Abstract
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.
Footnotes
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The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
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↵1 Supported by NIH Research Grant CA76176 and Department of Defense Breast Cancer Grant DAMD17-98-1-8060 (to G. F. W.). NIH Grant AI 12184 was awarded to H. C. The generation of the CD44 knockout mice was funded by grants from the Medical Research Council of Canada and the National Cancer Institute of Canada (to T. W. M.), as well as a fellowship from the Dr. Mildred-Scheel Stiftung in Germany (to R. S.).
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↵2 To whom requests for reprints should be addressed, at Department of Radiation Oncology, New England Medical Center and Tufts University Medical School, NEMC # 824, 750 Washington Street, Boston, MA 02111. Phone: (617) 636-9013; Fax: (617) 636-1766; E-mail: GWeber{at}lifespan.org
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↵3 Present address: Universitaet des Saarlandes, 66424 Homburg, Germany.
- Received September 25, 2001.
- Accepted February 26, 2002.
- ©2002 American Association for Cancer Research.
Volume 62, Issue 8
