Hsiu Ting Tsai

CONTRIBUTION OF GENETIC POLYMORPHISMS OF STROMAL CELL-DERIVED FACTOR-1 AND ITS RECEPTOR, CXCR4, TO THE SUSCEPTIBILITY AND CLINICOPATHOLOGIC DEVELOPMENT OF ORAL CANCER

The aim of this study was to evaluate the relations of SDF‐1 and its receptor, CXCR4, gene variants on oral cancer risk.

Hypoxia inducible factor-1α gene polymorphism G1790A and its interaction with tobacco and alcohol consumptions increase susceptibility to hepatocellular carcinoma†

The aim of this study was to examine the potential associations of two hypoxia inducible factor‐1α (HIF‐1α) gene polymorphisms, C1772T and G1790A, with the susceptibility and clinicopathological status of hepatocellular carcinoma.

The association between hypoxia inducible factor-1α gene polymorphisms and increased susceptibility to oral cancer

The aim of this study was to estimate the relations between hypoxia inducible factor-1alpha (HIF-1alpha) gene polymorphisms, C1772T and G1790A, to the susceptibility and clinicopathological status of oral cancer. A total of 521 subjects, including 347 controls and 174 oral cancer patients, were recruited in this study and subjected to polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) to analyze the impact of these two polymorphic variants on oral cancer. A significant association between oral cancer susceptibility and G1790A polymorphism was demonstrated since individuals with heterozygotes, that is GA, had a higher risk for oral cancer, compared to GG genotypes after adjusting for other confounders (AOR=3.31; 95%CI=1.27-8.61). Compared to individuals with both C1772C and G1790G homozygotes, individuals with at least one of either C1772T or G1790A of HIF-1alpha gene had a risk of 2.17-folds (95% CI=1.0-4.75) to develop oral cancer. Moreover, results also revealed the presence of synergistic effect between gene polymorphisms of HIF-1alpha and environmental risk factors, such as tobacco and betel nut consumptions while there was no significant association between HIF-1alpha gene polymorphism and clinicopathological parameters of oral cancer. Genetic polymorphism, including C1772T and G1790A, of HIF-1alpha is an important factor for the susceptibility to oral cancer.

Stromal cell-derived factor-1 but not its receptor, CXCR4, gene variants increase susceptibility and pathological development of hepatocellular carcinoma

Abstract Background: Hepatocellular carcinoma (HCC) is one of the most frequent malignant neoplasms worldwide. Genetic polymorphism has been reported as a predictive factor related to a higher risk for HCC. Because the stromal cell-derived factor-1 (SDF-1) and its receptor, CXCR4, have been reported to play important roles in tumor cell proliferation, angiogenesis, and metastasis of HCC, the aim of this study was to estimate the relationship between SDF-1 and CXCR4 gene variants to HCC risk and clinicopathological status. Methods: Polymerase chain reaction-restriction fragment length polymorphism was used to measure SDF-1 (rs1801157) and CXCR4 (rs2228014) gene polymorphisms in 311 healthy controls and 102 patients with HCC. Results: Compared to controls, individuals with at least one A allele had a higher risk of 1.57-fold (95% CI: 1.00–2.47) to induce HCC and had a risk of 2.81-fold (95% CI: 1.04–7.58) to develop a status of stage III or stage IV disease, after being adjusted for other confounders. However, there was no significant association between CXCR4 gene polymorphism and either HCC risk or pathological status. Additionally, both gene polymorphisms were not associated with the serum expression of liver-related clinical pathological markers. Conclusions: SDF-1–3′A gene polymorphism could be considered as a factor related to an increased susceptibility to the risk and pathological development of HCC. Clin Chem Lab Med 2009;47:412–8.

Glutathione S-Transferase P1 (GSTP1) gene polymorphism increases age-related susceptibility to hepatocellular carcinoma

BackgroundHepatocellular carcinoma (HCC) is one of the most frequent malignant neoplasms in the world. Genetic polymorphism has been reported to be a factor increasing the risk of HCC. Phase II enzymes such as glutathione s-transferases (GSTP1, GSTA1) play important roles in protecting cells against damage induced by carcinogens. The aim of this study was to estimate the relationship of the GSTP1 and GSTA1 gene polymorphisms to HCC risk and clinico-pathological status.MethodsPolymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) was used to measure GSTP1 (A→G) and GSTA1 (C→T) gene polymorphisms in 386 healthy controls and 177 patients with HCC.ResultsNeither gene polymorphism was associated with the clinico-pathological status of HCC and serum expression of liver-related clinico-pathological markers. No association between the GSTA1 gene polymorphism and HCC susceptibility was found. However, in the younger group, aged ≤ 57 years, individuals with AG or GG alleles of GSTP1 had a 2.18-fold (95%CI = 1.09-4.36; p = 0.02) and 5.64-fold (95%CI = 1.02-31.18; p = 0.04) risk, respectively, of developing HCC compared to individuals with AA alleles, after adjusting for other confounders.ConclusionAG and GG alleles of GSTP1 gene polymorphisms may be considered as factors increasing the susceptibility to and risk of HCC in Taiwanese aged ≤ 57 years.

Glutathione S-transferase P1 and alpha gene variants; role in susceptibility and tumor size development of oral cancer.

