ArticlePPAR research2008
Macrophages, PPARs, and Cancer.
Article in PPAR research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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
22 citing papers in PubMed, 53 citations in OpenAlex.
- Ferroptosis in idiopathic pulmonary fibrosis: mechanisms, impact, and therapeutic opportunities.Frontiers in immunology · 2025Review
- Review
- The Role of PPAR Alpha in the Modulation of Innate Immunity.International journal of molecular sciences · 2021Review
- Head and neck squamous cell carcinoma cell lines have an immunomodulatory effect on macrophages independent of hypoxia and toll-like receptor 9.BMC cancer · 2021Article
- Mannose-decorated hybrid nanoparticles for enhanced macrophage targeting.Biochemistry and biophysics reports · 2019Article
- Tumour-Associated Macrophages (TAMs) in Colon Cancer and How to Reeducate Them.Journal of immunology research · 2019Review
- Immune cell subset differentiation and tissue inflammation.Journal of hematology & oncology · 2018Review
- Dynamic Macrophages: Understanding Mechanisms of Activation as Guide to Therapy for Atherosclerotic Vascular Disease.Frontiers in cardiovascular medicine · 2018Review
- Fucosterol Protects against Concanavalin A-Induced Acute Liver Injury: Focus on P38 MAPK/NF-Gastroenterology research and practice · 2018Article
- PPAR Agonists for the Prevention and Treatment of Lung Cancer.PPAR research · 2017Review
- The PPAR-γ antagonist GW9662 elicits differentiation of M2c-like cells and upregulation of the MerTK/Gas6 axis: a key role for PPAR-γ in human macrophage polarization.Journal of inflammation (London, England) · 2015Article
- Functional Relationship between Tumor-Associated Macrophages and Macrophage Colony-Stimulating Factor as Contributors to Cancer Progression.Frontiers in immunology · 2014Review
- Mechanisms driving macrophage diversity and specialization in distinct tumor microenvironments and parallelisms with other tissues.Frontiers in immunology · 2014Review
- Inverse PPARβ/δ agonists suppress oncogenic signaling to the ANGPTL4 gene and inhibit cancer cell invasion.Oncogene · 2013Article
- Targeting tumor-infiltrating macrophages to combat cancer.Immunotherapy · 2013Review
- Review
- Monocytes link atherosclerosis and cancer.European journal of immunology · 2011Review
- Origins of injection-site sarcomas in cats: the possible role of chronic inflammation-a review.ISRN veterinary science · 2011Article
- Sex dimorphic actions of rosiglitazone in generalised peroxisome proliferator-activated receptor-gamma (PPAR-gamma)-deficient mice.Diabetologia · 2010Article
- The tumor microenvironment in colorectal carcinogenesis.Cancer microenvironment : official journal of the International Cancer Microenvironment Society · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mononuclear phagocytes often function as control switches of the immune system, securing the balance between pro- and anti-inflammatory reactions. For this purpose and depending on the activating stimuli, these cells can develop into different subsets: proinflammatory classically activated (M1) or anti-inflammatory alternatively activated (M2) macrophages. The expression of the nuclear peroxisome proliferator-activated receptors (PPARs) is regulated by M1- or M2-inducing stimuli, and these receptors are generally considered to counteract inflammatory M1 macrophages, while actively promoting M2 activation. This is of importance in a tumor context, where M1 are important initiators of inflammation-driven cancers. As a consequence, PPAR agonists are potentially usefull for inhibiting the early phases of tumorigenesis through their antagonistic effect on M1. In more established tumors, the macrophage phenotype is more diverse, making it more difficult to predict the outcome of PPAR agonism. Overall, in our view current knowledge provides a sound basis for the clinical evaluation of PPAR ligands as chemopreventive agents in chronic inflammation-associated cancer development, while cautioning against the unthoughtful application of these agents as cancer therapeutics.
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.