• Journal of the Korean Association of Oral and Maxillofacial Surgeons
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• v.32 no.1
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• pp.8-18
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• 2006

Purpose: The purpose of this study was to verify that the expressions of angiogenin, transforming growth factor-beta(TGF-${\beta}$), vascular endothelial growth factor(VEGF), human apurinic/apyrimidinic endonuclease(APEX) and tumor necrosis factor-alpha(TNF-${\alpha}$) were associated with the tumorigenesis of the oral squamous cell carcinoma(OSCC). Materials and Methods: Fifty-one samples of OSCC and fifteen normal oral mucosae were obtained to analyze the expression levels of above five factors. mRNA expressions were quantified by the quantitative competitive PCR(QC-PCR) method. After 2% agarose gel electrophoresis stained with ethidium bromide, the concentration of mRNA was calculated by a digital image analysis system. The expression levels of angiogenin, TGF-${\beta}$, VEGF, APEX and TNF-${\alpha}$ were compared by unpaired Student's t-tests between cancer and normal tissues. We analyzed statistically to find the cut-off values that would be useful as diagnostic markers, and the linear regression analysis between every two factors of these five factors by SAS system. Results: All of these five factors (angiogenin: P<0.0037, TGF-${\beta}$: P<0.0001, VEGF: P<0.0102, APEX: P<0.0023, TNF-${\alpha}$: P<0.0074) were significantly correlated with OSCC. In the analysis to find the cut-off values for the diagnosis, we could not find any value that had a reasonable sensitivity and specificity. In the linear regression analysis, there were correlations between angiogenin and TNF-${\alpha}$, TGF-${\beta}$ and VEGF, TGF-${\beta}$ and APEX, TGF-${\beta}$ and TNF-${\alpha}$, VEGF and APEX, VEGF and TNF-${\alpha}$, APEX and TNF-${\alpha}$. Conclusion: Our results suggest that not only angiogenin, TGF-${\beta}$, VEGF, APEX and TNF-${\alpha}$ are significantly associated with the tumorigenesis, but also the close relationship between these factors might enhance the tumorigenesis of OSCC. We can not find clinical availability for diagnosis.

• Tuberculosis and Respiratory Diseases
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• v.44 no.3
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• pp.547-558
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• 1997

Background : Tumor necrosis factor(TNF) has been considered as an important candidate for cancer gene therapy based on its potent anti-tumor activity. However, since the efficiency of current techniques of gene transfer is not satisfactory, the majorities of current protocols is aiming the in vitro gene transfer to cancer cells and re-introducing genetically modified cancer cells to hoot. In previous study, it was shown that TNF-sensitive cancer cells transfected with TNF-$\alpha$ cDNA would become highly resistant to TNF. Understanding the mechanisms of TNF-resistance in TNF-$\alpha$ gene transfected cancer cells would be an important step for improving the efficacy of cancer gene therapy as well as for better understandings of tumor biology. This study was designed to evaluate the role of new protective protein synthesis in the acquired resistance to TNF of TNF-$\alpha$ gene transfected cancer cells. Method : We transfected TNF-$\alpha$ c-DNA to WEHI164, a murine fibrosarcoma cell line, using retroviral vector(pLT12SN(TNF)) and confirm the expression of TNF with PCR, ELISA, MIT assay. Then we determined the TNF resistance of TNF gene transfected cells(WEHI164-TNF) and the changes of TNF sensitivities after treatments with actinomycin D(transcription inhibitor) and cycloheximide ( translation inhibitor). Results : WEHI164 which was sensitive to TNF became resistant to TNF after being transfected with TNF-$\alpha$ gene and the resistance to TNF was partially reversed after treatment with actinomycin D, but not with cycloheximide. Conclusion : The acquired resistance to TNF after TNF-$\alpha$ gene transfection may be associated with synthesis of some protective proteins.

