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JNCI Journal of the National Cancer Institute 2002 94(1):4-5; doi:10.1093/jnci/94.1.4
© 2002 by Oxford University Press
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Journal of the National Cancer Institute, Vol. 94, No. 1, 4-5, January 2, 2002
© 2002 Oxford University Press

EDITORIAL

Prostate Cancer in Bone: Importance of Context for Inhibition of Matrix Metalloproteinases

Mina J. Bissell, Johanne Le Beyec, Robin L. Anderson

Affiliations of authors: M. J. Bissell, J. Le Beyec, Lawrence Berkeley National Laboratory, Life Science Division, Berkeley, CA; R. L. Anderson, Peter MacCallum Cancer Institute, East Melbourne, and Victoria, Australia.

Correspondence to: Mina J. Bissell, Ph.D., Lawrence Berkeley National Laboratory, Life Science Division, 1 Cyclotron Rd., MS 83-101, Berkeley, CA 94720 (e-mail: mjbissell@lbl.gov).

Prostate cancer is the second most common cause of cancer death in American men. Once metastasis has occurred, there is no curative treatment, and the search for effective therapies for prostate cancer and, in particular, for metastasis to bone is hampered by a lack of suitable animal models of the disease.

In this issue of the Journal, Nemeth et al. (1) address aspects of these two difficult issues. They describe the use of the human fetal bone/severe combined immunodeficient (SCID) mouse model to explore the role of matrix metalloproteinases (MMPs) in metastasis of prostate cancer to bone and the ability of the broad-spectrum MMP inhibitor batimastat to reduce bone disease.

Most research into human prostate cancer uses just three cell lines, PC3, DU-145, and LnCaP. After subcutaneous inoculation into immunocompromised . . . [Full Text of this Article]

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