NF-κBp65 and Expression of Its Pro-Inflammatory Target Genes Are Upregulated in the Subcutaneous Adipose Tissue of Cachectic Cancer Patients.
Level 4 - case-series / case-control
Cross-sectional comparative case-control observational study
PubMed 26053616 · doi:10.3390/nu7064465
What was done
An observational study evaluated subcutaneous white adipose tissue samples from 35 participants divided into a control group (n = 12) and a cancer group (n = 23, subdivided into cachectic and non-cachectic patients). Investigators measured gene expression and binding activity of NF-κB subunits (NF-κBp65 and NF-κBp50), the inhibitory protein IκB-α, and downstream inflammatory target genes (IL-1β, IL-6, INF-γ, TNF-α, and MCP-1).
What was found
The abstract reports no numerical values, fold changes, or p-values. It reports that NF-κBp65 gene expression and target gene expression (TNF-α, IL-1β, MCP-1, and IκB-α) were significantly higher in cachectic cancer patients compared to controls and non-cachectic patients, with a positive correlation between NF-κBp65 expression and target gene expression.
Why it matters
The study demonstrates local NF-κB pathway upregulation and inflammatory gene expression directly within subcutaneous adipose tissue during human cancer cachexia.
Limits
The sample size is very small (n = 35 divided across three subgroups). The cross-sectional design cannot establish causality between NF-κB signaling and cachectic wasting. Numerical data, effect sizes, statistical thresholds, cancer types, and clinical stages are not provided in the abstract.
Cited by
- supports Cancer cachexia is characterized by marked elevation of inflammatory mediators including interleukin-1 beta (IL-1 beta) and tumor necrosis factor-alpha (TNF-alpha).