• Asian Pacific Journal of Cancer Prevention
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• v.14 no.5
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• pp.3275-3279
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• 2013

Background: Tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$) plays a very important role in the development and progression of cancer. Many epidemiological studies have evaluated associations between the TNF-${\alpha}$ 238 G/A polymorphism and hepatocellular carcinoma (HCC) risk, but the published data are inconclusive. Therefore, we performed the present meta-analysis. Methods: Electronic searches of several databases were conducted for all publications on the association between TNF-${\alpha}$ 238 G/A polymorphism and HCC through July 2012. Asummary odds ratio (OR) with its 95% confidence interval (CI) were calculated to evaluate the strength of this association. Results: Eleven case-control studies with a total of 1,572 HCC cases and 1,875 controls were finally included in this meta-analysis. Overall, the TNF-${\alpha}$ 238 G/A polymorphism was significantly associated with increased risk of hepatocellular carcinoma in three genetic comparison models (For A versus G: OR 1.32, 95%CI 1.04-1.69, P = 0.02, $I_2$ = 40%; for AG versus GG: OR 1.32, 95%CI 1.02-1.71, P = 0.03, $I_2$ = 40%; for AA/AG versus GG: OR 1.33, 95%CI 1.03-1.72, P = 0.03, $I_2$ = 41%) when all studies were pooled. Subgroup analysis by ethnicity further showed that there was a significant association between the TNF-${\alpha}$ 238 G/A polymorphism and risk of HCC in Asians under three genetic comparison models (For A versus G: OR 1.30, 95%CI 1.00-1.68, P = 0.05, $I_2$ = 45% for AA/AG versus GG: OR 1.31, 95%CI 1.00-1.71, P = 0.05, $I_2$ = 46%). Conclusions: This meta-analysis provided convincing evidence that the TNF-${\alpha}$ 238 G/A polymorphism is associated with increased susceptibility to HCC. However, more well-designed studies with large sample size are needed to validate this association in Caucasians.

• Journal of the Korean Society of Radiology
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• v.10 no.3
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• pp.195-200
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• 2016

Acute promyelocytic leukemia(APL) is not just the poor grades of treating a type of blood cancer hayeoteul combination with chemotherapy despite concurrent radiation therapy are known to exhibit a greater effect and also works on normal cells to result in side effects. In this study, when after treatment with gamma rays, such as $TNF-{\alpha}$ in order to reduce these side effects was confirmed how affected the cell death of normal cells and cancer cells. HL-60 cells were used as the APL cell line HL-60 cells were differentiated with DMSO for treatment are shown the properties of normal granulocytes was used as a control group. As a result, HL-60 cells treated with $TNF-{\alpha}$ and gamma rays with only showed a cytotoxic effect by inducing the apoptosis cells were put to death. Consequently, $TNF-{\alpha}$ is thought to active substances that can increase the efficiency of cancer treatment to increase the removal of cancer cells when used with low-density gamma-ray treatment in order to eliminate the side effects of chemotherapy.

• The Korean Journal of Pain
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• v.25 no.4
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• pp.213-220
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• 2012

Background: It has been demonstrated that the expression of tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$) and apoptotic cell death in the dorsal root ganglion (DRG) following spinal nerve constriction injury play a role in the initiation and continuation of hyperalgesia and allodynia. The present study was designed to investigate the effects of ethyl pyruvate (EP) on mechanical and cold allodynia, TNF-${\alpha}$ expression, and apoptosis in DRG after spinal nerve ligation injury. Methods: Rats were divided into 3 groups: control, pre-EP, and post-EP. EP (50 mg/kg) was intraperitoneally injected 30 minutes before (pre-EP) or after (post-EP) surgery. Behavioral tests to determine mechanical and cold allodynia were conducted before surgery and 4 and 7 days after surgery. Seven days after surgery, TNF-${\alpha}$ protein levels in DRG were evaluated by enzyme-linked immunosorbent assay, and DRG apoptosis was determined by immunohistochemical detection of activated caspase-3. Results: Treatment with EP significantly reduced mechanical and cold allodynia following spinal nerve ligation injury. TNF-${\alpha}$ protein levels in the pre-EP ($4.7{\pm}1.2$ pg/200 ${\mu}g$; P < 0.001) and post-EP ($6.4{\pm}1.8$ pg/200 ${\mu}g$; P < 0.001) groups were 2-3 times lower than the control group ($14.4{\pm}1.2$ pg/200 ${\mu}g$). The percentages of neurons and satellite cells that co-localized with caspase-3 were also significantly lower in the pre-EP and post-EP groups than the control group. Conclusions: These results demonstrate that EP has a strong anti-allodynic effect that acts through the inhibition of TNF-${\alpha}$ expression and apoptosis in DRG after spinal nerve ligation injury.

