ReviewThe Journal of clinical investigation2025
Cancer therapy and cachexia.
Review in The Journal of clinical investigation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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
24 citing papers in PubMed.
- Impact of oral nutritional supplements on chemotherapy tolerance and overall survival in postoperative colorectal cancer patients undergoing chemotherapy.Asia Pacific journal of clinical nutrition · 2026Trial
- Practical prescribing in cancer cachexia.Current opinion in supportive and palliative care · 2026Review
- Cancer-associated adipocytes: metabolic reprogramming, crosstalk and therapeutic implications in tumor progression.Signal transduction and targeted therapy · 2026Review
- Early Identification and Prognostic Stratification of Cancer Cachexia Using Explainable Machine Learning: A Multicentre Cohort Study.Journal of cachexia, sarcopenia and muscle · 2026Observational
- GDF15: A Hijacked Metabo-Hormone Orchestrating Cachexia and Immunosuppression in Cancer.Biomolecules · 2026Review
- Cardiac Biomarkers in Chronic Kidney Disease: Signal or Noise?Clinical journal of the American Society of Nephrology : CJASN · 2026Review
- Tumour-macrophage crosstalk initiated by NFIC/METTL3 negative feedback loop via exosomal miR-194-5p promotes NSCLC progression.Clinical and translational medicine · 2026Article
- Oxaliplatin triggers adipose and muscle wasting through cancer-independent metabolic and CNS pathways in mouse models.Communications biology · 2026Article
- Cancer IDO1-Mediated Tryptophan-Kynurenine Metabolic Reprogramming to Drive Skeletal Muscle Atrophy and Cachexia Acceleration.Journal of cachexia, sarcopenia and muscle · 2026Article
- Downregulation of Organ-Derived Activin A Attenuates Muscle Atrophy and Intramuscular Fat Infiltration in Cancer Cachexia Mice.Journal of cachexia, sarcopenia and muscle · 2026Article
- DNA delivered by lipid nanoparticles induces CD8+ T cell-dependent antitumor responses and enhances anti-PD-L1 therapy.JCI insight · 2026Article
- Ribosome Biogenesis and Translational Control in Skeletal Muscle Atrophy and Hypertrophy: Mechanisms and Therapeutic Perspectives.Biomolecules · 2026Review
- When adipose meets inflammation: a novel adiposity-inflammation signature predicts prognosis and chemotherapy benefit in locally advanced gastric cancer.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2026Article
- The effects of tissue inflammation on cancer cachexia.Biochimica et biophysica acta. Molecular basis of disease · 2026Review
- Article
- NF-κB Signaling as a Central Driver of Cancer Cachexia.Cancers · 2026Review
- Review
- Association between serum transferrin and overall survival in cancer patients: a multi-center cohort study.BMC cancer · 2026Observational
- CT Body Composition Changes Predict Survival in Immunotherapy-Treated Cancer Patients: A Retrospective Cohort Study.Cancers · 2026Article
- Limited Utility of the CALLY Index in Enhancing Mortality Prediction for Trauma Patients in Intensive Care Units: A Retrospective Analysis.Risk management and healthcare policy · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
Abstract
A central challenge in cancer therapy is the effective delivery of anticancer treatments while minimizing adverse effects on patient health. The potential dual impact of therapy is clearly illustrated in cancer-associated cachexia, a multifactorial syndrome characterized by involuntary weight loss, systemic inflammation, metabolic dysregulation, and behavioral alterations such as anorexia and apathy. While cachexia research often focuses on tumor-driven mechanisms, the literature indicates that cancer therapies themselves, particularly chemotherapies and targeted treatments, can initiate or exacerbate the biological pathways driving this syndrome. Here, we explore how therapeutic interventions intersect with the pathophysiology of cachexia, focusing on key organ systems including muscle, adipose tissue, liver, heart, and brain. We highlight examples such as therapy-induced upregulation of IL-6 and growth-differentiation factor 15, both contributing to reduced nutrient intake and a negative energy balance via brain-specific mechanisms. At the level of nutrient release and organ atrophy, chemotherapies also converge with cancer progression, for example, activating NF-κB in muscle and PKA/CREB signaling in adipose tissue. By examining how treatment timing and modality align with the natural trajectory of cancer cachexia, we underscore the importance of incorporating physiological endpoints alongside tumor-centric metrics in clinical trials. Such integrative approaches may better capture therapeutic efficacy while preserving patient well-being.
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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.