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NUPR1 works against the metabolic stress-induced autophagy-associated cell death in pancreatic cancer cells. Autophagy 2013 Jan;9(1):95-7 PMID: 23047430 PMCID: PMC3542222

Pubmed ID

23047430

DOI

10.4161/auto.22258

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.

Author List

Hamidi T, Cano CE, Grasso D, Garcia MN, Sandi MJ, Calvo EL, Dagorn JC, Lomberk G, Goruppi S, Urrutia R, Carracedo A, Velasco G, Iovanna JL

Authors

Gwen Lomberk PhD Associate Professor in the Surgery department at Medical College of Wisconsin
Raul A. Urrutia MD Center Director, Professor in the Surgery department at Medical College of Wisconsin




MESH terms used to index this publication - Major topics in bold

Aurora Kinases
Autophagy
Basic Helix-Loop-Helix Transcription Factors
Carcinoma, Pancreatic Ductal
Cell Death
Cell Survival
Drug Resistance, Neoplasm
Humans
Models, Biological
Neoplasm Proteins
Protein-Serine-Threonine Kinases
Stress, Physiological
jenkins-FCD Prod-353 9ccd8489072cb19f5b9f808bb23ed672c582f41e