Genetic variants in the tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) and death receptor (DR4) genes contribute to susceptibility to colorectal cancer in pakistani population.
No significant association was found between the TNF-<i>α</i> T-857C polymorphism and colorectal cancer, cervical cancer, and prostate cancer.<i>Conclusions</i>.
Because UC patients are at increased risk for developing colorectal cancer (CRC), we investigated if there was an association between SNPs in the promoter of the TNF-alpha gene and UC-CRC.
We have studied the association between single nucleotide polymorphisms in the interleukin (IL)-6 (-174 G>C), IL8 (-251T>A), tumor necrosis factor alpha (-308G>A), and PPARG (Pro12Ala) genes and the risk of CRC in a group of 377 cases and 326 controls from Barcelona, Spain.
Polymorphisms of LBP (rs1739654, rs2232596, rs2232618), CD14 (rs77083413, rs4914), TLR-4 (rs5030719), IL-6 (rs13306435) and TNF-α (rs35131721) were genotyped in 479 cases of sporadic colorectal carcinoma and 486 healthy controls of Han Chinese in a case-control study.
In conclusion, TNF-α serum levels and AA-AG genotypes of the TNF-α-308G>A polymorphism may significantly contribute to CRC susceptibility in the population examined in this investigation.
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.
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.
For rs1800629 of TNF-α, the allelic model showed that polymorphism at this locus significantly increased the risk of IBD-associated CRC in IBD patients (OR 4.45, 95% CI 3.18-6.21, P < 0.001).
Notably, rectal cancer (a subtype of CRC) patients with TNF-α -308 A allele had a very high risk of distant tumor metastasis [odds ratio (OR) = 4.481; 95% confidence interval (CI): 2.072-9.693; P = 0.00025].
We studied the association of SNPs in the IL-6 (-174G>C), IL-8 (-251T>A), TNFalpha (-308G>A), ICAM-1 (R241G and K469E), and PPARgamma (Pro12Ala) genes and the risk of CRC.
These results indicate that TNF plays a key role in determining the cytotoxic effectiveness of SN38 in colorectal cancer and suggests a re-evaluation of TNF-based interventions to enhance therapeutic efficacy.<b>Implications:</b> The capacity of RIP1 to influence drug sensitivity suggests RIP1 may have biomarker potential.<i></i>.
This study assessed the antitumor effect of circularly permuted tumor necrosis factor-related apoptosis-inducing ligand alone or with 5-fluorouracil in colorectal cancer cells in vitro and explored the underlying mechanisms.
This study demonstrates that combined treatment with subtoxic doses of Codium extracts (CE), a flavonoid found in many fruits and vegetables, and tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), induces apoptosis in TRAIL-resistant colorectal cancer (CRC) cells.
Tumor necrosis factor‑α‑mediated (TNF‑α) epithelial‑mesenchymal transition (EMT) is associated with distant metastasis in patients with colorectal cancer with poor prognosis.