Cited by 248Cancer, Hypoxia, and MetabolismAngiogenesis and VEGF in CancerErythropoietin and Anemia Treatment

Hypoxia-Inducible Factors and Cancer

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Jun, Jonathan C., Rathore, Aman, Younas, Haris, Gilkes, Daniele, Polotsky, Vsevolod Y.·2017·Current Sleep Medicine Reports

Abstract

Purpose of review Hypoxia inducible factors (HIFs) mediate the transcription of hundreds of genes that allow cells to adapt to hypoxic environments. In this review, we summarize the current state of knowledge about mechanisms of HIF activation in cancer, as well as downstream cancer-promoting consequences such as altered substrate metabolism, angiogenesis, and cell differentiation. In addition, we examine the proposed relationship between respiratory-related hypoxia, HIFs, and cancer. Recent findings HIFs are increased in many forms of cancer, and portend a poor prognosis and response to therapy. Conclusion HIFs play a critical role in various stages of carcinogenesis. HIF and its transcription targets may be useful as biomarkers of disease and therapeutic targets for cancer.

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Crossref · 10.1007/s40675-017-0062-7

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  • HIFs form the core regulatory axis governing cellular responses to hypoxic and oxidative stress, integrating redox signals with metabolic, vascular, and immune responses through genome-wide transcriptional reprogramming.

    “Hypoxia-inducible factors form the core regulatory axis governing cellular responses to hypoxic and oxidative stress, integrating redox signals with metabolic, vascular, and immune responses through genome-wide transcriptional reprogramming [[216], [217], [218], [219]].”

    From HIF inhibition: Current strategies and clinical challenges (2026) · cites this paper as [217]

    The Introduction (page unavailable) says HIF regulates hundreds of genes, and Normal Regulation says reactive oxygen species can activate HIF-1α. The Angiogenesis and Glucose metabolism sections describe vascular and metabolic effects. The paper does not establish the claimed governance of oxidative-stress responses or integration of immune responses; it discusses inflammatory cytokines chiefly as inputs that can activate HIF-1α. (LLM, conf=0.84)

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Authors
Jun, J. C., Rathore, A., Younas, H., Gilkes, D., & Polotsky, V. Y.
Affiliations
Johns Hopkins University (US)
Corresponding author
Jun, Jonathan C.
Venue
Current Sleep Medicine Reports
Published
2017-01-28
Volume
3
Issue
1
Pages
1-10
ISSN
2198-6401 (ISSN-L)
OpenAlex
W2581267196
Cited by
248
References
144
Citations by year
2026: 22 · 2025: 23 · 2024: 50 · 2023: 40 · 2022: 32 · 2021: 37 · 2020: 21 · 2019: 14 · 2018: 8 · 2017: 1
FWCI
4.04
Type
journal article
Language
en
Open access
Locations
  • Current Sleep Medicine Reports (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • Nutrition Obesity Research Center (NIH P30DK072488)
  • American Academy of Sleep Medicine Foundation (106-JF-14)
  • National Institutes of Health (R01 HL133100, P50 ES018176)
  • American Sleep Medicine Foundation (133-BS-15)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Hypoxia, and Metabolism
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Angiogenesis and VEGF in Cancer
  • Health Sciences › Medicine › Hematology › Erythropoietin and Anemia Treatment
Keywords
hypoxia-inducible factor, cancer, tumor hypoxia, HIF activation, angiogenesis, substrate metabolism, cell differentiation, carcinogenesis, prognostic factors, therapeutic target

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