Pathology of Incipient Pancreatic Cancer
Hruban, R. H. ; Wilentz, R.E. ; Goggins, M. ; Offerhaus, G.J.A. ; Yeo, C.J. ; Kern, S.E.
Springer
Published 1999
Springer
Published 1999
| ISSN: |
1569-8041
|
|---|---|
| Keywords: |
duct lesions ; hyperplasia ; K-ras ; p16 ; p53 ; pancreas ; pancreas cancer
|
| Source: |
Springer Online Journal Archives 1860-2000
|
| Topics: |
Medicine
|
| Notes: |
Abstract Background: An understanding of incipient pancreatic neoplasia is an essential foundation for the future development of effective screening tests for pancreatic cancer. Only when we understand early pancreatic neoplasms will be able to detect tumors that are curable with surgical resection. Method: Two approaches have helped define incipient pancreatic neoplasia. First, the histologic examination of pancreata has helped identify the most common histologic lesions in pancreatic tissues adjacent to infiltrating carcinomas. The assumption is that some of these lesions represent the precursors to the infiltrating cancers. Second, advances in molecular genetics now make it possible to define the genetic alterations present in small lesions. The demonstration that a suspected precursor lesion and an infiltrating pancreatic carcinoma share the same genetic alterations would help establish that the lesion is indeed a precursor to infiltrating pancreatic carcinoma. Results: A spectrum of intraductal proliferations in the pancreas has been found associated with infiltrating adenocarcinoma of the pancreas. These lesions, called "duct lesions," have even been identified in pancreas years before patients develop infiltrating carcinoma. Molecular genetic analysis of these lesions has revealed that they frequently harbor many of the same alterations present in infiltrating carcinoma of the pancreas. These alterations include activation of K-ras and inactivation of p16, p53 and, rarely BRCA2. Conclusions: From these morphologic and molecular observations, we can now develop a progression model for the development of infiltrating carcinoma of the pancreas. Infiltrating carcinomas of the pancreas may arise from pancreatic duct lesions, and the progression of duct lesions to infiltrating cancer is associated with the accumulation of generalized and specific genetic alterations.
|
| Type of Medium: |
Electronic Resource
|
| URL: |
| _version_ | 1798296352940097537 |
|---|---|
| autor | Hruban, R. H. Wilentz, R.E. Goggins, M. Offerhaus, G.J.A. Yeo, C.J. Kern, S.E. |
| autorsonst | Hruban, R. H. Wilentz, R.E. Goggins, M. Offerhaus, G.J.A. Yeo, C.J. Kern, S.E. |
| book_url | http://dx.doi.org/10.1023/A:1008359929858 |
| datenlieferant | nat_lic_papers |
| hauptsatz | hsatz_simple |
| identnr | NLM192892215 |
| issn | 1569-8041 |
| journal_name | Annals of oncology |
| materialart | 1 |
| notes | Abstract Background: An understanding of incipient pancreatic neoplasia is an essential foundation for the future development of effective screening tests for pancreatic cancer. Only when we understand early pancreatic neoplasms will be able to detect tumors that are curable with surgical resection. Method: Two approaches have helped define incipient pancreatic neoplasia. First, the histologic examination of pancreata has helped identify the most common histologic lesions in pancreatic tissues adjacent to infiltrating carcinomas. The assumption is that some of these lesions represent the precursors to the infiltrating cancers. Second, advances in molecular genetics now make it possible to define the genetic alterations present in small lesions. The demonstration that a suspected precursor lesion and an infiltrating pancreatic carcinoma share the same genetic alterations would help establish that the lesion is indeed a precursor to infiltrating pancreatic carcinoma. Results: A spectrum of intraductal proliferations in the pancreas has been found associated with infiltrating adenocarcinoma of the pancreas. These lesions, called "duct lesions," have even been identified in pancreas years before patients develop infiltrating carcinoma. Molecular genetic analysis of these lesions has revealed that they frequently harbor many of the same alterations present in infiltrating carcinoma of the pancreas. These alterations include activation of K-ras and inactivation of p16, p53 and, rarely BRCA2. Conclusions: From these morphologic and molecular observations, we can now develop a progression model for the development of infiltrating carcinoma of the pancreas. Infiltrating carcinomas of the pancreas may arise from pancreatic duct lesions, and the progression of duct lesions to infiltrating cancer is associated with the accumulation of generalized and specific genetic alterations. |
| package_name | Springer |
| publikationsjahr_anzeige | 1999 |
| publikationsjahr_facette | 1999 |
| publikationsjahr_intervall | 8004:1995-1999 |
| publikationsjahr_sort | 1999 |
| publisher | Springer |
| reference | 10 (1999), S. 9-11 |
