Defining normoxia, physoxia and hypoxia in tumours—implications for treatment response

McKeown, S R

doi:10.1259/bjr.20130676

Cited by 1,050Cancer, Hypoxia, and MetabolismMathematical Biology Tumor GrowthAngiogenesis and VEGF in Cancer

Defining normoxia, physoxia and hypoxia in tumours—implications for treatment response

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McKeown, S R·2014·The British Journal of Radiology

DOI 10.1259/bjr.20130676PMC PMC4064601

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Abstract

Tumour hypoxia is increasingly recognized as a major deleterious factor in cancer therapies, as it compromises treatment and drives malignant progression. This review seeks to clarify the oxygen levels that are pertinent to this issue. It is argued that normoxia (20% oxygen) is an extremely poor comparator for "physoxia", i.e. the much lower levels of oxygen universally found in normal tissues, which averages about 5% oxygen, and ranges from about 3% to 7.4%. Importantly, it should be recognized that the median oxygenation in untreated tumours is significantly much lower, falling between approximately 0.3% and 4.2% oxygen, with most tumours exhibiting median oxygen levels <2%. This is partially dependent on the tissue of origin, and it is notable that many prostate and pancreatic tumours are profoundly hypoxic. In addition, therapy can induce even further, often unrecognized, changes in tumour oxygenation that may vary longitudinally, increasing or decreasing during treatment in ways that are not always predictable. Studies that fail to take cognizance of the actual physiological levels of oxygen in tissues (approximately 5%) and tumours (approximately 1%) may fail to identify the real circumstances driving tumour response to treatment and/or malignant progression. This can be of particular importance in genetic studies in vitro when comparison to human tumours is required.

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Reduced oxygen tension activates a conserved hypoxic signaling network centered on hypoxia-inducible factors (HIFs).
“Reduced oxygen tension activates a conserved hypoxic signaling network centered on hypoxia-inducible factors (HIFs)”
From HIF inhibition: Current strategies and clinical challenges (2026) · cites this paper as [2]
The passage labeled Abstract says that falling oxygen levels stabilize HIF1α, allowing HIF1 to form and trigger many changes. It also describes HIF1 and HIF2 as predominant mediators of hypoxia-induced genetic changes and discusses other, sometimes integrated, response pathways. It does not establish that this signaling network is conserved. (LLM, conf=0.82)
Experimental — accuracy not yet measured
Both physiological and pathological states can transiently disrupt the equilibrium between oxygen supply and demand, resulting in tissue and cellular hypoxia.
“Nevertheless, both physiological and pathological states can transiently disrupt the equilibrium between oxygen supply and demand, resulting in tissue and cellular hypoxia”
From HIF inhibition: Current strategies and clinical challenges (2026) · cites this paper as [2]
The passages on physiological hypoxia (page unavailable) describe a transitory fall in tissue oxygen that homeostasis reverses. The passage on pathological hypoxia describes reduced oxygen delivery in acute or chronic ischaemia, but also says homeostasis may not be restored; it does not support characterizing pathological hypoxia generally as transient. (LLM, conf=0.82)
Experimental — accuracy not yet measured
In liver metastases of colorectal cancer, the median PO2 was 6 mmHg compared with 30 mmHg in normal liver tissue.
“In liver metastases of colorectal cancer, the median PO2 was 6 mmHg as compared with 30 mmHg in normal liver tissue (20).”
From HIF inhibitor 32-134D eradicates murine hepatocellular carcinoma in combination with anti-PD1 therapy (2022) · cites this paper as [20]
The hypoxia response features extensive transcriptional reprogramming aimed at preserving cellular integrity under low-oxygen conditions.
“This response features extensive transcriptional reprogramming aimed at preserving cellular integrity under low-oxygen conditions”
From HIF inhibition: Current strategies and clinical challenges (2026) · cites this paper as [2]

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Authors: McKeown, S. R.
Affiliations: University of Ulster (GB)
Corresponding author: McKeown, S R
Venue: The British Journal of Radiology
Publisher: Oxford University Press (OUP)
Published: 2014-03
Volume: 87
Issue: 1035
Pages: 20130676
ISSN: 0007-1285 (ISSN-L)
1748-880X
DOI: 10.1259/bjr.20130676
PMC: PMC4064601
OpenAlex: W2018722597
Cited by: 1,050
References: 126
Citations by year: 2026: 84 · 2025: 122 · 2024: 129 · 2023: 139 · 2022: 137 · 2021: 152 · 2020: 107 · 2019: 68 · 2018: 56 · 2017: 33 · 2016: 13 · 2015: 5 · 2014: 4
FWCI: 1.82
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Locations: British Journal of Radiology (publishedVersion)
Europe PMC (PubMed Central) (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Hypoxia, and Metabolism
Physical Sciences › Mathematics › Modeling and Simulation › Mathematical Biology Tumor Growth
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Angiogenesis and VEGF in Cancer
Keywords: tumor hypoxia, tumor oxygenation, normoxia, treatment response, prostate cancer, pancreatic cancer, malignant progression
MeSH terms: Animals, Hypoxia, Humans, Male, Neoplasms, Oxygen, Cell Hypoxia, Disease Progression

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Defining normoxia, physoxia and hypoxia in tumours—implications for treatment response

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