• Restorative Dentistry and Endodontics
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• v.23 no.1
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• pp.316-327
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• 1998

This study was designed to examine the tissue levels of interleukin-$1{\alpha}$(IL-$1{\alpha}$), interleukin-$1{\beta}$(IL-$1{\beta}$) and tumor necrosis factor-${\alpha}$(TNF-${\alpha}$) in inflamed human dental pulps and periapical lesions, and to determine the relationship between each cytokine and pulpal and periapical pathosis. The pulps used in this experiment, were obtained in routine endodontic treatment and the periapical lesions in periapical surgery after clinical diagnoses were performed. These specimens were divided into four groups as normal pulp group(control group, n=9), acute pulpitis group(n=g), chronic pulpitis group(n= 10) and periapical lesion group(n= 18) and stored in liquid N2. For extract preparation, tissues were finely minced with a scalpel, and the fragments were incubated in $0.5m\ell$ homogenizing buffer (0.1 mol/L potassium chloride, 0.02 mol/L TRIS; pH=7.6) for two hours and grinded with glass homogenizer. Debris was removed by centrifugation and supernatants were immediately tested with enzymelinked immunosorbent assay (ELISA, R&D Co., Minneapolis, USA). Following results were obtained; 1. The concentrations of IL-$1{\alpha}$ in all experimental groups were significantly higher than in control group(p<0.05). And the concentrations of IL-$1{\alpha}$ in periapical lesion group were somewhat higher than in two pulpitis groups, but the differences among those groups were not stastically significant (p>0.05). 2. The concentrations of IL-$1{\beta}$ in all experimental groups were significantly higher than in control group (p<0.05), and all the experimental groups expressed similar concentrations. 3. The concentrations of TNF-${\alpha}$ in all experimental groups were higher than in control group but only the differences between chronic pulpitis group and control group were statistically significant(p<0.05). And the concentrations of TNF-${\alpha}$ in acute and chronic pulpit is groups were higher than in periapical lesion group but only the differences between chronic pulpitis group and periapical lesion group were statistically significant (p<0.05). 4. There was significant correlation only between IL-$1{\alpha}$ and IL-$1{\beta}$ in periapical lesion group (p<0.05).

• Childhood Kidney Diseases
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• v.7 no.1
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• pp.16-22
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• 2003

Purpose : Minimal Change Disease(MCD) is the most common primary nephrotic syndrome in children. Some suggested that tumor necrosis factor-${\alpha}$ ($TNF-{\alpha}$) are involved in the pathogenesis of MCD. This study was done to see the changes of plasma and urinary $TNF-{\alpha}$, and their effects on the permeability of glomerular basement membrane. Methods : Study patients consisted of 19 biopsy-proven MCD children aged 2-15 years old. Both plasma and urinary $TNF-{\alpha}$ were measured. Employing the Millicell system, $TNF-{\alpha}$ were screened for the permeability factors. Results : Urinary $TNF-{\alpha}$ during relapse was significantly increased(P<0.01). No significant change was seen in the plasma $TNF-{\alpha}$ during relapse when compared to those in remission and the healthy controls. Furthermore, in the in vitro Millicell system, $TNF-{\alpha}$ did not produce a significant change in albumin permeability. Conclusion : Therefore, it seems that $TNF-{\alpha}$ may not play a disease-specific role in the pathogenesis of MCD.