| schlagwort | duct lesions hyperplasia K-ras p16 p53 pancreas pancreas cancer |
| search_space | articles |
| shingle_author_1 | Hruban, R. H. Wilentz, R.E. Goggins, M. Offerhaus, G.J.A. Yeo, C.J. Kern, S.E. |
| shingle_author_2 | Hruban, R. H. Wilentz, R.E. Goggins, M. Offerhaus, G.J.A. Yeo, C.J. Kern, S.E. |
| shingle_author_3 | Hruban, R. H. Wilentz, R.E. Goggins, M. Offerhaus, G.J.A. Yeo, C.J. Kern, S.E. |
| shingle_author_4 | Hruban, R. H. Wilentz, R.E. Goggins, M. Offerhaus, G.J.A. Yeo, C.J. Kern, S.E. |
| shingle_catch_all_1 | Hruban, R. H. Wilentz, R.E. Goggins, M. Offerhaus, G.J.A. Yeo, C.J. Kern, S.E. Pathology of Incipient Pancreatic Cancer duct lesions hyperplasia K-ras p16 p53 pancreas pancreas cancer duct lesions hyperplasia K-ras p16 p53 pancreas pancreas cancer Abstract Background: An understanding of incipient pancreatic neoplasia is an essential foundation for the future development of effective screening tests for pancreatic cancer. Only when we understand early pancreatic neoplasms will be able to detect tumors that are curable with surgical resection. Method: Two approaches have helped define incipient pancreatic neoplasia. First, the histologic examination of pancreata has helped identify the most common histologic lesions in pancreatic tissues adjacent to infiltrating carcinomas. The assumption is that some of these lesions represent the precursors to the infiltrating cancers. Second, advances in molecular genetics now make it possible to define the genetic alterations present in small lesions. The demonstration that a suspected precursor lesion and an infiltrating pancreatic carcinoma share the same genetic alterations would help establish that the lesion is indeed a precursor to infiltrating pancreatic carcinoma. Results: A spectrum of intraductal proliferations in the pancreas has been found associated with infiltrating adenocarcinoma of the pancreas. These lesions, called "duct lesions," have even been identified in pancreas years before patients develop infiltrating carcinoma. Molecular genetic analysis of these lesions has revealed that they frequently harbor many of the same alterations present in infiltrating carcinoma of the pancreas. These alterations include activation of K-ras and inactivation of p16, p53 and, rarely BRCA2. Conclusions: From these morphologic and molecular observations, we can now develop a progression model for the development of infiltrating carcinoma of the pancreas. Infiltrating carcinomas of the pancreas may arise from pancreatic duct lesions, and the progression of duct lesions to infiltrating cancer is associated with the accumulation of generalized and specific genetic alterations. 1569-8041 15698041 Springer |
| shingle_catch_all_2 | Hruban, R. H. Wilentz, R.E. Goggins, M. Offerhaus, G.J.A. Yeo, C.J. Kern, S.E. Pathology of Incipient Pancreatic Cancer duct lesions hyperplasia K-ras p16 p53 pancreas pancreas cancer duct lesions hyperplasia K-ras p16 p53 pancreas pancreas cancer Abstract Background: An understanding of incipient pancreatic neoplasia is an essential foundation for the future development of effective screening tests for pancreatic cancer. Only when we understand early pancreatic neoplasms will be able to detect tumors that are curable with surgical resection. Method: Two approaches have helped define incipient pancreatic neoplasia. First, the histologic examination of pancreata has helped identify the most common histologic lesions in pancreatic tissues adjacent to infiltrating carcinomas. The assumption is that some of these lesions represent the precursors to the infiltrating cancers. Second, advances in molecular genetics now make it possible to define the genetic alterations present in small lesions. The demonstration that a suspected precursor lesion and an infiltrating pancreatic carcinoma share the same genetic alterations would help establish that the lesion is indeed a precursor to infiltrating pancreatic carcinoma. Results: A spectrum of intraductal proliferations in the pancreas has been found associated with infiltrating adenocarcinoma of the pancreas. These lesions, called "duct lesions," have even been identified in pancreas years before patients develop infiltrating carcinoma. Molecular genetic analysis of these lesions has revealed that they frequently harbor many of the same alterations present in infiltrating carcinoma of the pancreas. These alterations include activation of K-ras and inactivation of p16, p53 and, rarely BRCA2. Conclusions: From these morphologic and molecular observations, we can now develop a progression model for the development of infiltrating carcinoma of the pancreas. Infiltrating carcinomas of the pancreas may arise from pancreatic duct lesions, and the progression of duct lesions to infiltrating cancer is associated with the accumulation of generalized and specific genetic alterations. 1569-8041 15698041 Springer |
