PubMed Health⌕ Search

Biomedical subjects

Wen-Chi Chen

Publications and source records attributed to Wen-Chi Chen.

64 records · Page 4Linked to original sources

Expression of p16 and cyclin D1 in bladder cancer and correlation in cancer progression.

INTRODUCTION: Gene p16 encodes a cyclin-dependent kinase inhibitor which functions to regulate cyclin D1, cell cycle progression and malignancies. The relationship between p16 and cyclin D1 is thought to alter bladder cancer formation and tumor progression. We aimed to investigate the expression of p16 and cyclin D1 genes in order to evaluate their clinical significance in bladder cancer. MATERIALS AND METHODS: Tissue samples from 67 patients with transitional cell carcinoma were examined with an immunohistochemical stain for the expression of p16 and cyclin D1 genes. The expression rate was compared to 12 normal urinary bladder mucosa samples obtained from transurethral surgery from noncancer patients. RESULTS: The results revealed significant differences between normal bladder mucosa (100%) and cancer tissue (40.3%) for the positive staining of p16 protein (p < 0.001), while positive staining for the cyclin D1 protein in the patient group (67.2%) was significantly higher (p = 0.003) than that in the control group (16.7%). With the progression of tumor grade and clinical staging the positive rate of p16 gene expression increased, whereas, that of cyclin D1 decreased. Expression of the p16 gene in the non-invasive group was greater than that in the invasive group and a lower expression rate of the cyclin D1 gene in the non-invasive group compared to the invasive group. CONCLUSIONS: The results revealed that expression of the p16 gene is inversely proportional to the expression of the cyclin D1 gene. Therefore, abnormal expression of the p16 and cyclin D1 genes play important roles in tumorigenesis and tumor progression.

Adult↗

Relation of vitamin D receptor FokI start codon polymorphism to bone mineral density and occurrence of osteoporosis in postmenopausal women in Taiwan.

BACKGROUND: Osteoporosis is a common disorder with a strong genetic component. Our aim was to evaluate the correlation of the vitamin D receptor FokI start codon polymorphism to bone mineral density and the occurence of osteoporosis. METHODS: We determined the vitamin D receptor FokI start codon polymorphism using polymerase chain reaction-based restriction analysis in 163 postmenopausal women in Taiwan. The vitamin D receptor gene polymorphism was detected by the restriction enzyme FokI, where the F allele indicated the absence of the cuttable site and the f allele its presence. We then related the genotypes to bone mineral density and the occurence of osteoporosis in these women. RESULTS: The allelic frequencies for 163 postmenopausal women in Taiwan were 59.2% for F and 40.8% for f in FokI restriction fragment length polymorphisms. The prevalence of each genotype in the study population was: 42.3% FF, 33.7% Ff and 24% ff. The three genotypic groups differed significantly in bone mineral density at the lumbar spine (P = 0.029). Bone mineral density was highest in the Ff group and lowest in the ff group at the lumbar spine and the femoral neck. The FokI vitamin D receptor genotype showed a significant effect on the prevalence of osteoporosis in the subjects at the lumbar spine. That is, women with genotype ff had a 2.8 times greater risk for osteoporosis (P < 0.05), and those with genotype FF had a 0.8 times greater risk than women with genotype Ff. CONCLUSION: Our findings indicate that the vitamin D receptor FokI start codon polymorphism is associated with reduced bone mineral density and predisposes women to osteoporosis at the lumbar spine.

Alleles↗

Effects of butylated hydroxyanisole and butylated hydroxytoluene on DNA adduct formation and arylamine N-acetyltransferase activity in human bladder tumour cells.

In this study, butylated hydroxyanisole (BHA) and butylated hydroxytoluene (BHT) were used to determine the inhibition of arylamine N-acetyltransferase (NAT) activity and DNA adduct formation in human bladder tumour cell line T-24. The activity of NAT was measured by high-performance liquid chromatography, assaying for the amounts of N-acetyl-2-aminofluorene and N-acetyl-p-aminobenzoic acid and remaining 2-aminofluorene and p-aminobenzoic acid. Human bladder tumour cell line T-24 cytosols and intact cells were used for examining NAT activity and carcinogen-DNA adduct formation. The results demonstrated that NAT activity and 2-aminofluorene-DNA adduct formation in human bladder tumour cells were inhibited and decreased by BHA and BHT in a dose-dependent manner. The effects of BHA and BHT on the values of the apparent K(m) and V(max) also were determined in both systems examined. The results indicated that BHA and BHT decreased the apparent values of K(m) and V(max) from human bladder tumour cells in both cytosol and intact cells.

2-Acetylaminofluorene↗

Protective effect of nicotinamide on neuronal cells under oxygen and glucose deprivation and hypoxia/reoxygenation.

