ReviewMedComm2022
Targeting cancer cachexia: Molecular mechanisms and clinical study.
Review in MedComm, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.
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
28 citing papers in PubMed, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.
- Host insulin resistance caused byFrontiers in cellular and infection microbiology · 2023Pooled it
- Bone Loss, Osteoporosis, and Skeletal Fragility: Hidden Consequences of Cancer Cachexia.Cells · 2026Review
- Oxaliplatin triggers adipose and muscle wasting through cancer-independent metabolic and CNS pathways in mouse models.Communications biology · 2026Article
- RAGE Re-Expressed at Myofibre Level Drives Muscle Wasting in Cancer Conditions.Journal of cachexia, sarcopenia and muscle · 2026Article
- Tumor-muscle communication in cancer-associated cachexia (Review).Oncology letters · 2026Review
- Downregulation of Organ-Derived Activin A Attenuates Muscle Atrophy and Intramuscular Fat Infiltration in Cancer Cachexia Mice.Journal of cachexia, sarcopenia and muscle · 2026Article
- Brain-cancer interactions outside the CNS.Oncogene · 2026Review
- Tumor-Derived LIF Promotes GDF15-Driven Cachexia and Adverse Outcomes in Gastric Cancer.Cells · 2026Article
- The evolving landscape of cancer cachexia prevention: A review of metronomic chemotherapy and drug repurposing strategies.Medical oncology (Northwood, London, England) · 2025Review
- Gut microbiota in cancer cachexia: a new frontier for research and therapy.Genes & nutrition · 2025Review
- LncRNA ADAMTS9-AS1 regulates the proliferation, migration, and invasion of esophageal cancer cells via miR-575/ CADM2.Discover oncology · 2025Article
- Physical Activity, Exerkines, and Their Role in Cancer Cachexia.International journal of molecular sciences · 2025Review
- Exercise therapy: an effective approach to mitigate the risk of cancer metastasis.World journal of surgical oncology · 2025Review
- The neuroscience of cancer: Focus on neuropeptidergic systems.Acta pharmaceutica Sinica. B · 2025Review
- TRIM22 governs tumorigenesis and protects against endometrial cancer-associated cachexia by inhibiting inflammatory response and adipose thermogenic activity.Cancer & metabolism · 2025Article
- Role, mechanisms and effects ofOncology letters · 2025Review
- Review
- Cancer cachexia: multilevel metabolic dysfunction.Nature metabolism · 2024Review
- Metabolic, Inflammatory, and Molecular Impact of Cancer Cachexia on the Liver.International journal of molecular sciences · 2024Review
- Testosterone replacement therapy in patients with cachexia: a contemporary review of the literature.Sexual medicine reviews · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cancer cachexia is a complex systemic catabolism syndrome characterized by muscle wasting. It affects multiple distant organs and their crosstalk with cancer constitute cancer cachexia environment. During the occurrence and progression of cancer cachexia, interactions of aberrant organs with cancer cells or other organs in a cancer cachexia environment initiate a cascade of stress reactions and destroy multiple organs including the liver, heart, pancreas, intestine, brain, bone, and spleen in metabolism, neural, and immune homeostasis. The role of involved organs turned from inhibiting tumor growth into promoting cancer cachexia in cancer progression. In this review, we depicted the complicated relationship of cancer cachexia with the metabolism, neural, and immune homeostasis imbalance in multiple organs in a cancer cachexia environment and summarized the treatment progress in recent years. And we discussed the molecular mechanism and clinical study of cancer cachexia from the perspective of multiple organs metabolic, neurological, and immunological abnormalities. Updated understanding of cancer cachexia might facilitate the exploration of biomarkers and novel therapeutic targets of cancer cachexia.
Indexed as
Identifiers
What Socratic holds
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.