Table of Contents
Conference Papers in Medicine
Volume 2013, Article ID 528909, 5 pages
http://dx.doi.org/10.1155/2013/528909
Conference Paper

Hypoxia Immunity, Metabolism, and Hyperthermia

1Centro Medico Demetra, Center for Clinical Hyperthermia and Immunity, Via Staderini, 19/B, 05100 Terni, Italy
2Blokhin Cancer Research Center, Russian Academy of Medical Sciences, Moscow 115478, Russia
3Laboratoire d’Informatique, Ecole Polytechnique, 91128 Palaiseau, France
4Department of Animal Biology and CNR Institute of Molecular Genetics, Section of Histochemistry and Cytometry, University of Pavia, 27100 Pavia, Italy
5Oncology Unit, Azienda Ospedaliera Ospedale San Salvatore, 6112 Pesaro, Italy
6Integrated Health Clinic, 23242 Mavis Avenue, Fort Langley, BC, Canada V1M 2R4

Received 14 January 2013; Accepted 3 April 2013

Academic Editors: M. Jackson, D. Lee, and A. Szasz

This Conference Paper is based on a presentation given by Gianfranco Baronzio at “Conference of the International Clinical Hyperthermia Society 2012” held from 12 October 2012 to 14 October 2012 in Budapest, Hungary.

Copyright © 2013 Gianfranco Baronzio et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Hypoxia is common in solid tumors and in many other disease states such as myocardial infarction, stroke, bone fracture, and pneumonitis. Once hypoxia has developed, the undernourished and hypoxic cells trigger signals in order to obtain new blood vessels to satisfy their increasing demands and to resolve hypoxia. The principal signal activated is an ancestral oxygen sensor, the hypoxia inducible factor (HIF). After its nuclear translocation, HIF triggers a series of mediators that recruit, into the hypoxic milieu, several immature myeloid, mesenchymal, and endothelial progenitors cells. Resident and recruited cells participate in the processes of neoangiogenesis, for resolving the hypoxia, while at the same time trigger an inflammatory reaction. The inflammatory reaction has as primary end point, the repair of the damaged area, but if an insufficient production of resolvins is produced, the inflammatory reaction becomes chronic and is unable to repair the damaged tissue. In this brief overview, we will show the differences and the similar events present in cancer, myocardial infarction, and stroke. Furthermore, the metabolic alterations produced in the tumor by hypoxia/HIF axis and the consequences on hyperthermic treatment are also discussed.