[Biological aspects of pancreatic cancer]
- PMID: 16172578
[Biological aspects of pancreatic cancer]
Abstract
Pancreatic ductal carcinoma still is an aggressive disease with a fatal prognosis due to late diagnosis and resistance to pharmacological and surgical treatments. Molecular investigations of pancreatic cancer are complicated by the restricted accessibility of the organ for biopsies. However, recent studies have indicated that pancreatic cancer is a multi-stage process resulting from the accumulation of genetic changes in the somatic DNA of normal cells. These molecular alterations, including overexpression of receptor-ligand systems, oncogene activation and loss of tumour suppressor genes, leads to a profound disturbance in cell cycle regulation and continuous growth. The molecular findings are now integrated in a pancreatic tumour progression model, with genetically and morphological defined precursor lesions. However, it remains unclear whether the initial target cells of this cancer develop from ductal or acinar cells. This review will present recent emerging questions on the biology of pancreatic cancer with particular emphasis on the cell origin and tumour microenvironment.
Similar articles
-
The molecular genetics of pancreatic ductal carcinoma.Minerva Chir. 2002 Oct;57(5):561-74. Minerva Chir. 2002. PMID: 12370658 Review.
-
[Precursors to pancreatic cancer].Tidsskr Nor Laegeforen. 2006 Mar 23;126(7):905-8. Tidsskr Nor Laegeforen. 2006. PMID: 16554881 Review. Norwegian.
-
Molecular pathogenesis of precursor lesions of pancreatic ductal adenocarcinoma.Pathology. 2003 Feb;35(1):14-24. Pathology. 2003. PMID: 12701679 Review.
-
Ductal neoplasia of the pancreas: nosologic, clinicopathologic, and biologic aspects.Semin Radiat Oncol. 2005 Oct;15(4):254-64. doi: 10.1016/j.semradonc.2005.04.001. Semin Radiat Oncol. 2005. PMID: 16183479 Review.
-
Tumor growth suppression in pancreatic cancer by a putative metastasis suppressor gene Cap43/NDRG1/Drg-1 through modulation of angiogenesis.Cancer Res. 2006 Jun 15;66(12):6233-42. doi: 10.1158/0008-5472.CAN-06-0183. Cancer Res. 2006. PMID: 16778198
Publication types
MeSH terms
Substances
LinkOut - more resources
Medical