دورية أكاديمية

A polymorphism in the G protein β3-subunit gene is associated with bone metastasis risk in breast cancer patients.

التفاصيل البيبلوغرافية
العنوان: A polymorphism in the G protein β3-subunit gene is associated with bone metastasis risk in breast cancer patients.
المؤلفون: H. Clar, U. Langsenlehner, P. Krippl, W. Renner, A. Leithner, G. Gruber, G. Hofmann, B. Yazdani-Biuki, T. Langsenlehner, R. Windhager
المصدر: Breast Cancer Research & Treatment; Oct2008, Vol. 111 Issue 3, p449-452, 4p, 1 Chart, 1 Graph
مصطلحات موضوعية: BREAST cancer patients, CANCER risk factors, BONE metastasis, CANCER in women, G proteins, GENETIC polymorphisms, CALCITONIN
مستخلص: Abstract  Breast cancer is the most frequently diagnosed cancer among women in western countries and bone metastases of breast cancer cause significant morbidity. G proteins are important components of a multitude of transmembrane receptors and are involved in the regulation of intracellular signaling pathways such as parathormone receptors 1 and 2 (PTH1 and 2), extracellular calcium-sensing receptor, the calcitonin receptor and the OPG/RANKL-system. A common polymorphism in the gene encoding the G protein β3-subunit, GNB3 825C > T, has been linked to increased G protein activation. To analyse the role of this polymorphism in bone metastasis of breast cancer, we determined GNB3 825C > T genotypes in 500 female breast cancer patients. According to breast cancer staging, patients were divided in three groups, representing patients without metastases (n = 250), those with metastases other than bone (n = 117), and those with bone metastasis (n = 133). Frequency of the GNB3 825 TT genotype was significantly lower among patients with bone metastases (3.1%) than among those with other metastases (12.8%; P = 0.004) or no metastases (13.3%; P P = 0.004) for bone metastasis. We conclude that the homozygous GNB3 825 TT genotype may be protective against development of bone metastasis in breast cancer patients. The precise mechanism for this remains to be determined, but could be due to a direct involvement of G protein-coupled receptors in bone metabolism. [ABSTRACT FROM AUTHOR]
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قاعدة البيانات: Complementary Index
الوصف
تدمد:01676806
DOI:10.1007/s10549-007-9808-0