ArticleCancer letters2020
Macrophages potentiate STAT3 signaling in skeletal muscles and regulate pancreatic cancer cachexia.
Article in Cancer letters, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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Who cites it
59 citing papers in PubMed, 1 synthesis or guideline pooled it, 71 citations in OpenAlex.
- Prognostic value of Prognostic Nutritional Index in cancer: an umbrella review of systematic review and meta-analysis.Frontiers in nutrition · 2025Pooled it
- Review
- Understanding cachexia and muscle dysfunction in the context of metastatic breast cancer.Cancer metastasis reviews · 2026Review
- C26 and CT26 colorectal cancer models exhibit divergent cachexia phenotypes, intramuscular inflammation, and protein turnover signaling.bioRxiv : the preprint server for biology · 2026Article
- A STING signaling relay from tumor cells to macrophages mediates the improved efficacy of combination chemotherapy in pancreatic cancer.Journal of biomedical science · 2026Article
- The effects of tissue inflammation on cancer cachexia.Biochimica et biophysica acta. Molecular basis of disease · 2026Review
- Patient-derived organoid xenografts model esophageal cancer cachexia and enable assessment of anti-inflammatory drug repositioning.iScience · 2026Article
- Cancer cachexia: molecular basis and therapeutic advances.Signal transduction and targeted therapy · 2026Review
- The Muscle-Liver Immunometabolic Axis in Liver Transplantation: A Decisive Role in Outcomes and Mechanisms.International journal of biological sciences · 2026Review
- Macrophage-Myocyte Cross Talk Induces M1 Polarization and Inflammatory Cytokine Production During Cancer Cachexia.Mediators of inflammation · 2026Article
- Cathepsin L as a dual-target to mitigate muscle wasting while enhancing anti-tumor efficacy of anti-PD-L1.Nature communications · 2025Article
- Profibrotic immune cells and fibro-adipogenic progenitors contribute to skeletal muscle extracellular matrix remodeling and fibrosis in cancer cachexia.American journal of physiology. Cell physiology · 2025Article
- Article
- Cancer-induced FOXP1 disrupts and reprograms skeletal-muscle circadian transcription in cachexia.Cell reports · 2025Article
- Identification of a senescence-associated transcriptional program in skeletal muscle of cachectic pancreatic-tumor-bearing mice.American journal of physiology. Cell physiology · 2025Article
- Deciphering molecular crosstalk mechanisms between skeletal muscle atrophy and KRAS-mutant pancreatic cancer: a literature review.Hepatobiliary surgery and nutrition · 2025Review
- Local Inflammation Precedes Diaphragm Wasting and Fibrotic Remodelling in a Mouse Model of Pancreatic Cancer.Journal of cachexia, sarcopenia and muscle · 2025Article
- Unraveling the role of STAT3 in Cancer Cachexia: pathogenic mechanisms and therapeutic opportunities.Frontiers in endocrinology · 2025Review
- Inflammation o'clock: interactions of circadian rhythms with inflammation-induced skeletal muscle atrophy.The Journal of physiology · 2024Review
- Cancer cachexia: multilevel metabolic dysfunction.Nature metabolism · 2024Review
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
Incidence of cachexia is highly prevalent in pancreatic ductal adenocarcinoma (PDAC); advanced disease stage directly correlates with decreased muscle and fat mass in PDAC patients. The pancreatic tumor microenvironment is central to the release of systemic factors that govern lipolysis, proteolysis, and muscle and fat degeneration leading to the cachectic phenotype in cancer patients. The current study explores the role of macrophages, a key immunosuppressive player in the pancreatic tumor microenvironment, in regulating cancer cachexia. We observed a negative correlation between CD163-positive macrophage infiltration and muscle-fiber cross sectional area in human PDAC patients. To investigate the role of macrophages in myodegeneration, we utilized conditioned media transplant assays and orthotopic models of PDAC-induced cachexia in immune-competent mice with and without macrophage depletion. We observed that macrophage-derived conditioned medium, in combination with tumor cell-conditioned medium, promoted muscle atrophy through STAT3 signaling. Furthermore, macrophage depletion attenuated systemic inflammation and muscle wasting in pancreatic tumor-bearing mice. Targeting macrophage-mediated STAT3 activation or macrophage-derived interleukin-1 alpha or interleukin-6 diminished myofiber atrophy. Taken together, the current study identified the critical association between macrophages and cachexia phenotype in pancreatic cancer.
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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.