Animal models of melanoma: Recent advances and future prospects

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This chapter reviews the current knowledge of the genetic basis of human melanoma and describes how this information is employed to construct and refine in vivo animal model systems for this disease. The focus is placed on the mouse and how genetics and transgenic technology are being used to generate an accurate melanoma model. The chapter discusses the clinical aspects and molecular basis for melanoma. It is suggested that receptor tyrosine kinases (RTKs) play crucial roles in coordinated development and proliferation of normal melanocytes and contribute to uncontrolled growth and progression of melanomas. The chapter discusses several RTKs that have been implicated in melanoma genesis or progression, either through correlative expression analyses in human melanoma cell lines or by genetic experiments in animal models. In addition, the chapter emphasizes the requirement to study cancer in an in vivo setting. Mouse tumor model systems, employing advances in transgenic technology and cancer genetics, are generated with varying fidelity. The development of inducible and conditional knockout strains may provide for a more physiologic approach enabling the stepwise acquisition of genetic lesions that is a hallmark of human malignancy. With these tools in hand, one can strive to achieve the ultimate goals of cancer research: improvement in the diagnosis, treatment, and prevention of cancer.

References (186)

  • A.C. Bell et al.

    Curr. Opin. Genet. Dev.

    (1999)
  • D.C. Bennett

    Int. Rev. Cytol.

    (1993)
  • A. Brehm et al.

    Trends Biochem. Sci.

    (1999)
  • S. Chen et al.

    J. Invest. Dermatol.

    (1996)
  • L. Chin et al.

    Trends Biochem. Sci.

    (1998)
  • A. de la Chapelle et al.

    Curr. Opin. Genet. Dev.

    (1998)
  • P.E. de Wit et al.

    J. Invest. Dermatol.

    (1992)
  • D.L. Ellis et al.

    J. Am. Acad. Dermatol.

    (1992)
  • B. Gardie et al.

    Blood

    (1998)
  • M.H. Greene
  • S. Grugel et al.

    J. Biol. Chem.

    (1995)
  • D.A. Haber

    Cell (Cambridge, Mass.)

    (1997)
  • G. Imokawa et al.

    J. Biol. Chem.

    (1992)
  • D. Jean et al.

    J. Biol. Chem.

    (1998)
  • M. Johnston

    Curr. Biol.

    (1998)
  • A. Kamb

    Trends Genet.

    (1995)
  • T. Kamijo et al.

    Cell

    (1997)
  • A.J. Levine

    Cell (Cambridge, Mass.)

    (1997)
  • N.U. Ahmed et al.

    Melanoma Res.

    (1997)
  • B.K. Armstrong et al.

    Melanoma Res.

    (1993)
  • C.M. Balch et al.
  • A. Bardelli et al.

    Oncogene

    (1999)
  • S. Bates et al.

    Nature (London)

    (1998)
  • D. Becker et al.

    EMBO J.

    (1989)
  • D. Becker et al.

    Oncogene

    (1992)
  • M. Bradl et al.
  • J.S. Butel et al.

    J. Natl. Cancer Inst.

    (1999)
  • S.L. Campbell et al.

    Oncogene

    (1998)
  • L.C. Cantley et al.
  • L. Chin et al.

    Genes Dev.

    (1997)
  • L. Chin et al.

    Nature (London)

    (1999)
  • B. Cohen

    Nat. Genet.

    (1999)
  • E. de Stanchina et al.

    Genes Dev.

    (1998)
  • A. Di Cristofano et al.

    Nat. Genet.

    (1998)
  • G.J. Draper et al.

    Br. J. Cancer

    (1986)
  • D. Duro et al.

    Oncogene

    (1995)
  • A. Dwenger et al.

    J. Hematother.

    (1996)
  • N. Dyson

    Genes Dev.

    (1998)
  • M.S. Eller et al.
  • E.R. Fearon

    Science

    (1997)
  • R.E. Finney et al.

    Science

    (1993)
  • R.A. Fleischman et al.
  • J.W. Fountain et al.

    Cancer Surv.

    (1990)
  • D.S. Franklin et al.

    Genes Dev.

    (1998)
  • S.Y. Fuchs et al.

    Oncogene

    (1998)
  • A. Fujimoto et al.

    Oncogene

    (1999)
  • R. Ganss et al.

    EMBO J.

    (1994)
  • P.R. Gause et al.

    Mol. Carcinog.

    (1997)
  • E.N. Geissler et al.

    Genetics

    (1981)
  • F.N. Ghadially

    IARC Sci. Publ.

    (1982)
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