Molecular pathology of pancreatic cancer: implications for molecular targeting therapy

Toru Furukawa

doi:10.1016/j.cgh.2009.07.035

Molecular pathology of pancreatic cancer: implications for molecular targeting therapy

Clin Gastroenterol Hepatol. 2009 Nov;7(11 Suppl):S35-9. doi: 10.1016/j.cgh.2009.07.035.

Author

Toru Furukawa¹

Affiliation

¹ International Research and Educational Institute for Integrated Medical Sciences, Tokyo Women's Medical University, Shinjuku, Tokyo, Japan. furukawa@imcir.twmu.ac.jp

PMID: 19896096
DOI: 10.1016/j.cgh.2009.07.035

Abstract

Pancreatic cancer develops through ductal dysplastic lesions or pancreatic intraepithelial neoplasia (PanIN). The origin of pancreatic cancer remains controversial. Some of the molecular origins of pancreatic cancer have been described. For example, KRAS, SHH, CDKN2A, TP53, SMAD4, and DUSP6 are crucial molecules in the development and progression of pancreatic cancer. Understanding the mechanisms of carcinogenesis could help researchers find the Achilles' heel of pancreatic cancer. Molecular targeting is a promising strategy for curing this devastating disease.

Publication types

Research Support, Non-U.S. Gov't
Review

MeSH terms

Gene Targeting*
Genetic Therapy*
Humans
Models, Biological
Pancreatic Neoplasms / etiology*
Pancreatic Neoplasms / genetics
Pancreatic Neoplasms / pathology*
Pathology, Molecular*