title: Exploiting molecular targets in pancreatic cancer.
abstract: Oncology has entered an era of molecular therapy. Given the multitude of molecular defects involved with pancreatic carcinogenesis, invasion, and metastasis, it is unlikely that single-agent targeted therapy will alter the course of this disease. Given the emergence of molecular targets and a growing number of agents available for clinical development, however, meaningful improvements in patient outcomes are expected, particularly if treatments are designed and delivered rationally.
authors.affiliation: Department of Gastrointestinal Medical Oncology, University of Texas, M. D. Anderson Cancer Center, 1515 Holcombe Boulevard, Box 426, Houston, TX 77030-4095, USA. rwolff@mdanderson.org
authors.forename: Robert A
authors.initials: RA
authors.lastname: Wolff
mesh_terms: D000230:Adenocarcinoma / Q000188:drug therapy / Q000235:genetics / Q000628:therapy*; D020533:Angiogenesis Inhibitors / Q000627:therapeutic use; D000911:Antibodies, Monoclonal / Q000627:therapeutic use; D061067:Antibodies, Monoclonal, Humanized; D017209:Apoptosis / Q000187:drug effects; D018797:Cell Cycle Proteins / Q000187:drug effects; D000068818:Cetuximab; D017326:Clinical Trials, Phase III as Topic; D004791:Enzyme Inhibitors / Q000627:therapeutic use; D066246:ErbB Receptors / Q000037:antagonists & inhibitors / Q000276:immunology; D006801:Humans; D006877:Hydroxamic Acids / Q000627:therapeutic use; D061965:Matrix Metalloproteinase Inhibitors; D009363:Neoplasm Proteins / Q000037:antagonists & inhibitors / Q000235:genetics; D010190:Pancreatic Neoplasms / Q000188:drug therapy / Q000235:genetics / Q000628:therapy*; D047428:Protein Kinase Inhibitors; D011494:Protein Kinases; D016283:Proto-Oncogene Proteins p21(ras) / Q000037:antagonists & inhibitors; D020794:Receptor Protein-Tyrosine Kinases / Q000037:antagonists & inhibitors; D018719:Erb-b2 Receptor Tyrosine Kinases / Q000037:antagonists & inhibitors / Q000276:immunology; D012107:Research Design; D015398:Signal Transduction / Q000187:drug effects; D058570:TOR Serine-Threonine Kinases; D000068878:Trastuzumab; D016159:Tumor Suppressor Protein p53 / Q000502:physiology
chemical_list: D020533:Angiogenesis Inhibitors; D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D018797:Cell Cycle Proteins; D000068818:Cetuximab; D004791:Enzyme Inhibitors; D066246:ErbB Receptors; D006877:Hydroxamic Acids; D061965:Matrix Metalloproteinase Inhibitors; D009363:Neoplasm Proteins; D047428:Protein Kinase Inhibitors; D011494:Protein Kinases; D016283:Proto-Oncogene Proteins p21(ras); D020794:Receptor Protein-Tyrosine Kinases; D018719:Erb-b2 Receptor Tyrosine Kinases; D058570:TOR Serine-Threonine Kinases; D000068878:Trastuzumab; D016159:Tumor Suppressor Protein p53; C100342:marimastat; C546842:MTOR protein, human; C501009:HRAS protein, human