title: Pancreatic Cancer Metabolism: Breaking It Down to Build It Back Up.
abstract: How do cancer cells escape tightly controlled regulatory circuits that link their proliferation to extracellular nutrient cues? An emerging theme in cancer biology is the hijacking of normal stress response mechanisms to enable growth even when nutrients are limiting. Pancreatic ductal adenocarcinoma (PDA) is the quintessential aggressive malignancy that thrives in nutrient-poor, hypoxic environments. PDAs overcome these limitations through appropriation of unorthodox strategies for fuel source acquisition and utilization. In addition, the interplay between evolving PDA and whole-body metabolism contributes to disease pathogenesis. Deciphering how these pathways function and integrate with one another can reveal novel angles of therapeutic attack.
  
  
  CONCLUSIONS
  Alterations in tumor cell and systemic metabolism are central to the biology of pancreatic cancer. Further investigation of these processes will provide important insights into how these tumors develop and grow, and suggest new approaches for its detection, prevention, and treatment.
authors.affiliation: Center for Cancer Research, Massachusetts General Hospital, Boston, Massachusetts. Center for Regenerative Medicine, Massachusetts General Hospital, Boston, Massachusetts. Department of Medicine, Harvard Medical School, Boston, Massachusetts. Bardeesy.Nabeel@mgh.harvard.edu rushika.perera@ucsf.edu.
authors.forename: Rushika M
authors.initials: RM
authors.lastname: Perera
authors.affiliation: Center for Cancer Research, Massachusetts General Hospital, Boston, Massachusetts. Center for Regenerative Medicine, Massachusetts General Hospital, Boston, Massachusetts. Department of Medicine, Harvard Medical School, Boston, Massachusetts. Bardeesy.Nabeel@mgh.harvard.edu rushika.perera@ucsf.edu.
authors.forename: Nabeel
authors.initials: N
authors.lastname: Bardeesy
mesh_terms: D000818:Animals; D001343:Autophagy; D021441:Carcinoma, Pancreatic Ductal / Q000188:drug therapy / Q000209:etiology / Q000378:metabolism / Q000473:pathology; D002471:Cell Transformation, Neoplastic; D004734:Energy Metabolism / Q000187:drug effects; D005947:Glucose / Q000378:metabolism; D018698:Glutamic Acid / Q000378:metabolism; D006801:Humans; D050356:Lipid Metabolism; D008247:Lysosomes / Q000378:metabolism; D058990:Molecular Targeted Therapy; D010084:Oxidation-Reduction; D010190:Pancreatic Neoplasms / Q000188:drug therapy / Q000209:etiology / Q000378:metabolism* / Q000473:pathology
chemical_list: D018698:Glutamic Acid; D005947:Glucose