ReviewFrontiers in immunology2018
Tumor Microenvironment-Induced Immunometabolic Reprogramming of Natural Killer Cells.
Review in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
48 citing papers in PubMed, 73 citations in OpenAlex.
- Multi-omics characterization of metabolic and immune interactions in prostate cancer.Translational andrology and urology · 2025Article
- Empowering hypoxia to convert cold tumors into hot tumors for breast cancer immunotherapy.Cell death discovery · 2025Review
- The diversity of natural killer cell functional and phenotypic states in cancer.Cancer metastasis reviews · 2025Review
- Engineered iPSC-derived natural killer cells: recent innovations in translational innate anti-cancer immunotherapy.Clinical & translational immunology · 2025Review
- Article
- Car T Cells in Solid Tumors: Overcoming Obstacles.International journal of molecular sciences · 2024Review
- synNotch-programmed iPSC-derived NK cells usurp TIGIT and CD73 activities for glioblastoma therapy.Nature communications · 2024Article
- The role of metabolic reprogramming in immune escape of triple-negative breast cancer.Frontiers in immunology · 2024Review
- The innate defenders: a review of natural killer cell immunotherapies in cancer.Frontiers in immunology · 2024Review
- Engineering the glioblastoma microenvironment with bioactive nanoparticles for effective immunotherapy.RSC advances · 2023Review
- Immunometabolism: a new dimension in immunotherapy resistance.Frontiers of medicine · 2023Review
- Targeting Immunosuppressive Adenosine Signaling: A Review of Potential Immunotherapy Combination Strategies.International journal of molecular sciences · 2023Review
- Challenges of chimeric antigen receptor-T/natural killer cell therapy in the treatment of solid tumors: focus on colorectal cancer and evaluation of combination therapies.Molecular and cellular biochemistry · 2023Review
- Metabolism of NK cells during viral infections.Frontiers in immunology · 2023Review
- Enhancement of immune surveillance in breast cancer by targeting hypoxic tumor endothelium: Can it be an immunological switch point?Frontiers in oncology · 2023Review
- Gene-edited and CAR-NK cells: Opportunities and challenges with engineering of NK cells for immunotherapy.Molecular therapy oncolytics · 2022Review
- Surface Plasmon Resonance Screening to Identify Active and Selective Adenosine Receptor Binding Fragments.ACS medicinal chemistry letters · 2022Article
- In vivo multidimensional CRISPR screens identifyScience advances · 2022Article
- Natural killer cells and immune-checkpoint inhibitor therapy: Current knowledge and new challenges.Molecular therapy oncolytics · 2022Review
- The 'Danse Macabre'-Neutrophils the Interactive Partner Affecting Oral Cancer Outcomes.Frontiers in immunology · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Energy metabolism is key to the promotion of tumor growth, development, and metastasis. At the same time, cellular metabolism also mediates immune cell survival, proliferation and cytotoxic responses within the tumor microenvironment. The ability of natural killer cells to eradicate tumors relies on their ability to functionally persist for the duration of their anti-tumor effector activity. However, a tumor's altered metabolic requirements lead to compromised functional responses of cytokine-activated natural killer cells, which result in decreased effectiveness of adoptive cell-based immunotherapies. Tumors exert these immunosuppressive effects through a number of mechanisms, a key driver of which is hypoxia. Hypoxia also fuels the generation of adenosine from the cancer-associated ectoenzymes CD39 and CD73. Adenosine's immunosuppression manifests in decreased proliferation and impaired anti-tumor function, with adenosinergic signaling emerging as an immunometabolic checkpoint blockade target. Understanding such immunometabolic suppression is critical in directing the engineering of a new generation of natural killer cell-based immunotherapies that have the ability to more effectively target difficult-to-treat solid tumors.
Indexed as
Identifiers
What OpenQuestion holds
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.