ArticleJCSM rapid communications
JAK Inhibitors Suppress Cancer Cachexia-Associated Anorexia and Adipose Wasting in Mice.
Article in JCSM rapid communications. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 43 citations in OpenAlex.
- Review
- Scutellarein attenuates cancer cachexia-induced muscle atrophy via targeted inhibition of the JAK/STAT pathway.Journal of advanced research · 2026Article
- Undetected Weight Loss Associates With Upstaging in Cancer Patients.Journal of cachexia, sarcopenia and muscle · 2026Article
- Fos-induced osteosarcoma growth causes a cachexia-like phenotype in mice and correlates with high Fgf21 serum levels.Cancer & metabolism · 2026Article
- Extracellular vesicles in cancer-associated cachexia: molecular mechanisms and therapeutic perspectives.Frontiers in cell and developmental biology · 2026Review
- JAK1/2 Inhibition Delays Cachexia and Improves Survival through Increased Food Intake.bioRxiv : the preprint server for biology · 2025Article
- Cancer-Associated Cachexia: Bridging Clinical Findings with Mechanistic Insights in Human Studies.Cancer discovery · 2025Review
- Comparative Efficacy and Safety of Baricitinib Against Traditional Therapies in Severe Alopecia Areata: A Retrospective Cohort Study.Journal of cosmetic dermatology · 2025Article
- Mechanisms and pharmacotherapy of cancer cachexia-associated anorexia.Pharmacology research & perspectives · 2025Review
- Pan-cancer secreted proteome and skeletal muscle regulation: insight from a proteogenomic data-driven knowledge base.Functional & integrative genomics · 2025Review
- Identification of Genes in Diagnosing Major Depressive Disorder with Anorexia Through Bioinformatics Analysis.Neuropsychiatric disease and treatment · 2025Article
- Unraveling the role of STAT3 in Cancer Cachexia: pathogenic mechanisms and therapeutic opportunities.Frontiers in endocrinology · 2025Review
- Article
- Immune System Disorder and Cancer-Associated Cachexia.Cancers · 2024Review
- R-ketorolac ameliorates cancer-associated cachexia and prolongs survival of tumour-bearing mice.Journal of cachexia, sarcopenia and muscle · 2024Article
- Leukemia inhibitory factor suppresses hepatic de novo lipogenesis and induces cachexia in mice.Nature communications · 2024Article
- STAT3 Signalling Drives LDH Up-Regulation and Adiponectin Down-Regulation in Cachectic Adipocytes.International journal of molecular sciences · 2023Article
- Melanoma cells induce dedifferentiation and metabolic changes in adipocytes present in the tumor niche.Cellular & molecular biology letters · 2023Article
- Tumor loss-of-function mutations in STK11/LKB1 induce cachexia.JCI insight · 2023Article
- New insights into the role of adipocytes in pancreatic cancer progression: paving the way towards novel therapeutic targets.Theranostics · 2023Review
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
backgroundCachexia, a syndrome of muscle atrophy, adipose loss, and anorexia, is associated with reduced survival in cancer patients. The colon adenocarcinoma C26c20 cell line secretes the cytokine leukemia inhibitory factor (LIF) which induces cachexia. We characterized how LIF promotes cachexia-associated weight loss and anorexia in mice through JAK-dependent changes in adipose and hypothalamic tissues.
methodsCachexia was induced
resultsTumor-secreted LIF induced changes in adipose tissue expression and serum levels of IL-6 and leptin in a JAK-dependent manner influencing cachexia-associated adipose wasting and anorexia. We identified two JAK inhibitors that block IL-6 family-mediated adipocyte lipolysis and IL-6 induction using an
conclusionsJAK inhibitors suppress LIF-associated adipose loss and anorexia in both
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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.