Perspective

Journal of Investigative Dermatology (2008) 128, 2381–2391; doi:10.1038/jid.2008.177

From UVs to Metastases: Modeling Melanoma Initiation and Progression in the Mouse

M Raza Zaidi1,2, Chi-Ping Day1,2 and Glenn Merlino1

1Laboratory of Cancer Biology and Genetics, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA

Correspondence: Dr Glenn Merlino, Chief Laboratory of Cancer Biology & Genetics, National Cancer Institute, NIH, 9000 Rockville Pike, Building 37, Room 5002, Bethesda, Maryland 20892-4264, USA. E-mail: gmerlino@helix.nih.gov

2These authors contributed equally to this work.

Received 14 March 2008; Revised 7 May 2008; Accepted 10 May 2008.

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Abstract

Cutaneous malignant melanoma is highly invasive and capable of metastasizing to distant sites where it is typically resistant to available therapy. While striving to prevent or eradicate melanoma, researchers have two significant advantages not shared by those working on many other cancers. The main environmental etiological agent, UV radiation, is known and melanocytic lesions are excisable for molecular analysis from most stages. Yet knowledge about how UV initiates melanoma has been insufficient to achieve prevention, and the understanding of metastatic mechanisms has been inadequate to reduce mortality. Here, we review the value of melanoma mouse models, focusing on these critical early and late stages.

Abbreviations:

CPD, cyclobutane pyrimidine dimer; CT, computed tomography; GEM, genetically engineered mouse; HGF/SF, hepatocyte growth factor/scatter factor; MAPK, mitogen-activated protein kinase; MRI, magnetic resonance imaging; PET, positron emission tomography; RGP, radial growth phase; VGP, vertical growth phase; UVR, ultraviolet radiation

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