Abstract
Our understanding of many aspects of cancer biology has been advanced through the use of modern genetics. These studies have already shown that germ line polymorphisms play a significant role in disease initiation and response to therapy. However, what is less well studied is the role of germ line polymorphisms in cancer progression. Studies in rodents indicate that differential susceptibility to cancer metastasis can be heritable; thus, the search for the genes that control cancer metastasis is underway. Although some provocative studies suggest potential candidates for metastasis regulating genes, the conclusive identification of a specific inherited genetic variant that alters metastatic potential awaits further studies.
Highlights
Recent studies in mice indicate that inherited genetic backgrounds can influence metastatic potential
This was due to a weaker interaction between the 739Thr Sipa1 protein with its inhibitor, AQP2, and, SNP = single nucleotide polymorphism
Less inhibition of Sipa1 activity. They showed that altered Sipa1 expression levels resulted in altered pulmonary metastases. This evidence is consistent with Sipa1 being a metastasis susceptibility gene, one could argue that these data are not sufficient to conclude for certain that the Sipa1 polymorphism is a “constitutional genetic polymorphism affecting tumor metastasis” [5]
Summary
Recent studies in mice indicate that inherited genetic backgrounds can influence metastatic potential. Recent genome-wide association studies have led to the identification of numerous polymorphisms associated with increased risk for breast cancer, with FGFR2 being one of the top candidate genes [2,3]. In the COS7 and U373MG non-breast cancer cell lines, functional studies showed that the Thr allele was associated with reduced concentrations of active, GTPbound Rap1.
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