Molecular Pathogenesis of Pancreatic Cancer.
- Author:
Yong Tae KIM
1
Author Information
1. Department of Internal Medicine, Seoul National University College of Medicine, Korea. yongtkim@snu.ac.kr
- Publication Type:Review
- Keywords:
Pancreatic cancer;
Molecular pathogenesis;
Gene
- MeSH:
Animals;
Carcinoma in Situ;
Early Diagnosis;
Mice;
Oncogenes;
Pancreatic Neoplasms*;
Biomarkers
- From:Hanyang Medical Reviews
2007;27(1):76-84
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Applying the growing body of knowledge of the molecular basis of pancreatic cancer to effective strategies for early diagnosis and treatment is a challenge for both clinicians and scientists. Although our knowledge of the molecular alterations in pancreatic cancer has grown significantly using genomic high-throughput technology, there is still much to learn. Molecular studies of pancreatic cancer have revealed that this cancer is associated with several genetic mutations. The genes targeted in pancreatic cancer include tumor-suppressor genes (p16, TP53 and SMAD4), oncogenes (K-RAS, BRAF, AKT2 and Shh), and genome-maintenance genes (MLH1, MSH2 and BRAC2). However, a better understanding of the relative contribution of each of these molecular alterations is necessary. Mutant mice that develop pancreatic intraepithelial neoplasms (PanIN), the preinvasive stage of pancreatic cancer, were produced and demonstrated promise in the pursuit of biomarkers of early pancreatic cancer. Mutant mice that develop PanIN also facilitate explorations of the cellular origins of pancreatic cancer and the development of treatment strategies.