Nicotinamide (vitamin B(3)) reduces the infarct volume following focal cerebral ischemia in rats; however, its mechanism of action has not been reported. After cerebral ischemia and/or reperfusion, reactive oxygen species (ROS) and reactive nitrogen species may be generated by inflammatory cells through several cellular pathways, which can lead to intracellular calcium influx and cell damage. Therefore, we investigated the mechanisms of action of nicotinamide in neuroprotection under conditions of hypoxia/reoxygenation. Results showed that nicotinamide significantly protected rat primary cortical cells from hypoxia by reducing lactate dehydrogenase release with 1 h of oxygen-glucose deprivation (OGD) stress. ROS production and calcium influx in neuronal cells during OGD were dose-dependently diminished by up to 10 mM nicotinamide (p < 0.01). This effect was further examined with OGD/reoxygenation (H/R). Cells were stained with the fluorescent dye 4,6-diamidino-2-phenylindole (DAPI) or antibodies against anti-microtubule-associated protein-2 and cleaved caspase-3. Apoptotic cells were studied using Western blotting of cytochrome c and cleaved caspase-3. Results showed that vitamin B(3) reduced cell injury, caspase-3 cleavage and nuclear condensation (DAPI staining) in neuronal cells under H/R. In addition, nicotinamide diminished c-fos and zif268 immediate-early gene expressions following OGD. Taken together, these results indicate that the neuroprotective effect of nicotinamide might occur through these mechanisms in this in vitro ischemia/reperfusion model.

Animals↗

Glutathione S-transferase M1 gene but not insulin-like growth factor-2 gene or epidermal growth factor gene is associated with prostate cancer.

Prostate cancer is the most common urologic malignancy involving multiple factors. There is evidence that suggests that detoxification enzymes and growth factors may play a role in the formation of prostate cancer. Our aim was to investigate whether polymorphisms of glutathione S-transferase M1 (GST M1), insulin-like growth factor-2 (IGF-2), and epidermal growth factor (EGFR) genes could be used as genetic markers for risk of prostate cancer. In this study, we compared the frequency of the polymorphisms of GST M1, IGF-2, and EGFR genes among 96 patients with prostate cancer and 121 healthy male volunteers from the same geographic area (age, older than 60 years). There was significant difference in the GST M1 genotype between the prostate cancer group and the control group (P=0.042). The GST M1 null genotype was significantly higher in the cancer group (59.4%) than in the control group (45.5%). However, our study did not reveal a significant association between prostate cancer and the distribution of the IGF-2 or EGFR genotypes. This study suggests that the GST M1 gene, but not the IGF-2 or the EGFR genes, may be a risk factor of developing prostate cancer in Taiwan.

Aged↗

p21 gene codon 31 polymorphism is associated with bladder cancer.

The function of p21 is related to cell apoptosis, progression and malignancies. It is thought that p21 is related to cancer formation but is not related to tumor grade. We aimed to investigative the polymorphism of p21 codon 31 as a candidate for the genetic marker of bladder cancer and its progression. The distribution was analyzed in 53 bladder cancer patients, 119 healthy controls in Taiwanese patients. Polymerase chain reaction based restriction analysis was used for the study of the association of p21 codon 31 polymorphism with bladder cancer. There was a significant difference in p21 codon 31 polymorphism between the control and the cancer patients (p < 0.01). The arginine form was prominent in the cancer patient (per copy of the A allele, odds ratio = 2.03, 95% confidence interval = 1.23-3.37). Furthermore, the distribution of this polymorphism was significantly different from non-invasive to invasive bladder cancer (p < 0.05). Serine heterozygote was more prominent in the invasive group with 25 to 1% respectively when compared with the non-invasive group. The polymorphism of p21 codon 31 is associated with bladder cancer. An individual possessing one allele of arginine form in p21 codon 31 has a higher risk of developing bladder cancer than the serine form. Although the mechanism is unclear, our results show p21 gene is associated with tumor grade.

Aged↗

CYP17 gene promoter allelic variant is not associated with prostate cancer.

Prostate cancer is the most common urological malignancy in Taiwan. The formation of prostate cancer has been reported to be associated with androgen. Two key steps in the sex steroid synthesis are mediated by the enzyme cytochrome p450c17alpha which is encoded in the CYP17 gene. Our aim was to investigate whether a polymorphism of CYP17 gene could be used as a genetic marker for associating prostate cancer. In this study, we compared the frequency of the C/T polymorphism of CYP17 gene 5'-UTR promoter region between 93 patients with prostate cancer and 121 healthy male volunteers (age, >60 years). The result revealed no significant association between the CYP17 genotype and prostate cancer (P =.781). Therefore, CYP17 C/T polymorphism is not a valid genetic marker for prostate cancer. Although a possible interaction between CYP17 gene C/T polymorphism and SP-1 transcription factor has been reported in the literature, we did not find any evidence for this the difference among clinical staging, pathological grading, or responsiveness to hormonal therapy in prostate cancer.

