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Carcinogenesis |
Department of Cancer Immunology and AIDS, Dana-Farber Cancer Institute, Boston, Massachusetts [G. F. W., J. I., H. C.]; Departments of Medicine [G. F. W.] and Pathology [J. I., H. C.], Harvard Medical School, Boston, Massachusetts 02115; USDA Human Nutrition Research Center on Aging, Tufts University, Boston, Massachusetts 02111 [R. T. B.]; and Department of Cellular and Molecular Biology, Ontario Cancer Institute, Toronto, Ontario M56 2M9, Canada [R. S., T. W. M.]
To test the role of the CD44 gene in tumorigenesis, mice with the min mutationof the APC gene or with the tm1 mutation of the p53 gene were crossedwith CD44 knockout mice. The absence of CD44 gene products did not affect tumor incidence or survival; however, mice with disruption of the CD44 gene showed virtually aborted metastasis formation of osteosarcomas. This is in agreement with the role attributed to CD44 variants in the spread of cancer. Therefore, CD44 gene products are not essential for tumor incidence and growth but are important in regulating metastasis formation.
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