Two studies in the October issue of Nature Genetics report findings that improve our understanding of metastasis, the process by which cancer cells break free of a localized tumor and migrate to other parts of the body where they give rise to more widespread disease.
Kent Hunter and colleagues show that mice that have been engineered to develop mammary cancer have an increased incidence of metastatic disease when they harbor a particular variant of the gene Sipa1.
This gene encodes a protein that is induced by signals promoting cell proliferation. Its expression alters the adhesive properties of cells and increases their ability to metastasize. This finding lends support to the idea that normal variants may predispose certain individuals to metastatic cancer once a tumor has developed.
In the accompanying study, Robert Weinberg and colleagues describe a new mouse model of melanoma. Melanomas typically have a very high likelihood of metastasizing, and the authors show that this may in part be due to the program of gene expression that is found in normal melanocytes before they become cancerous. Melanocytes are derived from migratory cells called neural crest cells, and Weinberg and co-workers show that a protein called Slug, which is required for cell migration in normal melanocytes, also promotes metastasis in melanomas. Like the results of Hunter and colleagues, this work is consistent with the idea that normal variation in genetic background may explain why some individuals are more likely than others to develop metastatic cancer.
Kent Hunter (National Cancer Institute, NIH, Bethesda, MD, USA)
Robert Weinberg (Whitehead Institute for Biomedical Research, MIT, Cambridge, MA, USA)
For abstracts, click here: Abstract 1, and Abstract 2.
(C) Nature Genetics press release.
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