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Previous Volume 355:51-65 July 6, 2006 Number 1 Next

	Since this article has no abstract, we have provided an extract of the first 100 words of the full text and any section headings.

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Although melanoma accounts for only 4 percent of all dermatologic cancers, it is responsible for 80 percent of deaths from skin cancer; only 14 percent of patients with metastatic melanoma survive for five years.¹ The intractability of advanced melanoma shows how much we have to learn about the changes that facilitate the vertical growth and deep invasion of melanoma and about the mechanisms that block the effectiveness of chemotherapy.

The Clark model of the progression of melanoma emphasizes the stepwise transformation of melanocytes to melanoma (Figure 1). The model depicts the proliferation of melanocytes in the process of . . . [Full Text of this Article]

Environmental and Genetic Interactions

Risk Factors

Photosensitivity, Tanning, and Melanoma

A Molecular Model of Melanoma Progression

Hyperplasia and Nevus Formation

Cytologic Atypia and Tumor-Suppressor Genes

            CDKN2A

PTEN, AKT, and Cell Death

MITF and Melanocyte Differentiation

MITF in Development

MITF in Differentiation

MITF in Melanoma

Cell Adhesion and Invasion

Cadherins

Integrins

Patterns of Genetic Alteration

Modeling Melanoma Progression

Source Information

From the Dermatopathology Unit, Massachusetts General Hospital, and Harvard Medical School — both in Boston.

Address reprint requests to Dr. Mihm at the Department of Dermatopathology, Massachusetts General Hospital, 55 Fruit St., Warren 827, Boston, MA 02114.

Related Letters:

Molecular Mechanisms in Melanoma
Diaz-Cano S. J., Ugurel S., Houben R., Becker J. C., Vale S., Miller A., Mihm M. C. Jr.
Extract | Full Text | PDF  
N Engl J Med 2006; 355:1395-1396, Sep 28, 2006. Correspondence

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