Women with stage I and II breast cancer experienced variability in the severity of fatigue and levels of IL-6 and TNF-α throughout their treatment trajectories.
Since experimental studies have shown that tumour necrosis factor-alpha (TNF-alpha) has potent anti-tumour activity that can be potentiated with cytokines, we tested the efficacy of TNF-alpha with interferon-gamma (IFN-gamma) on different human breast cancer cell lines, particularly comparing hormone-dependent and -independent phenotypes.
CpG methylation within the TNF promoter may provide an additional mechanism through which TNF alters the risk for mild persistent breast pain after breast cancer surgery.
Although tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) can induce apoptosis in a wide range of cancer cells, such as breast cancer, it also has cytotoxicity to normal cells.
Expression of tumor necrosis factor receptor-assicated factor 4 correlates with expression of Girdin and promotes nuclear translocation of Girdin in breast cancer.
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.
The overexpression of CMTM1_v17 in the breast cancer cell line MDA-MB-231 promoted cell proliferation and resistance to tumor necrosis factor-α (TNF-α)-induced apoptosis.
Cellular FLICE (FADD-like IL-1beta-converting enzyme)-inhibitory protein (c-FLIP) is a major resistance factor for the tumor necrosis factor-related apoptosis-inducing ligand TRAIL and in drug resistance in human malignancies. c-FLIP is an antagonist of caspases-8 and -10, which inhibits apoptosis and is expressed as long (c-FLIP(L)) and short (c-FLIP(S)) splice forms. c-FLIP is often overexpressed in various human cancers, including breast cancer.
This study aims to investigate the possible anticancer activity of two clinically used drugs: a natural antioxidant agent (salicin) and an antihyperlipidemic agent (fenofibrate) against two breast cancer models (in vivo EAC and in vitro MCF7) and the pancreatic cancer cell line (Panc-1).Our results have shown that both salicin and fenofibrate exerted an in vivo anticancer activity as evidenced by the decrease in tumor weight, tumor volume, CEA level, and reduced tumor cholesterol content through an antioxidant (reduced MDA level and increased GSH and catalase content) and an antiinflammatory activity (reduced TNF-∝ level).
We evaluated the association of gene polymorphisms ATM Asp1853Asn, IL-6 G-174C and TNF-αG-308A involved in central phenotype pathways and development of individual radiosensitivity in BC patients with an exacerbated response to RT.
Decreased concentrations of adiponectin, and increased concentrations of leptin, IL-6, IL-8, TNF-α, resistin and visfatin were significantly associated with risk of breast cancer.
In this study, we observed that tumor necrosis factor-alpha (TNFalpha) up-regulates the expression of Bcl10 and induces a fraction of Bcl10 nuclear translocation in human breast carcinoma MCF7 cells.
Despite intensive study of the mechanisms of chemotherapeutic drug resistance in human breast cancer, few reports have systematically investigated the mechanisms that underlie resistance to the chemotherapy-sensitizing agent tumor necrosis factor (TNF)-alpha.
Patient-control comparisons revealed a non-significant trend for association between the TNF-alpha-308 GG genotype and breast cancer compared to controls (79.7 vs. 68.2%, P = 0.03, Pc = 0.54).
The present results suggested that sClu confers breast cancer cells resistance to TNF-alpha-induced apoptosis through NF-kappaB activation and Bcl-2 overexpression.
Recently, we showed the implication of the polymorphism in tumor necrosis factor-alpha (TNF-alpha) gene in the susceptibility and prognosis of breast carcinoma.