ReviewCells2022
Transforming Growth Factor-Beta Signaling in Cancer-Induced Cachexia: From Molecular Pathways to the Clinics.
Review in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
19 citing papers in PubMed, 26 citations in OpenAlex.
- Otopetrin 1 protects against adipose tissue wasting during cancer cachexia progression.iScience · 2026Article
- Pro-inflammatory cytokine-driven molecular signaling in skeletal muscle during cancer cachexia.Biochemical Society transactions · 2026Review
- Sarcopenia as a Marker of Immunometabolic Vulnerability in Pancreatic Ductal Adenocarcinoma.Cancers · 2026Review
- Driving innovation in cancer symptom science through translational research: bridging science and practice.Current opinion in supportive and palliative care · 2026Review
- From Therapeutic Dilemma to Precision Modulation: Harnessing Biomaterials to Target the Dual Face of TGF-β in Osteoarthritis.Journal of inflammation research · 2026Review
- Identification of Anticancer Target Combinations to Treat Pancreatic Cancer and Its Associated Cachexia Using Constraint-Based Modeling.Molecules (Basel, Switzerland) · 2025Article
- Article
- Cancer-Associated Fibroblast-Derived GDF15 Induces Oxidative Stress and Neutrophil Infiltration in Head and Neck Squamous Cell Carcinoma through the PI3K/AKT/STAT3 Axis Cascade.Research (Washington, D.C.) · 2025Article
- Role of diet, physical activity and new drugs in the primary management of cancer cachexia in gastrointestinal tumors - a comprehensive review.Frontiers in oncology · 2025Review
- Extracellular vesicles in cancer cachexia: deciphering pathogenic roles and exploring therapeutic horizons.Journal of translational medicine · 2024Review
- GDF15 ameliorates sepsis-induced lung injury via AMPK-mediated inhibition of glycolysis in alveolar macrophage.Respiratory research · 2024Article
- TNF in Human Tuberculosis: A Double-Edged Sword.Immune network · 2024Review
- A Phase Ib First-In-Patient Study Assessing the Safety, Tolerability, Pharmacokinetics, and Pharmacodynamics of Ponsegromab in Participants with Cancer and Cachexia.Clinical cancer research : an official journal of the American Association for Cancer Research · 2024Article
- Methyltransferase-like 14 promotes the tumorigenesis and proliferation of pancreatic cancer cells through myc proto-oncogene signaling pathway.CytoJournal · 2024Article
- Development of a nutritional screening and assessment indicator system for patients with esophageal cancer in China: Findings from the Delphi method.Cancer medicine · 2023Article
- Role of growth differentiation factor 15 in cancer cachexia (Review).Oncology letters · 2023Review
- Role of Cytokines and Other Soluble Factors in Tumor Development: Rationale for New Therapeutic Strategies.Cells · 2023Article
- Physical Activity as the Best Supportive Care in Cancer: The Clinician's and the Researcher's Perspectives.Cancers · 2022Review
- Safety and Efficacy of Treatment with/without Ramucirumab in Advanced or Metastatic Cancer: A Meta-Analysis of 11 Global, Double-Blind, Phase 3 Randomized Controlled Trials.Journal of oncology · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cachexia is a metabolic syndrome consisting of massive loss of muscle mass and function that has a severe impact on the quality of life and survival of cancer patients. Up to 20% of lung cancer patients and up to 80% of pancreatic cancer patients are diagnosed with cachexia, leading to death in 20% of them. The main drivers of cachexia are cytokines such as interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), macrophage inhibitory cytokine 1 (MIC-1/GDF15) and transforming growth factor-beta (TGF-β). Besides its double-edged role as a tumor suppressor and activator, TGF-β causes muscle loss through myostatin-based signaling, involved in the reduction in protein synthesis and enhanced protein degradation. Additionally, TGF-β induces inhibin and activin, causing weight loss and muscle depletion, while MIC-1/GDF15, a member of the TGF-β superfamily, leads to anorexia and so, indirectly, to muscle wasting, acting on the hypothalamus center. Against this background, the blockade of TGF-β is tested as a potential mechanism to revert cachexia, and antibodies against TGF-β reduced weight and muscle loss in murine models of pancreatic cancer. This article reviews the role of the TGF-β pathway and to a minor extent of other molecules including microRNA in cancer onset and progression with a special focus on their involvement in cachexia, to enlighten whether TGF-β and such other players could be potential targets for therapy.
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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 Socratic graph.