Further subgroup analyses based on ethnicity of participants revealed that <i>TNF-α</i> -238 G/A was significantly correlated with the risk of CRC in Caucasians (dominant model: <i>P</i> = 0.01, OR = 0.47, 95%CI 0.26-0.86; overdominant model: <i>P</i> = 0.01, OR = 2.27, 95%CI 1.20-4.30; allele model: <i>P</i> = 0.02, OR = 0.51, 95%CI 0.29-0.90), while -308 G/A polymorphism was significantly correlated with the risk of CRC in Asians (recessive model: <i>P</i> = 0.001, OR = 2.23, 95%CI 1.38-3.63).<b>Conclusions:</b> Our findings indicated that <i>TNF-α</i> -238 G/A polymorphism may serve as a potential biological marker for CRC in Caucasians, and <i>TNF-α</i> -308 G/A polymorphism may serve as a potential biological marker for CRC in Asians.
To explore zinc-α2-glycoprotein (ZAG), leptin, high-molecular-weight adiponectin (HMW-ADPN), and tumor necrosis factor-alpha (TNF-α) levels in serum and subcutaneous and visceral white adipose tissue (sWAT and vWAT) among normal weight (NW) and overweight/obese (OW/OB) patients with colorectal cancer (CRC).
Although miR-20a has been reported to be altered in a range of cancers, the role of miR-20a in colorectal cancer is not fully characterized, and the relationship between miR-20a dysregulation and the tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) sensitivity is not defined.
Overall, in this study, we demonstrate that the oncolytic radiotherapy-tumor necrosis factor-related apoptosis-inducing ligand construct can sensitize human colorectal cancer cells to radiation-induced apoptosis both in vitro and in vivo.
PRKCDBP is a proapoptotic tumor suppressor which is commonly altered in colorectal cancer by promoter hypermethylation, and its gene transcription is directly activated by NF-κB in response to TNFα.
It has been hypothesized that the VDR-mediated signaling antagonizing TNF-α and IL-6 receptor-activated pro-inflammatory and proliferative intracellular pathways, may prevent development of IBD and colitis-associated colorectal cancer.
Pooled odd ratios (ORs) and 95% confidence intervals (95% CIs) were calculated on the basis of data from 14, 18, and 7 studies from a total of 27 studies for the associations between the polymorphism of TNF-α-308 G>A and ulcerative colitis, Crohn's disease (CD) and CRC.
In addition, we also examined paired normal and tumor DNA from the colorectal cancer group for microsatellite alterations at the TNF alpha locus, including allelic loss of heterozygosity and microsatellite instability.
The novel marker tumor necrosis factor receptor-associated protein 1 (TRAP1) is a mitochondrial heat shock protein that has been related to drug resistance and protection from apoptosis in colorectal cancer.
The tumor necrosis factor⁻related weak inducer of apoptosis (TWEAK) belongs to the tumor necrosis factor ligand superfamily, which was shown to play an important role in inflammatory and malignant gastrointestinal diseases, including colitis or colorectal cancer.
The HT29 adenocarcinoma is a common model of epithelial cell differentiation and colorectal cancer and its death is an oft-analyzed response to TNF family receptor signaling.
<b>Background:</b> This study sought to evaluate the efficacy of a novel intraoperative chemotherapy (IOC) regimen that consists of hydroxycamptothecin, tumor necrosis factor (TNF), 5-fluorouracil (5-FU), and calcium folinate (CF) on the outcomes of colorectal cancer (CRC).
Restoration of RUNX1 abolished the inhibitory effects of miR-20a on the secretions of IFN-γ and TNF-α, as well as the killing effect of NK cells to colorectal cancer cells.
Inflammation and pro-inflammatory cytokines produced by Th1 and Th17 cells like IL-6, TNF, IL-17 and IL-23 promote the development and growth of colorectal cancer (CRC).
Tumor necrosis factor-α is associated with positive lymph node status in patients with recurrence of colorectal cancer-indications for anti-TNF-α agents in cancer treatment.