Association of glutathione S-transferase T1, M1, and P1 polymorphisms in the breast cancer risk: a meta-analysis

There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

Abstract

Background

Several case–control studies investigating the relationship between genetic polymorphisms of glutathione S-transferase (GST) M1, GSTT1, and GSTP1 (rs1695) and the risk of breast cancer have reported contradictory results. We therefore performed a meta-analysis to clarify this issue.

Materials and methods

An updated meta-analysis using PubMed and Web of Knowledge databases for the eligible case–control studies was performed. Random- or fixed-effects model was used.

Results

A total of 10,067 cancer cases and 12,276 controls in 41 independent case–control studies from 19 articles were included in this meta-analysis. Significant increase in risk of breast cancer for Asians was found in GSTM1-null genotype ( P=0.012, odds ratio [OR] =1.17, 95% confidence interval [CI] =1.04–1.32) and GSTT1-null genotype ( P=0.039, OR =1.19, 95% CI =1.01–1.41). In addition, our results showed that the GSTP1 (rs1695) polymorphisms can significantly increase the risk among Caucasians ( P=0.042, OR =1.16, 95% CI =1.01–1.34). Sensitivity analysis and publication bias further confirmed the dependability of the results in this meta-analysis.

Conclusion

Our results demonstrate that both GSTM1- and GSTT1-null polymorphisms are associated with an increased risk of breast cancer in Asians and that GSTP1 Val105Ile (rs1695) polymorphism is associated with an increased breast cancer risk in Caucasians.

Most cited references 43

Record: found
Abstract: found
Article: not found

Glutathione transferases.

John Hayes, Jack U. Flanagan, Ian R Jowsey (2005)

This review describes the three mammalian glutathione transferase (GST) families, namely cytosolic, mitochondrial, and microsomal GST, the latter now designated MAPEG. Besides detoxifying electrophilic xenobiotics, such as chemical carcinogens, environmental pollutants, and antitumor agents, these transferases inactivate endogenous alpha,beta-unsaturated aldehydes, quinones, epoxides, and hydroperoxides formed as secondary metabolites during oxidative stress. These enzymes are also intimately involved in the biosynthesis of leukotrienes, prostaglandins, testosterone, and progesterone, as well as the degradation of tyrosine. Among their substrates, GSTs conjugate the signaling molecules 15-deoxy-delta(12,14)-prostaglandin J2 (15d-PGJ2) and 4-hydroxynonenal with glutathione, and consequently they antagonize expression of genes trans-activated by the peroxisome proliferator-activated receptor gamma (PPARgamma) and nuclear factor-erythroid 2 p45-related factor 2 (Nrf2). Through metabolism of 15d-PGJ2, GST may enhance gene expression driven by nuclear factor-kappaB (NF-kappaB). Cytosolic human GST exhibit genetic polymorphisms and this variation can increase susceptibility to carcinogenesis and inflammatory disease. Polymorphisms in human MAPEG are associated with alterations in lung function and increased risk of myocardial infarction and stroke. Targeted disruption of murine genes has demonstrated that cytosolic GST isoenzymes are broadly cytoprotective, whereas MAPEG proteins have proinflammatory activities. Furthermore, knockout of mouse GSTA4 and GSTZ1 leads to overexpression of transferases in the Alpha, Mu, and Pi classes, an observation suggesting they are part of an adaptive mechanism that responds to endogenous chemical cues such as 4-hydroxynonenal and tyrosine degradation products. Consistent with this hypothesis, the promoters of cytosolic GST and MAPEG genes contain antioxidant response elements through which they are transcriptionally activated during exposure to Michael reaction acceptors and oxidative stress.

0 comments Cited 678 times – based on 0 reviews      Review now

Bookmark

Record: found
Abstract: found
Article: not found

Breast and cervical cancer in 187 countries between 1980 and 2010: a systematic analysis.

