ReviewSeminars in cell & developmental biology2016
STAT3 in the systemic inflammation of cancer cachexia.
Review in Seminars in cell & developmental biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 144 papers, 3 of them syntheses that pooled it.
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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
144 citing papers in PubMed, 3 syntheses or guidelines pooled it, 220 citations in OpenAlex.
- Pooled it
- Cancer- and cardiac-induced cachexia: same fate through different inflammatory mediators?Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022Pooled it
- The Pathway to Cancer Cachexia: MicroRNA-Regulated Networks in Muscle Wasting Based on Integrative Meta-Analysis.International journal of molecular sciences · 2019Pooled it
- Geriatric Nutritional Risk Index as a prognostic marker in patients with extensive-stage disease small cell lung cancer: Results from a randomized controlled trial.Thoracic cancer · 2020Trial
- An iron-regulated methionine redox axis governs adipose browning and cancer cachexia.Nature cancer · 2026Article
- Ribosome dynamics during skeletal muscle repair and regeneration in mice and humans.American journal of physiology. Cell physiology · 2026Article
- Phloretin Attenuates Cancer Cachexia-Induced Skeletal Muscle Wasting Associated with the Modulation of STAT3 Signaling.Biomedicines · 2026Article
- Biosacetalin (1,1-Diethoxyethane) Prolongs Survival and Alleviates Cachexia in the NSG Mice Bearing Neuroblastoma SH-SY5Y Cells.Antioxidants (Basel, Switzerland) · 2026Article
- NF-κB Signaling as a Central Driver of Cancer Cachexia.Cancers · 2026Review
- Review
- Cancer cachexia: molecular basis and therapeutic advances.Signal transduction and targeted therapy · 2026Review
- MOTS-c partially protects against skeletal muscle deterioration in C26 cachexia.Frontiers in medicine · 2026Article
- Sex impacts inflammatory signaling, body composition, and physical function in tumor-bearing mice receiving chemotherapy.American journal of physiology. Cell physiology · 2026Article
- Cachexia-induced reprogramming of visceral organ metabolism by human pancreatic cancer xenografts.International journal of cancer · 2025Article
- Cold, Hot, and Lethal-The Tumour Microenvironment and the Immunology of Head and Neck Squamous Cell Carcinoma.International journal of molecular sciences · 2025Review
- B0092 tumor-bearing mice are a new model for the study of cachexia in head and neck cancer.American journal of physiology. Cell physiology · 2025Article
- Tomatidine Attenuates Inflammatory Responses to Exercise-Like Stimulation in Donor-derived Skeletal Muscle Myobundles.Medical research archives · 2025Article
- Article
- mtSTAT3 suppresses rheumatoid arthritis by regulating Th17 and synovial fibroblast inflammatory cell death with IL-17-mediated autophagy dysfunction.Experimental & molecular medicine · 2025Article
- Cardioprotection of voluntary exercise against breast cancer-induced cardiac injury via STAT3.Basic research in cardiology · 2025Article
84 more citing papers are in PubMed but not listed here.
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
Weight loss is diagnostic of cachexia, a debilitating syndrome contributing mightily to morbidity and mortality in cancer. Most research has probed mechanisms leading to muscle atrophy and adipose wasting in cachexia; however cachexia is a truly systemic phenomenon. Presence of the tumor elicits an inflammatory response and profound metabolic derangements involving not only muscle and fat, but also the hypothalamus, liver, heart, blood, spleen and likely other organs. This global response is orchestrated in part through circulating cytokines that rise in conditions of cachexia. Exogenous Interleukin-6 (IL6) and related cytokines can induce most cachexia symptomatology, including muscle and fat wasting, the acute phase response and anemia, while IL-6 inhibition reduces muscle loss in cancer. Although mechanistic studies are ongoing, certain of these cachexia phenotypes have been causally linked to the cytokine-activated transcription factor, STAT3, including skeletal muscle wasting, cardiac dysfunction and hypothalamic inflammation. Correlative studies implicate STAT3 in fat wasting and the acute phase response in cancer cachexia. Parallel data in non-cancer models and disease states suggest both pathological and protective functions for STAT3 in other organs during cachexia. STAT3 also contributes to cancer cachexia through enhancing tumorigenesis, metastasis and immune suppression, particularly in tumors associated with high prevalence of cachexia. This review examines the evidence linking STAT3 to multi-organ manifestations of cachexia and the potential and perils for targeting STAT3 to reduce cachexia and prolong survival in cancer patients.
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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.