• Childhood Kidney Diseases
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• v.8 no.1
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• pp.1-9
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• 2004

Purpose : Minimal Change Disease (MCD) is the most common primary nephrotic syndrome in children. Some suggested that tumor necrosis $factor-{\alpha}$ ($TNF-{\alpha}$) are involved in the pathogenesis of MCD. Methods : This study was done to see the changes of plasma and urinary $TNF-{\alpha}$, and its effect on the determination of permeability of the glomerular basement membrane (BM) contributed by heparan sulfate proteoglycan (HSPG). Study patients consisted of 19 biopsy-proven MCD children aged 2-15 years old. Both plasma and urinary $TNF-{\alpha}$ were measured. Employing the Millicell system, $TNF-{\alpha}$ was screened for the permeability factors. We examined whether $TNF-{\alpha}$ regulated BM HSPG gene expression and HS synthesis in the glomerular epithelial cells (GECs). Results : Urinary $TNF-{\alpha}$ during relapse was significantly increased when compared with that of during remission or controls ($364.4{\pm}51.2$ vs $155.3{\pm}20.8,\;36.0{\pm}4.5$ ng/mg cr) (P<0.05). However, negative results were obtained in the permeability assay using the Millicell system. No difference was seen in the BM HSPG gene expression and HS synthesis in the GECs. Conclusion : It seems that $TNF-{\alpha}$ may not play a disease-specific role in the pathogenesis of MCD.

• Advances in Traditional Medicine
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• v.7 no.4
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• pp.341-347
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• 2007

Red seaweed (Callophyllis japonica) has long formed part of the diet of Asians, but the pharmacological properties of this plant have not been evaluated. In this study, we examined the effect of an ethanol extract of C. japonica on the generation of nitric oxide (NO) in RAW 264.7 cells. The C. japonica extract increased the generation of NO and tumor necrosis $factor-{\alpha}$ ($TNF-{\alpha}$), which were detected by the Griess method and an enzyme-linked immunosorbent assay, respectively. The increased production of NO by C. japonica extract was inhibited by $N^G$-monomethyl-L-arginine ($100{\mu}M$), a specific inhibitor of NO production in the L-arginine-dependent pathway, and by the nuclear $factor-{\kappa}B$ ($NF-{\kappa}B$) inhibitor, pyrrolidine dithiocarbamate ($10-100{\mu}M$) in a dose-dependent manner. These findings demonstrate that C. japonica extract stimulates the production of NO and $TNF-{\alpha}$ in RAW 264.7 cells through the activation of $NF-{\kappa}B$ and that this extract might also inhibit the growth of the human leukemic cells.

• Journal of Life Science
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• v.24 no.7
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• pp.721-727
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• 2014

Mushroom-derived ${\beta}$-glucan, a polysaccharide (GLP) isolated from the mycelium of Ganoderma lucidum, was previously shown to have inhibitory effects against tumor-bearing mice in vivo. We investigated the apoptotic effect of mushroom-derived ${\beta}$-glucan in a sarcoma-180 tumor cell- bearing mice model using an ELISA to determine the levels of tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$) in the mice. The morphology of the tumor cells was assessed with transmission electron microscopy (TEM). GLP was injected into the tumor-bearing mice at a dose (i.p.) of 20 mg/kg for 10 days. After 30 days, the tumor mass from the inguinal region was collected, weighed, and assayed using TEM and a TNF-${\alpha}$ ELISA kit. The tumors that developed in the mice treated with GLP were 71.4% smaller than those in the control group, showing the ability of GLP to inhibit tumor growth. The levels of TNF-${\alpha}$ in the serum of the sarcoma-180 bearing mice were 12 times greater than in the serum of the nonbearing tumor mice. An ultrastructural study demonstrated that the GLP-treated sarcoma-180 tumor cells were condensed, with rearranged chromatin. In addition, the marginated chromatin in nucleus induced the nuclear compartment, and there were many vacuolization in the cell. GLP could be an effective apoptosis-inducing compound in sarcoma-type cancers.