Apparent absence of a benign precursor lesion: Implications for the pathogenesis of malignant melanoma
- Rockefeller Univ., New York, NY (USA)
This review relates concepts derived from the study of chemically induced skin cancer in animal models to the pathogenesis of malignant melanoma in humans. Most chemically induced experimental cancers in animals, including melanomas in rodents, arise within a benign precursor lesion. The initiation-promotion-progression sequence is a central concept in animal models for carcinogenesis. Many human melanomas appear to arise from epidermal melanocytes, with no associated precursor lesion. This article considers why there is no apparent precursor in many human melanomas and the consequences of this absence. Melanocyte physiology and factors that govern escape from defenses such as DNA repair, local tissue environment, and immunity presumably influence melanocyte conversion to melanoma. These factors may determine the absence of a precursor lesion in primary melanomas. In addition, it is possible that some human melanomas arise by cellular mechanisms different from those causing cancer in rodent models. Both molecular and prospective clinical studies will be required to explain this apparent paradox in the pathogenesis of melanoma. A similar approach may help to explain the origin of basal cell carcinoma and perhaps other human cancers that appear to arise directly from normal cells. From a clinical point of view, the absence of an identifiable, benign precursor lesion requires even greater emphasis on melanoma prevention. Research on mechanisms of ultraviolet carcinogenesis indicates that appropriate postexposure treatments may be useful in preventing long-term consequences of sunburn, including melanoma. 69 references.
- OSTI ID:
- 5345540
- Journal Information:
- Journal of the American Academy of Dermatology; (USA), Vol. 21; ISSN 0190-9622
- Country of Publication:
- United States
- Language:
- English
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Related Subjects
59 BASIC BIOLOGICAL SCIENCES
MELANOMAS
PATHOGENESIS
SKIN
XENOBIOTICS
CARCINOGENESIS
BIOLOGICAL MODELS
DNA REPAIR
EXPERIMENTAL NEOPLASMS
GENES
MICE
ONCOGENIC TRANSFORMATIONS
REVIEWS
ULTRAVIOLET RADIATION
ANIMALS
BIOLOGICAL RECOVERY
BIOLOGICAL REPAIR
BODY
CELL TRANSFORMATIONS
DISEASES
DOCUMENT TYPES
ELECTROMAGNETIC RADIATION
MAMMALS
NEOPLASMS
ORGANS
RADIATIONS
RECOVERY
REPAIR
RODENTS
VERTEBRATES
560300* - Chemicals Metabolism & Toxicology
550900 - Pathology