ReviewCancer letters2022
Macrophage inhibitory cytokine-1 in cancer: Beyond the cellular phenotype.
Review in Cancer letters, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed, 29 citations in OpenAlex.
- Osteocyte-Derived GDF15 Promotes Paclitaxel Resistance, Tumor Growth, and Bone Microenvironment Regulation in Prostate Cancer.Current issues in molecular biology · 2026Article
- Extracellular vesicles in prostate cancer: current understanding and future perspectives.Journal of the National Cancer Center · 2026Review
- 6-Gingerol enhances the anti-tumor activity of temozolomide by inhibiting EGR1/GDF15 signaling in glioblastoma.Scientific reports · 2025Article
- Liver X Receptor-Growth Differentiation Factor 15 Activation Drives Profibrotic Changes in the Aqueous Outflow Tract of Uveitic Glaucoma.The American journal of pathology · 2025Article
- Growth differentiation factor 15: a promising biomarker in oral cancer.Journal of the Korean Association of Oral and Maxillofacial Surgeons · 2025Article
- Hallmarks of Cancer Cachexia: Sexual Dimorphism in Related Pathways.International journal of molecular sciences · 2025Review
- The importance of growth differentiation factor 15 and interleukin 6 serum levels in inflammatory bowel diseases.Journal of physiology and biochemistry · 2025Article
- The metabolic basis of cancer-related fatigue.Neuroscience and biobehavioral reviews · 2025Review
- Relationship Between MIC-1, VEGF, and TGF-β1 and Clinicopathologic Stage and Lymph Node Metastasis in Gastric Cancer.International journal of general medicine · 2025Article
- GDF15/MIC-1: a stress-induced immunosuppressive factor which promotes the aging process.Biogerontology · 2024Review
- GDF-15 Predicts Epithelioid Hemangioendothelioma Aggressiveness and Is Downregulated by Sirolimus through ATF4/ATF5 Suppression.Clinical cancer research : an official journal of the American Association for Cancer Research · 2024Article
- GDF15 induces chemoresistance to oxaliplatin by forming a reciprocal feedback loop with Nrf2 to maintain redox homeostasis in colorectal cancer.Cellular oncology (Dordrecht, Netherlands) · 2024Article
- Tumor associated macrophages as key contributors and targets in current and future therapies for melanoma.Expert review of clinical immunology · 2024Review
- Metabolic Crosstalk between Liver and Brain: From Diseases to Mechanisms.International journal of molecular sciences · 2024Review
- Macrophages as a Source and Target of GDF-15.International journal of molecular sciences · 2024Review
- Role and Mechanism of Growth Differentiation Factor 15 in Chronic Kidney Disease.Journal of inflammation research · 2024Review
- Emerging Roles of Growth Differentiation Factor 15 in Immunoregulation and Pathogenesis.Journal of immunology (Baltimore, Md. : 1950) · 2023Review
- The Upregulation of Caffeic Acid Phenethyl Ester on Growth Differentiation Factor 15 Inhibits Transforming Growth Factor β/Smad Signaling in Bladder Carcinoma Cells.Biomedicines · 2022Article
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 2 institutions in 1 country.
Funding
Abstract
Despite technological advances in diagnostic abilities and improved treatment methods, the burden of cancers remains high, leading to significant morbidity and mortality. One primary reason is that cancer cell secretory factors modulate the tumor microenvironment, supporting tumor growth and circumvents anticancer activities of conventional therapies. Macrophage inhibitory cytokine-1 (MIC-1) is a pleiotropic cytokine elevated in various cancers. MIC-1 regulates various cancer hallmarks, including sustained proliferation, tumor-promoting inflammation, avoiding immune destruction, inducing invasion, metastasis, angiogenesis, and resisting cell death. Despite these facts, the molecular regulation and downstream signaling of MIC-1 in cancer remain elusive, partly because its receptor (GFRAL) was unknown until recently. Binding of MIC-1 to GFRAL recruits the coreceptor tyrosine kinase RET to execute its downstream signaling. So far, studies have shown that GFRAL expression is restricted to the brain stem and is responsible for MIC-1/GFRAL/RET-mediated metabolic disorders. Nevertheless, abundant levels of MIC-1 expression have been reported in all cancer types and have been proposed as a surrogate biomarker. Given the ubiquitous expression of MIC-1 in cancers, it is crucial to understand both upstream regulation and downstream MIC-1/GFRAL/RET signaling in cancer hallmark traits.
Indexed as
Identifiers
What Socratic 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 Socratic graph.