Breast Cancer Research and Treatment

, Volume 124, Issue 1, pp 243–249 | Cite as

Association of TGFB1 -509 C>T polymorphism with breast cancer: evidence from a meta-analysis involving 23,579 subjects

  • Wenquan NiuEmail author
  • Yue Qi
  • Pingjin Gao
  • Dingliang Zhu


Although a number of genetic studies have attempted to link transforming growth factor beta 1 gene (TGFB1) -509 C>T polymorphism to breast cancer, the results were often irreproducible. We therefore aimed to meta-analyze all available case–control studies from the English-published literature to explore the association of this polymorphism with breast cancer. A total of 6 studies with 9 populations involving 10,197 patients and 13,382 controls were identified as of February 20, 2010. A random-effects model was performed irrespective of the between-study heterogeneity. Study quality was assessed in duplicate. The frequencies of TGFB1 -509 T allele in patients and controls ranged from 21.72 to 51.74%, and 24.53 to 52.40%, respectively. The presence of -509 T allele conferred a nonsignificant protective effect on breast cancer [odds ratio (OR) = 0.99; 95% confidence interval (CI) 0.93–1.05; P = 0.72]. This lack of association persisted under co-dominant, dominant, and recessive models. However, exclusion of the initial study significantly strengthened the magnitude of this protective effect. For example, under the dominant assumption, carriers of -509 T allele had a moderate reduced risk for breast cancer compared with the -509 CC homozygous (OR = 0.94; 95% CI 0.88–1.00; P = 0.04). Subgroup analyses by study designs and geographic areas did not substantially affect the present associations. No publication biases were observed by the fail-safe number. Taken together, our results demonstrated that TGFB1 -509 T allele was associated with a reduced risk to develop breast cancer and this allele appeared to act in an additive mode.


Breast cancer Transforming growth factor beta 1 gene (TGFB1) -509 C>T Meta-analysis Association 



This study was financially supported by the Shanghai “Chen Guang” Project (09CG12), the Natural Science Foundation of Shanghai (09ZR1426200), two Excellent Young Teachers Programs, one from Ruijin Hospital (W.N.) and the other from Shanghai City (W.N.), the Science Fund of Shanghai Jiaotong University School of Medicine (09XJ21019), and the National Science Foundation for Young Scientists of China (Grant Number: 30900808).


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Copyright information

© Springer Science+Business Media, LLC. 2010

Authors and Affiliations

  • Wenquan Niu
    • 1
    • 2
    • 3
    • 4
    Email author
  • Yue Qi
    • 5
  • Pingjin Gao
    • 1
    • 2
    • 4
  • Dingliang Zhu
    • 1
    • 2
    • 3
  1. 1.State Key Laboratory of Medical Genomics, Ruijin HospitalShanghai Jiaotong University School of MedicineShanghaiChina
  2. 2.Sino-French Research Center for Life Science and Genomics, Ruijin HospitalShanghai Jiaotong University School of MedicineShanghaiChina
  3. 3.Shanghai Key Laboratory of Vascular Biology, Ruijin HospitalShanghai Jiaotong University School of MedicineShanghaiChina
  4. 4.Shanghai Institute of Hypertension, Ruijin HospitalShanghai Jiaotong University School of MedicineShanghaiChina
  5. 5.Department of Epidemiology, Beijing Institute of Heart, Lung & Blood Vessel DiseasesCapital Medical University Affiliated Beijing Anzhen HospitalBeijingChina

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