Mohammad Forouzanfar, Kyle J Foreman, Allyne M Delossantos … (2011)

Breast and cervical cancer are important causes of mortality in women aged ≥15 years. We undertook annual age-specific assessments of breast and cervical cancer in 187 countries. We systematically collected cancer registry data on mortality and incidence, vital registration, and verbal autopsy data for the period 1980-2010. We modelled the mortality-to-incidence (MI) ratio using a hierarchical model. Vital registration and verbal autopsy were supplemented with incidence multiplied by the MI ratio to yield a comprehensive database of mortality rates. We used Gaussian process regression to develop estimates of mortality with uncertainty by age, sex, country, and year. We used out-of-sample predictive validity to select the final model. Estimates of incidence with uncertainty were also generated with mortality and MI ratios. Global breast cancer incidence increased from 641,000 (95% uncertainty intervals 610,000-750,000) cases in 1980 to 1,643,000 (1,421,000-1,782,000) cases in 2010, an annual rate of increase of 3·1%. Global cervical cancer incidence increased from 378,000 (256,000-489,000) cases per year in 1980 to 454,000 (318,000-620,000) cases per year in 2010-a 0·6% annual rate of increase. Breast cancer killed 425,000 (359,000-453,000) women in 2010, of whom 68,000 (62,000-74,000) were aged 15-49 years in developing countries. Cervical cancer death rates have been decreasing but the disease still killed 200,000 (139,000-276,000) women in 2010, of whom 46,000 (33,000-64,000) were aged 15-49 years in developing countries. We recorded pronounced variation in the trend in breast cancer mortality across regions and countries. More policy attention is needed to strengthen established health-system responses to reduce breast and cervical cancer, especially in developing countries. Susan G Komen for the Cure and the Bill & Melinda Gates Foundation. Copyright © 2011 Elsevier Ltd. All rights reserved.

0 comments Cited 310 times – based on 0 reviews      Review now

Bookmark

Record: found
Abstract: found
Article: not found

The global breast cancer burden: variations in epidemiology and survival.

Hussein Khaled, Mei Liu, Kathleen Pritchard … (2005)

Breast cancer is the most common type of cancer and the most common cause of cancer-related mortality among women worldwide. However, the burden is not evenly distributed, and, according to the best available data, there are large variations in the incidence, mortality, and survival between different countries and regions and within specific regions. Many complex factors underlie these variations, including population structure (eg, age, race, and ethnicity), lifestyle, environment, socioeconomic status, risk factor prevalence, mammography use, disease stage at diagnosis, and access to high-quality care. We review recent breast cancer incidence and mortality statistics and explore why these vary so greatly across the world. Further research is needed to fully understand the reasons for variations in breast cancer outcomes. This will aid the development of tailored strategies to improve outcomes in general as well as the standard of care for underserved populations and reduce the burden of breast cancer worldwide.

0 comments Cited 154 times – based on 0 reviews      Review now

Bookmark

All references

Author and article information

Journal

Journal ID (nlm-ta): Ther Clin Risk Manag

Journal ID (iso-abbrev): Ther Clin Risk Manag

Journal ID (publisher-id): Therapeutics and Clinical Risk Management

Title: Therapeutics and Clinical Risk Management

Publisher: Dove Medical Press

ISSN (Print): 1176-6336

ISSN (Electronic): 1178-203X

Publication date Collection: 2016

Publication date (Electronic): 12 May 2016

Volume: 12

Pages: 763-769

Affiliations

[1 ]Department of Oncology, Shanghai East Hospital, Tongji University, Shanghai, People’s Republic of China

[2 ]Department of Neurosurgery, The Second Clinical Medical College of North Sichuan Medical College, Nanchong, Sichuan, People’s Republic of China

Author notes

Correspondence: Chunyan Dong, Department of Oncology, Shanghai East Hospital, Tongji University, 150 Jimo Road, Shanghai 200120, People’s Republic of China, Tel +86 133 7002 9736, Email chunyan_dong@ 123456yeah.net .

Article

Publisher ID: tcrm-12-763

DOI: 10.2147/TCRM.S104339

PMC ID: 4869650

PubMed ID: 27274261

SO-VID: cc4a55b7-288b-421a-87b0-e7a1b9fdfe9a

License:

The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

Association of glutathione S-transferase T1, M1, and P1 polymorphisms in the breast cancer risk: a meta-analysis

Read this article at

Abstract

Background

Materials and methods

Results

Conclusion

Most cited references 43

Glutathione transferases.

Breast and cervical cancer in 187 countries between 1980 and 2010: a systematic analysis.

The global breast cancer burden: variations in epidemiology and survival.

Author and article information

Journal

Affiliations

Author notes

Article

History

Categories

Comments

Comment on this article

Similar content 445

Cited by 9

Most referenced authors 1,251