| shingle_catch_all_3 | Hruban, R. H. Wilentz, R.E. Goggins, M. Offerhaus, G.J.A. Yeo, C.J. Kern, S.E. Pathology of Incipient Pancreatic Cancer duct lesions hyperplasia K-ras p16 p53 pancreas pancreas cancer duct lesions hyperplasia K-ras p16 p53 pancreas pancreas cancer Abstract Background: An understanding of incipient pancreatic neoplasia is an essential foundation for the future development of effective screening tests for pancreatic cancer. Only when we understand early pancreatic neoplasms will be able to detect tumors that are curable with surgical resection. Method: Two approaches have helped define incipient pancreatic neoplasia. First, the histologic examination of pancreata has helped identify the most common histologic lesions in pancreatic tissues adjacent to infiltrating carcinomas. The assumption is that some of these lesions represent the precursors to the infiltrating cancers. Second, advances in molecular genetics now make it possible to define the genetic alterations present in small lesions. The demonstration that a suspected precursor lesion and an infiltrating pancreatic carcinoma share the same genetic alterations would help establish that the lesion is indeed a precursor to infiltrating pancreatic carcinoma. Results: A spectrum of intraductal proliferations in the pancreas has been found associated with infiltrating adenocarcinoma of the pancreas. These lesions, called "duct lesions," have even been identified in pancreas years before patients develop infiltrating carcinoma. Molecular genetic analysis of these lesions has revealed that they frequently harbor many of the same alterations present in infiltrating carcinoma of the pancreas. These alterations include activation of K-ras and inactivation of p16, p53 and, rarely BRCA2. Conclusions: From these morphologic and molecular observations, we can now develop a progression model for the development of infiltrating carcinoma of the pancreas. Infiltrating carcinomas of the pancreas may arise from pancreatic duct lesions, and the progression of duct lesions to infiltrating cancer is associated with the accumulation of generalized and specific genetic alterations. 1569-8041 15698041 Springer |
| shingle_catch_all_4 | Hruban, R. H. Wilentz, R.E. Goggins, M. Offerhaus, G.J.A. Yeo, C.J. Kern, S.E. Pathology of Incipient Pancreatic Cancer duct lesions hyperplasia K-ras p16 p53 pancreas pancreas cancer duct lesions hyperplasia K-ras p16 p53 pancreas pancreas cancer Abstract Background: An understanding of incipient pancreatic neoplasia is an essential foundation for the future development of effective screening tests for pancreatic cancer. Only when we understand early pancreatic neoplasms will be able to detect tumors that are curable with surgical resection. Method: Two approaches have helped define incipient pancreatic neoplasia. First, the histologic examination of pancreata has helped identify the most common histologic lesions in pancreatic tissues adjacent to infiltrating carcinomas. The assumption is that some of these lesions represent the precursors to the infiltrating cancers. Second, advances in molecular genetics now make it possible to define the genetic alterations present in small lesions. The demonstration that a suspected precursor lesion and an infiltrating pancreatic carcinoma share the same genetic alterations would help establish that the lesion is indeed a precursor to infiltrating pancreatic carcinoma. Results: A spectrum of intraductal proliferations in the pancreas has been found associated with infiltrating adenocarcinoma of the pancreas. These lesions, called "duct lesions," have even been identified in pancreas years before patients develop infiltrating carcinoma. Molecular genetic analysis of these lesions has revealed that they frequently harbor many of the same alterations present in infiltrating carcinoma of the pancreas. These alterations include activation of K-ras and inactivation of p16, p53 and, rarely BRCA2. Conclusions: From these morphologic and molecular observations, we can now develop a progression model for the development of infiltrating carcinoma of the pancreas. Infiltrating carcinomas of the pancreas may arise from pancreatic duct lesions, and the progression of duct lesions to infiltrating cancer is associated with the accumulation of generalized and specific genetic alterations. 1569-8041 15698041 Springer |
| shingle_title_1 | Pathology of Incipient Pancreatic Cancer |
| shingle_title_2 | Pathology of Incipient Pancreatic Cancer |
| shingle_title_3 | Pathology of Incipient Pancreatic Cancer |
| shingle_title_4 | Pathology of Incipient Pancreatic Cancer |
| sigel_instance_filter | dkfz geomar wilbert ipn albert fhp |
| source_archive | Springer Online Journal Archives 1860-2000 |
| timestamp | 2024-05-06T09:50:43.499Z |
| titel | Pathology of Incipient Pancreatic Cancer |
| titel_suche | Pathology of Incipient Pancreatic Cancer |
| topic | WW-YZ |
| uid | nat_lic_papers_NLM192892215 |