Oral mucosal melanoma: epidemiology and pathobiology.
The vast majority of healthy individuals have some form of melanocytic lesions with most having several cutaneous melanocytic nevocellular nevi. The incidence of cutaneous melanoma, despite improved prevention and early diagnosis of precursor melanocytic lesions, is on the increase with a projection that one in 75 persons born in the year 2000 will develop cutaneous melanoma in his/her lifetime. With cutaneous melanoma, the number, location and type of nevi, sun exposure and inability to tan, and presence or absence of dysplastic nevi affect transformation to a malignant process. Certain familial factors, syndromes, cytogenetic abnormalities, and mutations in tumor suppressor genes also influence tumor formation. In contrast, mucosal melanoma involving the oral cavity and head and neck regions is not as well understood or characterized. No doubt, this is due to the fact that this subtype of melanoma accounts for less than 1% of all cases. Mucosal melanomas tend to present at a higher stage, are more aggressive, and in a vertical growth phase of disease. A definitive precursor lesion for mucosal melanoma has not been identified; however, atypical melanocytic hyperplasia may represent a proliferative phase before overt tumorigenesis occurs. Melanoma-related antigens, growth factors, and proliferation markers have been identified in cutaneous melanoma, and allow for development of immunotherapy directed against melanoma-associated entities. It is currently possible to evaluate the cytogenetic make-up of precursor melanocytic lesions and frank melanoma, and the constitutional genetic background of individuals at risk for melanoma. No doubt, as concerted investigations of mucosal melanomas of the oral cavity and head and neck evolve, similar factors will be identified which will direct therapy and predict recurrence and survival. In the not too distant future, innovative retroviral transfection, antibodies against specific melanoma-associated factors, vaccination against melanoma, and gene therapy to repair cytogenetic abnormalities and tumor suppressor gene mutations may provide effective therapy and protection against melanomas.
Hicks
M J
MJ
Director of Surgical and Ultrastructural Pathology, Department of Pathology, MC1-2261, Baylor College of Medicine, Texas Childrens Hospital, 6621 Fannin Street, Houston, TX 77030-2399, USA. mjhicks@texaschildrenhospital.org
Flaitz
C M
CM
D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D005260:Female; D006801:Humans; D006965:Hyperplasia; D008297:Male; D008545:Melanoma / Q000453:epidemiology / Q000473:pathology*; D008875:Middle Aged; D009062:Mouth Neoplasms / Q000453:epidemiology / Q000473:pathology*