| セッション情報 | 特別講演10 |
|---|---|
| タイトル | SL-10：Familial aggregation and the early detection of pancreatic cancer |
| 演者 | Hruban Ralph H.（The Johns Hopkins University School of Medicine, USA） |
| 共同演者 | |
| 抄録 | Pancreatic cancer runs in some families. Mutations in a number of genes, including BRCA2, PALB2, ATM, BRCA1, p16/CDKN2A, STK11, PRSS1, and the genes responsible for hereditary nonpolyposis colorectal cancer（HNPCC）syndrome, have been shown to increase the risk of pancreatic cancer. Importantly, the risk of pancreatic and extra-pancreatic cancers can be quantified when the gene is known, providing a unique opportunity for targeted screening and early detection. Once individuals at risk are identified, the next step in developing early detection tests is to characterize the non-invasive precursor lesions that give rise to invasive pancreatic cancer. For pancreatic cancer, these precursors include small“pancreatic intraepithelial neoplasia（PanIN）”lesions and larger cystic precursor lesions including intraductal papillary mucinous neoplasms（IPMNs）and mucinous cystic neoplasms（MCNs）. The next step in developing early detection tests is to establish a method to detect these precursor lesions and to show that they can be detected. Promising approaches in the pancreas include endoscopic ultrasound（EUS）and novel techniques to detect mutant DNA shed by neoplastic lesions. Finally, the most challenging step in developing an early detection test is to develop an evidence base establishing that screening at-risk individuals is beneficial. |
| 索引用語 |