title: NUPR1 works against the metabolic stress-induced autophagy-associated cell death in pancreatic cancer cells.
abstract: The incidence of pancreatic adenocarcinoma is increasing with more than 43,000 predicted new cases in the US and 65,000 in Europe this year. Pancreatic cancer patients have a short life expectancy with less than 3-4% 5-y survival, which results in an equivalent incidence and mortality rate. One of the major challenges in pancreatic cancer is the identification of pharmacological approaches that overcome the resistance of this cancer to therapy. Intensive research in the past decades has led to the classification of pancreatic cancers and the identification of the driver key genetic events. Despite the advances in understanding the molecular mechanisms responsible for pancreatic cancer pathogenesis, this knowledge had little impact on significantly improving the treatment for this dismal disease. In particular, we know today that the lack of therapeutic response in pancreatic cancer is due to the intrinsic high resistance of these tumors to chemotherapy and radiation, rather than to the inappropriate design of these therapeutic approaches. Thus, in order to ensure a better outcome for pancreatic cancer patients, there is a strong need for research focused on the mechanism that determines this resistant phenotype and the means that might drive enhanced response to therapy.
authors.affiliation: Cancer Research Center of Marseille, INSERM U1068, Marseille, France.
authors.forename: Tewfik
authors.initials: T
authors.lastname: Hamidi
authors.forename: Carla E
authors.initials: CE
authors.lastname: Cano
authors.forename: Daniel
authors.initials: D
authors.lastname: Grasso
authors.forename: Maria Noé
authors.initials: MN
authors.lastname: Garcia
authors.forename: Maria José
authors.initials: MJ
authors.lastname: Sandi
authors.forename: Ezequiel L
authors.initials: EL
authors.lastname: Calvo
authors.forename: Jean-Charles
authors.initials: JC
authors.lastname: Dagorn
authors.forename: Gwen
authors.initials: G
authors.lastname: Lomberk
authors.forename: Sandro
authors.initials: S
authors.lastname: Goruppi
authors.forename: Raul
authors.initials: R
authors.lastname: Urrutia
authors.forename: Arkaitz
authors.initials: A
authors.lastname: Carracedo
authors.forename: Guillermo
authors.initials: G
authors.lastname: Velasco
authors.forename: Juan L
authors.initials: JL
authors.lastname: Iovanna
mesh_terms: D064127:Aurora Kinases; D001343:Autophagy / Q000187:drug effects / Q000502:physiology*; D051792:Basic Helix-Loop-Helix Proteins / Q000378:metabolism*; D021441:Carcinoma, Pancreatic Ductal / Q000378:metabolism* / Q000473:pathology* / Q000628:therapy; D016923:Cell Death; D002470:Cell Survival; D019008:Drug Resistance, Neoplasm; D006801:Humans; D008954:Models, Biological; D009363:Neoplasm Proteins / Q000378:metabolism*; D017346:Protein Serine-Threonine Kinases / Q000378:metabolism; D013312:Stress, Physiological / Q000502:physiology
chemical_list: D064127:Aurora Kinases; D051792:Basic Helix-Loop-Helix Proteins; D009363:Neoplasm Proteins; D017346:Protein Serine-Threonine Kinases; C491643:NUPR1 protein, human