dysplastic nevus syndrome

Dysplastic nevus

A dysplastic nevus, (or naevus; pl. nevi or naevi) is an atypical mole; a mole whose appearance is different from that of common moles. Dysplastic nevi are generally larger than ordinary moles and have irregular and indistinct borders. Their color frequently is not uniform and ranges from pink to dark brown; they usually are flat, but parts may be raised above the skin surface. Dysplastic nevi can be found anywhere, but are most common on the trunk in men, and on the calves in women. In 1992, the NIH recommended that the term "dysplastic nevus" be avoided in favor of more descriptive language.


According to the National Cancer Institute, doctors believe that dysplastic nevi are more likely than ordinary moles to develop into a type of skin cancer called melanoma. Because of this, moles should be checked regularly by a doctor or nurse specialist, especially if they look unusual; grow larger; or change in color, or outline; or if any changes occur.


When an atypical mole has been identified, a biopsy takes place in order to best diagnose it. Local anesthetic is used to numb the area, then the mole is biopsied. The biopsy material is then sent to a laboratory to be evaluated by a pathologist.

Dysplastic Nevus Syndrome

Dysplastic Nevus Syndrome is an autosomal dominant hereditary condition which causes the person to have a large quantity of nevi (moles), often 100 or more. There is a propensity for these nevi to become dysplastic in these individuals. Dysplastic nevi are a precursor to malignant melanoma, and these patients are therefore at a higher risk of developing this malignant form of skin cancer. A slight majority of melanomas do not form in an existing mole, but rather create a new growth on the skin. Nevertheless, those with more dysplastic nevi are at a higher risk of this type of melanoma occurrence. Such persons need to be checked regularly for any changes in their moles and to note any new ones. In 40-50% of cases, the disorder has been linked with germline mutations in the CDKN2A gene, which codes for p16 (a regulator of cell division).


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