBC compared to normal mammary tissue.Results: We found that a number of these proteins were overexpressed and that the cellular localization was altered in human breast cancer tissue.Conclusions: Our studies suggest that oxidative stress and DNA repair proteins not only protect normal cells from the damaging effects of ROS, but may also promote survival of mammary tumor cells.
AB - Background: During the course of normal cellular metabolism, oxygen is consumed and reactive oxygen species (ROS) are produced. If not effectively dissipated, ROS can accumulate and damage resident proteins, lipids, and DNA. Enzymes involved in redox regulation and DNA repair dissipate ROS and repair the resulting damage in order to preserve a functional cellular environment. Because increased ROS accumulation and/or unrepaired DNA damage can lead to initiation and progression of cancer and we had identified a number of oxidative stress and DNA repair proteins that influence estrogen responsiveness of MCF-7 breast cancer cells, it seemed possible that these proteins might be differentially expressed in normal mammary tissue, benign hyperplasia (BH), ductal carcinoma in situ (DCIS) and invasive breast cancer (IBC).Methods: Immunohistochemistry was used to examine the expression of a number of oxidative stress proteins, DNA repair proteins, and damage markers in 60 human mammary tissues which were classified as BH, DCIS or IBC. The relative mean intensity was determined for each tissue section and ANOVA was used to detect statistical differences in the relative expression of BH, DCIS and IBC compared to normal mammary tissue.Results: We found that a number of these proteins were overexpressed and that the cellular localization was altered in human breast cancer tissue.Conclusions: Our studies suggest that oxidative stress and DNA repair proteins not only protect normal cells from the damaging effects of ROS, but may also promote survival of mammary tumor cells.
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U2 - 10.1186/1471-2407-10-9
DO - 10.1186/1471-2407-10-9
M3 - Article
C2 - 20064251
AN - SCOPUS:77649106763
SN - 1471-2407
VL - 10
JO - BMC Cancer
JF - BMC Cancer
M1 - 9
ER -