© 2001 by Oxford University Press
Journal of the National Cancer Institute, Vol. 93, No. 4, 266-276,
February 21, 2001
© 2001 Oxford University Press
REVIEW |
Tumor Hypoxia: Definitions and Current Clinical, Biologic, and Molecular Aspects
Affiliations of authors: M. Höckel, Department of Obstetrics and Gynecology, University of Leipzig, Germany; P. Vaupel, Institute of Physiology and Pathophysiology, University of Mainz, Germany.
Correspondence to: Professor Dr. Peter Vaupel, Institute of Physiology and Pathophysiology, University of Mainz, Duesbergweg 6, 55099 Mainz, Germany (e-mail: VAUPEL{at}mail.uni-mainz.de).
Tissue hypoxia results from an inadequate supply of oxygen (O2) that compromises biologic functions. Evidence from experimental and clinical studies increasingly points to a fundamental role for hypoxia in solid tumors. Hypoxia in tumors is primarily a pathophysiologic consequence of structurally and functionally disturbed microcirculation and the deterioration of diffusion conditions. Tumor hypoxia appears to be strongly associated with tumor propagation, malignant progression, and resistance to therapy, and it has thus become a central issue in tumor physiology and cancer treatment. Biochemists and clinicians (as well as physiologists) define hypoxia differently; biochemists define it as O2-limited electron transport, and physiologists and clinicians define it as a state of reduced O2 availability or decreased O2 partial pressure that restricts or even abolishes functions of organs, tissues, or cells. Because malignant tumors no longer execute functions necessary for homeostasis (such as the production of adequate amounts of adenosine triphosphate), the physiology-based definitions of the term "hypoxia" are not necessarily valid for malignant tumors. Instead, alternative definitions based on clinical, biologic, and molecular effects that are observed at O2 partial pressures below a critical level have to be applied.
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