To explain these observations, we investigated actions of Th1 cytokines (TNF-α and IFN-γ) on murine and human breast cancer cell lines that varied in the surface expression of HER-family receptor tyrosine kinases.
A cross-sectional study was conducted to examine the extent to which perceived social support, cortisol-awaking response (CAR) and tumour necrosis factor alpha (TNF-α) interact to statistically predict psychological distress in breast cancer survivors.
No significant changes in B cell cytokine profiles were observed during breast cancer progression from stage I to III, but the percentage of B cells with high TNF-α expression (TNF<sup>hi</sup>) showed a negative relationship with lymph node involvement and Her2 expression (p < 0.05).
Recent studies have suggested that tumour necrosis factor (TNF) and its receptor 2 (TNFR2) expressed on breast cancer cells have important functional consequences.
This pilot study aims to determine whether different coping strategies are associated with differences in psychological distress, cortisol, and tumor necrosis factor alpha (TNF-a) levels in breast cancer survivors.
Therefore, in the present study, we explored the effect of <i>HLA-G</i> 3'UTR (14-bp Ins/Del and +3142 C/G) and <i>TNF-α</i> promoter (-238 G/A and -308 G/A) polymorphisms on breast cancer risk among South Indian women.
Here, we identified serum amyloid A (SAA) for proinflammatory predisposition in BC through the signature profiles of APPs, interleukin (IL) and tumor necrosis factor (TNF) superfamily using publicly available datasets of tumor samples and cell lines.
ELISA was conducted to check the concentrations of proteins involved in multiple intracellular signaling pathways, responsible for the promotion of tumor growth and breast cancer progression, namely matrix metalloproteinase (MMP)‑2, matrix MMP‑9, tumor necrosis factor‑α (TNF‑α), cyclooxygenase‑2 (COX‑2), soluble intercellular adhesion molecule 1 (sICAM1) and mTOR.
We used Doxorubicin as a therapeutic agent, TNFα as marker and mediator of an inflammatory microenvironment and 17β-Estradiol (E2) as an agonist of Estrogen Receptors, known predisposing factor for hormone-driven breast cancer, whose pharmacological inhibition reduces the risk of breast cancer recurrence.
With a view toward improving complete response rates, we investigated whether the principle Th1 cytokines (IFN-γ and TNF-α) could act in concert with lapatinib to suppress activity of breast cancer lines in vitro.
Sub-group analysis for the pro-inflammatory markers indicated that combined aerobic and resistance training had the greatest effect (SMD: -0.3, 95% CI: -0.5, -1.9, p < 0.001), that prostate (SMD: -0.5, 95% CI: -0.8, 0.1, p = 0.004) and breast cancer populations were most responsive (SMD: -0.2, 95% CI: -0.3, -0.1, p = 0.001), and that C-reactive protein (SMD: -0.5, 95% CI: -0.9, -0.06, p = 0.025) and tumor necrosis factor (SMD: -0.3, 95% CI: -0.5, -0.06, p = 0.004) were the most sensitive to change.
Overexpression of A20 not only protects luminal breast cancer cell lines from TNFα-induced cell death via inducing HSP70-mediated anti-apoptotic pathway but also promotes a robust EMT/CSC phenotype by activating the pStat3-mediated inflammatory signaling.
Tumour necrosis factor receptor associated factor 2 (TRAF2), a key component of NFκB signalling, has been identified as an oncogene, but its role in the regulation of breast cancer osteolytic metastasis remains unknown.
The two TNF superfamily members, APRIL (TNFSF13), and BAFF (TNFSF13B), which are type II membrane proteins, released in active forms by proteolytic cleavage and are primarily involved in B-lymphocyte maturation, have also been associated with tumor growth and aggressiveness in several solid tumors, including breast cancer.
Previous studies have indicated that the sensitivity of breast cancer cells to tumor necrosis factor‑related apoptosis‑inducing ligand (TRAIL)‑induced apoptosis is associated with the expression of death receptors on the cell membrane.
Factors including the secretion of adipokines such as leptin and adiponectin, as well as autotaxin, interleukin 6, tumor necrosis factor alpha, and hepatic growth factor, metabolic remodeling that supports the growth of breast cancer by transfer of fatty acids to increase mitochondrial β-oxidation, extracellular matrix remodeling and endotrophin production from type IV collagen, and cancer-associated fibroblast phenotype changes have all been implicated in this comprehensive process.
Inhibitory Effect of <i>Alisma canaliculatum</i> Ethanolic Extract on NF-κB-Dependent CXCR3 and CXCL10 Expression in TNFα-Exposed MDA-MB-231 Breast Cancer Cells.
These results demonstrate that TNF differentially regulates gangliosides expression in breast cancer cell lines and establish a possible link between inflammation at the tumor site environment, expression of complex gangliosides and tumor development.
Furthermore, cell from normal mammary epithelium and breast cancer cell lines expressed ICAM1 upon stimulation with the proinflammatory cytokines TNFα, IL1β and IFNγ.