Unformatted text preview: tes. Thus, nevus cells show limited proliferation and cells in common
acquired nevi have no apparent chromosomal aberrations. Nevi can develop not just
through a stimulatory event, but also through loss of control of keratinocytes over
melanocytes. Progression from the melanocyte or common acquired nevus cell to a
dysplastic nevus or RGP melanoma most likely involves the onset of genetic
aberrations. The cells show cytologic atypia, they can separate from the basement
membrane without undergoing apoptosis, and the entire lesion shows architectural
atypia. Cells from RGP lesions have biologic properties in vitro that are intermediate
between benign and malignant. VGP primary melanomas are characterized as
expanding nodules that invade deep into the dermis. VGP primary melanomas are
6 highly aneuploid. Biologically, the cells are relatively plastic, some also acquire
metastatic competence. Metastatic cells show a high level of genetic instability, and
phenotypic plasticity, depending on the environment and any selective pressure
placed on the cells (5, 6). Metastatic cells are highly motile and independent of
growth factors, and have acquired the capacity to invade other tissues and organs Melanoma risk factors
As in most types of cancers, there are two sets of factors that present significant risk
for melanoma in humans: host characteristics and environmental factors.
Epidemiologic studies have identified host factors important for risk of melanoma.
These include family history of melanoma, alterations in melanoma susceptibility
genes, number and type of nevi, skin type and pigmentation (7). Melanoma is more
common in individuals with fair skin, blue or green eyes, red or blond hair, many
freckles and in individuals who react to sunlight by burning rather than tanning.
UV radiation is the most important environmental factor in the development of
melanoma. Intermittent repeated exposures to sunlight from childhood are
epidemiologically shown to be a major cause of melanom...
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