TY - JOUR
T1 - Molecular Pathology of Pancreatic Cancer
T2 - Implications for Molecular Targeting Therapy
AU - Furukawa, Toru
N1 - Funding Information:
Funding The author was supported by the Program for Promoting the Establishment of Strategic Research Centers, Special Coordination Funds for Promoting Science and Technology, Ministry of Education, Culture, Sports, Science and Technology (Japan).
PY - 2009/11
Y1 - 2009/11
N2 - 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.
AB - 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.
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U2 - 10.1016/j.cgh.2009.07.035
DO - 10.1016/j.cgh.2009.07.035
M3 - Article
C2 - 19896096
AN - SCOPUS:71849092585
SN - 1542-3565
VL - 7
SP - S35-S39
JO - Clinical Gastroenterology and Hepatology
JF - Clinical Gastroenterology and Hepatology
IS - 11 SUPPL.
ER -