The aim of this study was to estimate the relationship of glutathione S‐transferases (GST)P1, GSTA1, GSTM1, and GSTT1 gene polymorphisms to oral cancer risk.

Genetic polymorphism of CCR2-64I increased the susceptibility of hepatocellular carcinoma†

The purpose of this study was to investigate genetic impact of monocyte chemoattractant protein‐1 (MCP‐1) and its receptor chemokine receptor‐2 (CCR2) gene polymorphisms on the susceptibility and clinicopathological characteristics of hepatocellular carcinoma (HCC).

Impact of interleukin-18 polymorphisms -607A/C and -137G/C on oral cancer occurrence and clinical progression.

Background The purpose of this study was to identify gene polymorphisms of interleukin-18 (IL-18) -607A/C and -137G/C specific to patients with oral cancer susceptibility and clinicopathological status. Methodology and Principal Findings A total of 1,126 participants, including 559 healthy people and 567 patients with oral cancer, were recruited for this study. Allelic discrimination of -607A/C (rs1946518) and -137G/C (rs187238) polymorphisms of the IL-18 gene was assessed by a real-time PCR with the TaqMan assay. There was no significant association between IL-18 -607A/C polymorphism and oral cancer risk. However, among alcohol consumers, people with A/A homozygotes of IL-18 -607A/C polymorphism had a 2.38-fold (95% CI=1.17-4.86; p=0.01) increased risk of developing oral cancer compared with those with C/C homozygotes. The participants with G/C heterozygotes of IL-18 -137 polymorphism had a 1.64-fold (95% CI: 1.08-2.48; p=0.02) increased risk of developing oral cancer compared with those with G/G wild type homozygotes. Both sets of statistics were determined after adjusting for confounding factors. Among people who had exposure to oral cancer-related environmental risk factors such as areca, alcohol, and tobacco consumption, the adjusted odd ratios and 95% confidence intervals were increased to a 2.02-fold (95% CI=1.01-4.04; p=0.04), 4.04 (95% CI=1.65-9.87; p=0.002) and a 1.66-fold (95% CI=1.00-2.84; p=0.05) risk of developing oral cancer. However, patients with G/C alleles of IL-18 -137 were correlated with a lower clinical stage (AOR=0.59; 95% CI=0.39-0.89; p=0.01), smaller tumor size (AOR=0.56; 95% CI=0.35-0.87; p=0.01), and non-lymph node metastasis (AOR=0.51; 95% CI=0.32-0.80; p=0.003). Conclusion IL-18 -137 G/C gene polymorphism may be a factor that increases the susceptibility to oral cancer, as well as a protective factor for oral cancer progression. The interactions of gene to oral cancer-related environmental risk factors have a synergetic effect that can further enhance oral cancer development.

Significant elevation and correlation of plasma neutrophil gelatinase associated lipocalin and its complex with matrix metalloproteinase-9 in patients with pelvic inflammatory disease.

BACKGROUNDS To detect the expression of plasma neutrophil gelatinase associated lipocalin (NGAL) and its complex with matrix metalloproteinase-9 (MMP-9) in patients with pelvic inflammatory disease (PID). METHODS Enzyme-linked immunosorbent assay was used to measure the levels of plasma NGAL and NGAL/MMP-9 complex. RESULTS The levels of plasma NGAL or NGAL/MMP-9 complex were increased in patients with PID compared with those in normal controls and decreased significantly after treatment. Pre-treatment plasma level of NGAL was significantly correlated with WBC and neutrophil counts. In patients with PID, plasma level of NGAL/MMP-9 complex was correlated with plasma level of NGAL or MMP-9 significantly. In predicting PID, the sensitivities of NGAL and NGAL/MMP-9 complex were 76.6% and 78.1%; the negative predictive values, 72.7% and 74.5%. CONCLUSIONS Plasma NGAL and NGAL/MMP-9 complex may act as diagnostic adjuvant biomarkers for PID. In patients with PID, about 80% have plasma levels of NGAL or NGAL/MMP-9 complex level >10.04 ng/ml or 2.33 ng/ml, respectively.

Plasma interleukin-1β, -6, -8 and tumor necrosis factor-α as highly informative markers of pelvic inflammatory disease

Abstract Background: The role of proinflammatory cytokines in pelvic inflammatory disease (PID) is unclear. We therefore determined whether plasma proinflammatory cytokines, interleukin-1β (IL-1β), IL-6, IL-8 and tumor necrosis factor-α (TNF-α) were useful plasma markers in PID patients. Methods: Multiplex bead array analysis was used to measure the plasma levels of proinflammatory cytokines in 50 healthy controls as well as in 41 PID patients before and after routine protocol treatments. Results: IL-1β, IL-6, IL-8 and TNF-α were significantly elevated in PID patients before antibiotic treatment than after treatment. However, IL-8 was not significantly different between healthy controls and PID patients. The relative increase in ratio of IL-6 was significantly correlated with white blood cell count (r=0.448, p=0.003), neutrophil count (r=0.472, p=0.002) and C-reactive protein level (r=0.412, p=0.008). Conclusions: IL-1β, IL-6, IL-8 and TNF-α may play an important role in the pathogenesis of PID. These biomarkers, particularly IL-6, could be useful adjuncts for the clinical diagnosis of PID. Clin Chem Lab Med 2008;46:997–1003.