G J Bullock1, J L Green, P L Baron. 1. Department of Surgery, Medical University of South Carolina, Charleston 29425, USA.
Abstract
BACKGROUND: Recent advances in molecular oncology have provided explanations at the DNA level for the malignant transformation and metastatic potential of various cancers. Malignant melanoma and pancreatic cancer may be classified together in both these cancers exhibit mutations in, or loss of, the cell-cycle inhibitory gene, p16. This paper reviews the current literature on p16 expression in melanoma and pancreatic cancer, explores factors that place patients with these cancers in categories of high risk for metastases or recurrence, and addresses whether aberrant gene expressions should influence awareness of and current recommendations for the management of these aggressive cancers. METHODS: A computerized literature search was performed utilizing OVID Technology's Medline database from 1993 to 1998. RESULTS: Both familial as well as sporadic cases of malignant melanoma and pancreatic carcinoma are reported in the literature. Although a low percentage of cases of either malignancy have p16 mutations, a higher risk of their development has been reported to occur in certain families with p16 germline mutations. CONCLUSIONS: The increased risk determined in these families may serve to heighten awareness of the influence of positive family history of these cancers in the evaluation of patients.
BACKGROUND: Recent advances in molecular oncology have provided explanations at the DNA level for the malignant transformation and metastatic potential of various cancers. Malignant melanoma and pancreatic cancer may be classified together in both these cancers exhibit mutations in, or loss of, the cell-cycle inhibitory gene, p16. This paper reviews the current literature on p16 expression in melanoma and pancreatic cancer, explores factors that place patients with these cancers in categories of high risk for metastases or recurrence, and addresses whether aberrant gene expressions should influence awareness of and current recommendations for the management of these aggressive cancers. METHODS: A computerized literature search was performed utilizing OVID Technology's Medline database from 1993 to 1998. RESULTS: Both familial as well as sporadic cases of malignant melanoma and pancreatic carcinoma are reported in the literature. Although a low percentage of cases of either malignancy have p16 mutations, a higher risk of their development has been reported to occur in certain families with p16 germline mutations. CONCLUSIONS: The increased risk determined in these families may serve to heighten awareness of the influence of positive family history of these cancers in the evaluation of patients.