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Hypoxia Induced Tumor Metabolic Switch Contributes to Pancreatic Cancer Aggressiveness

Abstract

Pancreatic ductal adenocarcinoma remains one of the most lethal of all solid tumors with an overall five-year survival rate of only 3–5%. Its aggressive biology and resistance to conventional and targeted therapeutic agents lead to a typical clinical presentation of incurable disease once diagnosed. The disease is characterized by the presence of a dense stroma of fibroblasts and inflammatory cells, termed desmoplasia, which limits the oxygen diffusion in the organ, creating a strong hypoxic environment within the tumor. In this review, we argue that hypoxia is responsible for the highly aggressive and metastatic characteristics of this tumor and drives pancreatic cancer cells to oncogenic and metabolic changes facilitating their proliferation. However, the molecular changes leading to metabolic adaptations of pancreatic cancer cells remain unclear. Cachexia is a hallmark of this disease and illustrates that this cancer is a real metabolic disease. Hence, this tumor must harbor metabolic pathways which are probably tied in a complex inter-organ dialog during the development of this cancer. Such a hypothesis would better explain how under fuel source limitation, pancreatic cancer cells are maintained, show a growth advantage, and develop metastasis.
Authors:
Vasseur, Sophie; Tomasini, Richard; Tournaire, Roselyne; Iovanna, Juan L. [1] 
  1. INSERM U624, Stress Cellulaire, Parc Scientifique et Technologique de Luminy, 163 Avenue de Luminy, BP 915,13288 Marseille cedex 9 (France)
Publication Date:
Dec 16, 2010
Product Type:
Journal Article
Resource Relation:
Journal Name: Cancers (Basel); Journal Volume: 2; Journal Issue: 4; Other Information: PMCID: PMC3840441; PMID: 24281221; PUBLISHER-ID: cancers-02-02138; OAI: oai:pubmedcentral.nih.gov:3840441; Copyright (c) 2010 by the authors; licensee MDPI, Basel, Switzerland.; This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license (http://creativecommons.org/licenses/by/3.0/).; Country of input: International Atomic Energy Agency (IAEA)
Subject:
60 APPLIED LIFE SCIENCES; 62 RADIOLOGY AND NUCLEAR MEDICINE; ANOXIA; BIOLOGICAL PATHWAYS; CARCINOMAS; DRUGS; METABOLIC DISEASES; METABOLISM; PANCREAS
OSTI ID:
22432474
Country of Origin:
Switzerland
Language:
English
Other Identifying Numbers:
Journal ID: ISSN 2072-6694; TRN: CH15$0368001916
Availability:
Available from http://dx.doi.org/10.3390/cancers2042138; Available from http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3840441
Submitting Site:
CHN
Size:
page(s) 2138-2152
Announcement Date:
Feb 20, 2016

Citation Formats

Vasseur, Sophie, Tomasini, Richard, Tournaire, Roselyne, and Iovanna, Juan L. Hypoxia Induced Tumor Metabolic Switch Contributes to Pancreatic Cancer Aggressiveness. Switzerland: N. p., 2010. Web. doi:10.3390/CANCERS2042138.
Vasseur, Sophie, Tomasini, Richard, Tournaire, Roselyne, & Iovanna, Juan L. Hypoxia Induced Tumor Metabolic Switch Contributes to Pancreatic Cancer Aggressiveness. Switzerland. doi:10.3390/CANCERS2042138.
Vasseur, Sophie, Tomasini, Richard, Tournaire, Roselyne, and Iovanna, Juan L. 2010. "Hypoxia Induced Tumor Metabolic Switch Contributes to Pancreatic Cancer Aggressiveness." Switzerland. doi:10.3390/CANCERS2042138. https://www.osti.gov/servlets/purl/10.3390/CANCERS2042138.
@misc{etde_22432474,
title = {Hypoxia Induced Tumor Metabolic Switch Contributes to Pancreatic Cancer Aggressiveness}
author = {Vasseur, Sophie, Tomasini, Richard, Tournaire, Roselyne, and Iovanna, Juan L.}
abstractNote = {Pancreatic ductal adenocarcinoma remains one of the most lethal of all solid tumors with an overall five-year survival rate of only 3–5%. Its aggressive biology and resistance to conventional and targeted therapeutic agents lead to a typical clinical presentation of incurable disease once diagnosed. The disease is characterized by the presence of a dense stroma of fibroblasts and inflammatory cells, termed desmoplasia, which limits the oxygen diffusion in the organ, creating a strong hypoxic environment within the tumor. In this review, we argue that hypoxia is responsible for the highly aggressive and metastatic characteristics of this tumor and drives pancreatic cancer cells to oncogenic and metabolic changes facilitating their proliferation. However, the molecular changes leading to metabolic adaptations of pancreatic cancer cells remain unclear. Cachexia is a hallmark of this disease and illustrates that this cancer is a real metabolic disease. Hence, this tumor must harbor metabolic pathways which are probably tied in a complex inter-organ dialog during the development of this cancer. Such a hypothesis would better explain how under fuel source limitation, pancreatic cancer cells are maintained, show a growth advantage, and develop metastasis.}
doi = {10.3390/CANCERS2042138}
journal = {Cancers (Basel)}
issue = {4}
volume = {2}
journal type = {AC}
place = {Switzerland}
year = {2010}
month = {Dec}
}