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SHR Neuro Krebs Kardio Lipid Stoffw Microb

Clar, H; Langsenlehner, U; Krippl, P; Renner, W; Leithner, A; Gruber, G; Hofmann, G; Yazdani-Biuki, B; Langsenlehner, T; Windhager, R.
A polymorphism in the G protein beta3-subunit gene is associated with bone metastasis risk in breast cancer patients.
Breast Cancer Res Treat. 2008; 111(3):449-452 Doi: 10.1007/s10549-007-9808-0
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Führende Autor*innen der Med Uni Graz
Clar Heimo
Langsenlehner Uwe
Co-Autor*innen der Med Uni Graz
Gruber Gerald
Hofmann Guenter
Langsenlehner Tanja
Leithner Andreas
Renner Wilfried
Windhager Reinhard
Yazdani-Biuki Babak

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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 beta3-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 < 0.001). In a Cox regression analysis, relative risk of the GNB3 TT genotype for bone metastasis was 0.22 (95% CI 0.08-0.61; 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.
Find related publications in this database (using NLM MeSH Indexing)
Adult -
Aged -
Bone Neoplasms - genetics
Breast Neoplasms - genetics
Female - genetics
Gene Expression Regulation, Neoplastic - genetics
Gene Frequency - genetics
Genetic Predisposition to Disease - genetics
Heterotrimeric GTP-Binding Proteins - genetics
Humans - genetics
Middle Aged - genetics
Neoplasm Staging - genetics
Polymorphism, Genetic - genetics
Proportional Hazards Models - genetics
Retrospective Studies - genetics
Risk Assessment - genetics
Risk Factors - genetics
Time Factors - genetics

Find related publications in this database (Keywords)
breast cancer
bone metastases
gene polymorphism
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