3' Untranslated Regions↗

Association of interleukin 1beta and receptor antagonist gene polymorphisms with primary open-angle glaucoma.

PURPOSE: Genetic factors are known to play a role in the etiology of glaucoma. More specifically, the role of the immune system is highly suspected. We evaluated the association between 2 polymorphisms in the interleukin (IL) 1beta gene (IL-1 promoter 511, IL-1 exon 5) and 1 polymorphism in the IL-1 gene receptor antagonist (IL-1Ra) intron 2 with primary open-angle glaucoma (POAG). PATIENTS AND METHODS: Fifty-eight POAG patients and 105 healthy volunteers were enrolled in this study. Analysis based on polymerase chain reaction was used to resolve the 2 IL-1beta polymorphisms and the IL-1Ra intron 2 polymorphism. RESULTS: There were significant differences in the distribution of the IL-1beta exon 5 polymorphism between the POAG patients and the control subjects (p < 0.05). The E2 allele of IL-1beta exon 5 was more frequently found in POAG patients than in healthy patients (odds ratio: 4.224, 95% confidence interval = 1.135-15.717). The distributions of the other 2 polymorphisms, IL-1beta promoter 511 and IL-1Ra intron 2, were not significantly different between the POAG patients and the healthy control group. CONCLUSIONS: The frequency of the E2 allele of the IL-1beta exon 5 polymorphism was high in POAG patients. Therefore the E2 allele can be used as a marker to predict or search for the genetic causes of glaucoma in Chinese POAG patients. Furthermore, we have concluded that the other 2 polymorphisms (IL-1 promoter 511 and IL-1Ra) are not helpful in predicting Chinese POAG.

Adult↗

Arginine and proline alleles of the p53 gene are associated with different locations of gastric cancer.

BACKGROUND/AIMS: Abnormal function of gene p53 is associated with the formation of various cancers including gastric cancer. Recently, p53 codon 72 polymorphism was extensively studied to determine the risk factors responsible for cancer formation using the concept of single nucleotide polymorphism. In this study, we evaluated the risk factors associated with p53 codon 72 polymorphism and gastric cancer carcinogenesis. METHODOLOGY: This study consisted of 51 patients and 59 control subjects. We then evaluated the patient's age, sex, smoking and alcohol consumption habits, tumor location, cell differentiation, lymph node involvement, distant metastasis and tumor stage. Finally the p53 gene codon 72 polymorphism was analyzed by polymerase chain reaction (PCR). The results of polymorphic genotype were stratified with the above risk factors and the associations were analyzed. RESULTS: There was no significant difference between the polymorphic genotypes and the two study groups. However, when the genotypes were further stratified with co-factors, the results revealed a significant association with tumor location. The proline homozygote was more frequent in the patients with gastric cancer at the cardia than in those with cancer at the antral or corpus locations. (55.56% of cardia vs. 14.28% of corpus and antrum, p=0.024). The arginine allele was associated with antral and corpus location of gastric cancer and the proline allele was associated with cardial location (OR=3.25, p=0.026). Also, these polymorphisms do not seem to be associated with age, sex, smoking and alcohol consumption, cell differentiation, lymph node involvement, tumor stage and distant metastasis. CONCLUSIONS: The proline allele at p53 codon 72 is associated with adenocarcinoma of the gastric cardia, and the arginine allele is associated with cancer of the antral and corpus locations. These findings suggest that different genotypes of the p53 gene in different locations of stomach might implicate a different cause of tumor growth.

Alcohol Drinking↗

Glutathione S-transferase M1 gene null genotype and gastric cancer risk in Taiwan.

BACKGROUND/AIMS: Glutathione S-transferases (GST) are involved in the detoxification of many potential carcinogens and appear to play an important role in the protection from carcinogens. The association between different GSTM1 genotypes and gastric cancer risk is still controversial. The aim of this study was to determine the association between the GSTM1-null genotype and gastric cancer risk. METHODOLOGY: A retrospective, hospital-based case-control study of 123 primary gastric cancer patients and 121 healthy controls was conducted to evaluate the presence or absence of the GSTM1 gene from peripheral blood samples by a PCR-based method. RESULTS: The frequency of the GSTM1-null was 59.3% in the gastric cancer group and 45.5% in the control group. An increase in risk for gastric cancer was found among carriers of GSTM1-null genotype. The odds ratio (OR) was 1.752, with 95% confidence interval (CI) = 2.963 approximately 1.035. CONCLUSIONS: GSTM1-null polymorphism was associated with genetic susceptibility of gastric cancer in Taiwan.

Adult↗