Observational studyNutrients2015
NF-κBp65 and Expression of Its Pro-Inflammatory Target Genes Are Upregulated in the Subcutaneous Adipose Tissue of Cachectic Cancer Patients.
Observational study in Nutrients, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 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
30 citing papers in PubMed, 43 citations in OpenAlex.
- Cancer-Associated Cachexia in the Era of Obesity.International journal of molecular sciences · 2025Review
- Nutrients Lowering Obesity-Linked Chemokines Blamable for Metastasis.International journal of molecular sciences · 2025Review
- Supportive care of female hormones in brain health: what and how?Frontiers in pharmacology · 2024Review
- Cachexia causes time-dependent activation of the inflammasome in the liver.Journal of cachexia, sarcopenia and muscle · 2023Article
- Intranasal administration of interleukin-4 ameliorates depression-like behavior and biochemical alterations in mouse submitted to the chronic unpredictable mild stress: modulation of neuroinflammation and oxidative stress.Psychopharmacology · 2023Article
- Lipocalin-2 and neutrophil activation in pancreatic cancer cachexia.Frontiers in immunology · 2023Article
- Exosomal IL-8 derived from Lung Cancer and Colon Cancer cells induced adipocyte atrophy via NF-κB signaling pathway.Lipids in health and disease · 2022Article
- Alcohol Induces Zebrafish Skeletal Muscle Atrophy through HMGB1/TLR4/NF-κB Signaling.Life (Basel, Switzerland) · 2022Article
- Review
- MicroRNAs: Novel players in the diagnosis and treatment of cancer cachexia (Review).Experimental and therapeutic medicine · 2022Review
- Whole-body and adipose tissue metabolic phenotype in cancer patients.Journal of cachexia, sarcopenia and muscle · 2022Article
- The ambiguous role of obesity in oncology by promoting cancer but boosting antitumor immunotherapy.Journal of biomedical science · 2022Review
- Non-coding RNAs in cancer-associated cachexia: clinical implications and future perspectives.Translational oncology · 2021Review
- Tumor-derived IL-6 and trans-signaling among tumor, fat, and muscle mediate pancreatic cancer cachexia.The Journal of experimental medicine · 2021Article
- Carnosol and its analogues attenuate muscle atrophy and fat lipolysis induced by cancer cachexia.Journal of cachexia, sarcopenia and muscle · 2021Article
- A Pound of Flesh: What Cachexia Is and What It Is Not.Diagnostics (Basel, Switzerland) · 2021Review
- Activation of the Adipose Tissue NLRP3 Inflammasome Pathway in Cancer Cachexia.Frontiers in immunology · 2021Article
- Pharmacological Inhibition of HMGB1 Prevents Muscle Wasting.Frontiers in pharmacology · 2021Article
- Small-Molecule Inhibitor of 8-Oxoguanine DNA Glycosylase 1 Regulates Inflammatory Responses duringJournal of immunology (Baltimore, Md. : 1950) · 2020Article
- Cancer Cachexia and Related Metabolic Dysfunction.International journal of molecular sciences · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cancer cachexia, of which the most notable symptom is severe and rapid weight loss, is present in the majority of patients with advanced cancer. Inflammatory mediators play an important role in the development of cachexia, envisaged as a chronic inflammatory syndrome. The white adipose tissue (WAT) is one of the first compartments affected in cancer cachexia and suffers a high rate of lipolysis. It secretes several cytokines capable of directly regulating intermediate metabolism. A common pathway in the regulation of the expression of pro-inflammatory cytokines in WAT is the activation of the nuclear transcription factor kappa-B (NF-κB). We have examined the gene expression of the subunits NF-κBp65 and NF-κBp50, as well as NF-κBp65 and NF-κBp50 binding, the gene expression of pro-inflammatory mediators under NF-κB control (IL-1β, IL-6, INF-γ, TNF-α, MCP-1), and its inhibitory protein, nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha (IκB-α). The observational study involved 35 patients (control group, n = 12 and cancer group, n = 23, further divided into cachectic and non-cachectic). NF-κBp65 and its target genes expression (TNF-α, IL-1β, MCP-1 and IκB-α) were significantly higher in cachectic cancer patients. Moreover, NF-κBp65 gene expression correlated positively with the expression of its target genes. The results strongly suggest that the NF-κB pathway plays a role in the promotion of WAT inflammation during cachexia.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.