title: Targeting signal transduction in pancreatic cancer treatment.
abstract: Pancreatic cancer is a lethal disease with a 5-year survival rate of 4%. The only opportunity for improved survival continues to be complete surgical resection for those with localized disease. Although chemotherapeutic options are limited for the few patients with resectable disease, this problem is even more magnified in the majority (85%) of patients with unresectable or metastastic disease. Therefore, there is an urgent need for improved therapeutic options. The recent success of inhibitors of signal transduction for the treatment of other cancers supports the need to identify and validate aberrant signaling pathways important for pancreatic tumor growth. This review focuses on the validation of specific signaling networks and the present status of inhibitors of these pathways as therapeutic approaches for pancreatic cancer treatment.
authors.affiliation: University of North Carolina at Chapel Hill, Lineberger Comprehensive Cancer Center, Division of Surgical Oncology, Chapel Hill, NC 27599, USA. jjyeh@med.unc.edu
authors.forename: Jen Jen
authors.initials: JJ
authors.lastname: Yeh
authors.forename: Channing J
authors.initials: CJ
authors.lastname: Der
mesh_terms: D000911:Antibodies, Monoclonal / Q000494:pharmacology / Q000627:therapeutic use; D000970:Antineoplastic Agents / Q000494:pharmacology / Q000627:therapeutic use; D021441:Carcinoma, Pancreatic Ductal / Q000188:drug therapy* / Q000235:genetics / Q000401:mortality / Q000628:therapy; D018450:Disease Progression; D016503:Drug Delivery Systems; D015195:Drug Design; D066246:ErbB Receptors / Q000502:physiology; D005544:Forecasting; D011905:Genes, ras; D053823:Hedgehog Proteins / Q000037:antagonists & inhibitors / Q000502:physiology; D006801:Humans; D007167:Immunotherapy; D020935:MAP Kinase Signaling System / Q000187:drug effects; D016328:NF-kappa B / Q000037:antagonists & inhibitors / Q000378:metabolism; D009363:Neoplasm Proteins / Q000037:antagonists & inhibitors* / Q000502:physiology; D015689:Oncogene Protein p21(ras) / Q000037:antagonists & inhibitors; D010190:Pancreatic Neoplasms / Q000188:drug therapy* / Q000235:genetics / Q000401:mortality / Q000628:therapy; D047428:Protein Kinase Inhibitors / Q000494:pharmacology / Q000627:therapeutic use; D051567:Proto-Oncogene Proteins c-vav / Q000037:antagonists & inhibitors / Q000502:physiology; D016283:Proto-Oncogene Proteins p21(ras) / Q000502:physiology; D051880:Receptors, Notch / Q000037:antagonists & inhibitors / Q000502:physiology; D015398:Signal Transduction / Q000187:drug effects* / Q000502:physiology; D051901:Smad4 Protein / Q000502:physiology; D016212:Transforming Growth Factor beta / Q000037:antagonists & inhibitors / Q000502:physiology
chemical_list: D000911:Antibodies, Monoclonal; D000970:Antineoplastic Agents; D053823:Hedgehog Proteins; D016328:NF-kappa B; D009363:Neoplasm Proteins; D047428:Protein Kinase Inhibitors; D051567:Proto-Oncogene Proteins c-vav; D051880:Receptors, Notch; D051901:Smad4 Protein; D016212:Transforming Growth Factor beta; C496618:VAV1 protein, human; D066246:ErbB Receptors; D015689:Oncogene Protein p21(ras); D016283:Proto-Oncogene Proteins p21(ras)