Skip Navigation

This Article
Right arrow FREE Full Text (PDF) Freely available
Right arrow E-letters: Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when E-letters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Goggins, M.
Right arrow Articles by Hruban, R.H.
Right arrow Search for Related Content
PubMed
Right arrow Articles by Goggins, M.
Right arrow Articles by Hruban, R.H.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Annals of Oncology 10:S4-S8, 1999
© 1999 European Society for Medical Oncology

Review

Progress in cancer genetics: Lessons from pancreatic cancer

M. Goggins1, S.E. Kern1, J.A. Offerhaus2 and R.H. Hruban1

1 Departments of Oncology and Pathology, Johns Hopkins Medical Institutions Baltimore, MD, USA
2 The Department of Pathology, Academic Medical Center, University of Amsterdam Amsterdam, The Netherlands

Correspondence to: Michael Goggins, MD, MRCPI, Department of Pathology, Gastrointestinal Division, 628 Ross Building, Johns Hopkins Medical Institutions, 720 Rutland Ave, Baltimore, MD, 21205, USA.

Background: In the near future advances in the molecular basis of cancer are expected to facilitate cancer diagnosis, to rationalize treatment, to facilitate screening, and to identify individuals requiring cancer prevention strategies.

Methods: The literature was reviewed concerning the genetic alterations that contribute to pancreatic cancer development.

Results: Virtually all pancreatic cancers have inactivation of the pl6 pathway, and the majority inactivate the TGF beta/DPC4 and p53 tumor-suppressive pathways. Pancreatic cancers with mismatch repair deficiency have a characteristic histology and may have an improved prognosis. The recently discovered tumor suppressor genes, ALK-5, MKK4, and STK11 (the gene responsible for Peutz-Jeghers syndrome) are all targeted for mutation in a small proportion of sporadic pancreatic cancers. Germline mutations of the BRCA2 gene are present in 5–10% of patients with pancreatic cancer. Typically such patients do not have a family history of pancreatic cancer and are mistaken as patients with sporadic disease. Five to 10% of patients with pancreatic cancer have first-degree relatives that will develop pancreatic cancer. Some such families also have a family history of melanoma and harbor germline pl6 mutations. However, the gene(s) responsible for much of the inherited predisposition to pancreatic cancer remain to be identified.

Conclusion: Further advances in pancreatic cancer molecular genetics are needed to facilitate the development of molecular screening tests, to identify additional familial susceptibility genes, and to identify targets for rational therapeutic targeting.

ALK-5, BRCA2, DPC4, mismatch repair, pancreas cancer, pl6, tumor suppressor genes


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?




Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.