Molecular biology of pancreatic cancer; oncogenes, tumour suppressor genes, growth factors, and their receptors from a clinical perspective

Pancreatic cancer represents the fourth leading cause of cancer death in me n and the fifth in women. Prognosis remains dis mat, mainly because the dia gnosis is made late in the clinical course of the disease,The need to impro ve the diagnosis, detection, and treatment of pancreatic cancer is great. i t is in this type of cancer; in which the mortality is so great and the cli nical detection so difficult that the recent advances of molecular biology may have a significant impact. Genetic alterations can be detected at diffe rent levels. These alterations include oncogene mutations (most commonly, K -ras mutations, which occur in 75% to more than 95% of pancreatic cancer ti ssues), tumour suppressor genes alterations (mainly, p53, p16, DCC, etc.), overexpression of growth factors (such as EGF,TGF alpha,TGF beta I-3, aFGF, bTGF, etc.) and their receptors (i.e., EGF receptor; TGF beta receptor I-I II, etc.). Insights into the molecular genetics of pancreatic carcinogenesi s are beginning to form a genetic model for pancreatic cancer and its precu rsors. These improvements in our understanding of the molecular biology of pancreatic cancer are not simply of research interest, but may have clinica l implications, such as risk assessment, early diagnosis, treatment, and pr ognosis evaluation. (C) 2000 Harcourt Publishers Ltd.