Evidence map›Paper›PMID 35659268›Full record

ReviewJournal of hematology & oncology2022

Hypoxia-inducible factors: master regulators of hypoxic tumor immune escape.

Qinghua Wu, Li You, Eugenie Nepovimova, Zbynek Heger, Wenda Wu, Kamil Kuca, Vojtech Adam

Registry-linked trialOpen access · goldAbstract readReview
In one paragraph

Review in Journal of hematology & oncology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06309459 (Carbonic Anhydrase IX Enzyme in Triple Negative Breast Carcinoma), which is not on this map. Cited by 277 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
277citing papers in PubMed, 3 pooled it
35.6field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

NCT06309459 completednot on this map

Carbonic Anhydrase IX Enzyme in Triple Negative Breast Carcinoma: Relationship With Prognostic Factors and Response to Neoadjuvant Chemotherapy

TypeobservationalSponsorKahramanmaras Sutcu Imam UniversityRan2018 to 2023Enrolled40ConditionsTriple Negative Breast Cancer, Carbonic Anhydrase IXArmsCarbonic anhydrase staining levels
3 · Its place in the literature

Who cites it

277 citing papers in PubMed, 3 syntheses or guidelines pooled it, 408 citations in OpenAlex.

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217 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 4 institutions in 2 countries.

Qinghua Wu *College of Life Science, Yangtze University, Jingzhou, 434025, China.
Li You *College of Life Science, Yangtze University, Jingzhou, 434025, China.
Eugenie NepovimovaDepartment of Chemistry, Faculty of Science, University of Hradec Kralove, 50003, Hradec Kralove, Czech Republic.
Zbynek HegerDepartment of Chemistry and Biochemistry, Mendel University in Brno, Brno, 613 00, Czech Republic.
Wenda WuMOE Joint International Research Laboratory of Animal Health and Food Safety, College of Veterinary Medicine, Nanjing Agricultural University, Nanjing, 210095, China. wuwenda@njau.edu.cn.
Kamil KucaDepartment of Chemistry, Faculty of Science, University of Hradec Kralove, 50003, Hradec Kralove, Czech Republic. kamil.kuca@uhk.cz.
Vojtech AdamDepartment of Chemistry and Biochemistry, Mendel University in Brno, Brno, 613 00, Czech Republic. vojtech.adam@mendelu.cz.ORCID 0000-0002-8527-286X
Central European Institute of Technology · CZUniversity of Hradec Králové · CZYangtze University · CNNanjing Agricultural University · CN

Funding

H2020 European Research Council 759585Natural Science Foundation of Jilin Province 31972741Postdoctoral Science Foundation of Jiangsu Province 2016T90477
6 · The paper itself

Abstract

Hypoxia, a common feature of the tumor microenvironment in various types of cancers, weakens cytotoxic T cell function and causes recruitment of regulatory T cells, thereby reducing tumoral immunogenicity. Studies have demonstrated that hypoxia and hypoxia-inducible factors (HIFs) 1 and 2 alpha (HIF1A and HIF2A) are involved in tumor immune escape. Under hypoxia, activation of HIF1A induces a series of signaling events, including through programmed death receptor-1/programmed death ligand-1. Moreover, hypoxia triggers shedding of complex class I chain-associated molecules through nitric oxide signaling impairment to disrupt immune surveillance by natural killer cells. The HIF-1-galactose-3-O-sulfotransferase 1-sulfatide axis enhances tumor immune escape via increased tumor cell-platelet binding. HIF2A upregulates stem cell factor expression to recruit tumor-infiltrating mast cells and increase levels of cytokines interleukin-10 and transforming growth factor-β, resulting in an immunosuppressive tumor microenvironment. Additionally, HIF1A upregulates expression of tumor-associated long noncoding RNAs and suppresses immune cell function, enabling tumor immune escape. Overall, elucidating the underlying mechanisms by which HIFs promote evasion of tumor immune surveillance will allow for targeting HIF in tumor treatment. This review discusses the current knowledge of how hypoxia and HIFs facilitate tumor immune escape, with evidence to date implicating HIF1A as a molecular target in such immune escape. This review provides further insight into the mechanism of tumor immune escape, and strategies for tumor immunotherapy are suggested.

Indexed as

NeoplasmsTumor EscapeHumansHypoxiaHypoxia-Inducible Factor 1, alpha SubunitImmunologic SurveillanceTumor MicroenvironmentHypoxia-Inducible Factor 1, alpha SubunitHypoxiaHypoxia-inducible factorsImmunotherapyPersonalized medicineTumor disease

Identifiers

PMID35659268
PMCPMC9166526
OpenAlexW4281707807

What OpenQuestion holds

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Registered trials

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.