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Sheng-Yow Ho

Publications and source records attributed to Sheng-Yow Ho.

13 recordsLinked to original sources

Room scatter factor modelling and measurement error analysis of 192Ir HDR calibration by a Farmer chamber.

We introduce an empirical formula to directly calculate the room scatter factor in the calibration of (192)Ir HDR using a Farmer chamber. Compared to the data of Selvam et al (2001 Phys. Med. Biol. 46 2299), our formula is accurate to within 0.3%. Our method saves time because the room scatter can be obtained in one calculation rather than being deduced through a series of setups of different source-chamber distances. It could also be cost effective because a calibration jig might be no longer necessary. We only need to position the applicator and chamber at a fixed space in air and measure its distance. We also analysed the effects of two possible errors arising from ignoring the room scatter and the measurement error of the source-chamber distance. We recommend that the source-chamber distance should be at least 10 cm.

Biophysical Phenomena↗

Evaluation of the associations between the single nucleotide polymorphisms of the promoter region of the tumor necrosis factor-alpha gene and nasopharyngeal carcinoma.

BACKGROUND: Tumor necrosis factor-alpha (TNF-alpha) is a pro-inflammatory cytokine and may act as an endogenous tumor promoter. Single nucleotide polymorphisms (SNPs) of the TNF-alpha gene promoter region have been found to be associated with certain cancers. We conducted a case-control study to evaluate the association between these SNPs and nasopharyngeal carcinoma (NPC). METHODS: We used polymerase chain reaction followed by restriction fragment length polymorphism analysis to determine the -308 TNF-alpha promoter genotypes of 89 NPC patients and 360 healthy controls. In 23 NPC patients and 50 controls, we determined the sequence from -1065 to -101 nucleotides of the TNF-alpha gene promoter region to detect SNPs. RESULTS: In comparison with the controls, the NPC patients had higher proportions of men and carriage of IgA antibodies against the capsid antigen of Epstein-Barr virus, but had a similar carrier rate of the -308A allele (odds ratio [OR], 1.2; 95% confidence interval [CI], 0.7-2.0). The carriage of the -308A allele was not associated with the occurrence of NPC in comparison with -308G homozygosity. We also found no significant differences in the distributions of allelic variants of the -1031, -863, -857, and -806 loci of the TNF-alpha promoter region, but observed a lower carrier rate of the novel -806T allele in the NPC patients (OR, 0.3; 95% Cl, 0.0-2.9). CONCLUSION: Allelic variants of the TNF-alpha promoter gene may not be used as biomarkers of susceptibility to NPC. The role of the -806T allele needs to be studied further.

Adult↗

Staurosporine modulates radiosensitivity and radiation-induced apoptosis in U937 cells.

PURPOSE: The present study aims at investigating the involvement of several genes in the cell cycle distribution and apoptosis in U937 cells, a cell line lacking functional p53 protein, after combined treatment with staurosporine and irradiation. MATERIALS AND METHODS: Using a DNA fragmentation assay, flow cytometry and western blot analysis, the molecular basis for the effects of staurosporine in combination with the irradiation of leukemia cells was investigated. RESULTS: Our results indicated that combined treatment led to an increased apoptotic cell death in U937 cells, which is correlated with the phosphorylation of the V-Jun sarcoma virus 17 oncogene homolog (c-JUN) NH(2)-terminal kinase protein (JNK), the activation of caspases, the increase in B cell leukemia/lymphoma 2 (Bcl-2) associated X protein (Bax), the decrease in Bcl xL protein (Bcl-XL) levels, the loss of mitochondria membrane potential and the release of cytochrome c. CONCLUSIONS: Abrogation of the G2 checkpoint should be an effective strategy against p53-deficient leukemia cells to irradiation-induced cell killing.

Apoptosis↗

Mechanisms of apoptosis induction and cell cycle regulation in irradiated leukemia U937 cells and enhancement by arsenic trioxide.

Apoptosis is a common mode of cell death after exposure of tumor cells to radiation and/or chemotherapy. The factors that determine the rate of induction of apoptosis are generally related to the functioning of cell cycle checkpoints. In the present study, we investigated the involvement of several genes in cell cycle redistribution and induction of apoptosis in U937 cells after low and high doses of radiation. Activation of CDC2 was observed after both low and high doses of radiation in U937 cells that underwent apoptosis. Expression of CDK2, CDC2 and cyclin A was induced rapidly in the process of radiation-induced apoptosis. In addition, we investigated the use of a clinically relevant dose of radiation to promote As2O3-induced apoptosis in U937 cells. We found that combining radiation and As2O3 may be a new and more effective means of cancer treatment.

Apoptosis↗

Increased expression of nitric oxide synthase and cyclooxygenase-2 is associated with poor survival in cervical cancer treated with radiotherapy.

PURPOSE: To investigate the expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) in cervical cancer and their association with clinical outcome in patients treated with radical radiotherapy. METHODS AND MATERIALS: One hundred sixty-seven consecutive patients with FIGO Stages IB-IVA squamous cell cervical cancer underwent radical radiotherapy, including external-beam radiotherapy or high-dose-rate brachytherapy, or both, between 1989 and 2002. Immunohistochemical studies of their formalin-fixed, paraffin-embedded tissues were performed. Univariate and multivariate analyses were performed to identify and evaluate the effects of the factors affecting patient survival. RESULTS: Positive immunostainings of iNOS and COX-2 were observed in 58.7% and 64.1% of the participants, respectively. The expression of both iNOS and COX-2 was positively correlated (Spearman correlation coefficient = 0.49, p < 0.01), and their overexpression provided independent predictors of distant metastasis (odds ratio = 5.22 and 10.07, respectively; p < 0.01 for all). iNOS- and COX-2-expressing patients had significantly shorter disease-free survival (p < 0.01, both) and cause-specific overall survival (p = 0.01, p < 0.01, respectively). Patients with iNOS-positive/COX-2-positive tumors had the poorest survival rates. Coexpression of iNOS/COX-2, together with bulky tumor and advanced stage were independent prognostic factors for disease-free survival. CONCLUSION: Overexpression of iNOS or COX-2 or both was associated with decreased survival and a greater propensity to metastasize in cervical cancer patients treated with radiotherapy. Coexpression of iNOS and COX-2 may represent a useful biologic marker in patients receiving radical radiotherapy for cervical cancer.

Adult↗

Merkel cell carcinoma in patients with long-term ingestion of arsenic.

Merkel cell carcinoma (MCC) is a rare primary neuroendocrine carcinoma of the skin, mostly occurring late in life on sun-exposed body parts. Little is known about the specific etiological factors in the pathogenesis of MCC. A previous report indicated that arsenic exposure might cause MCC, which might be another specific type of skin cancer associated with arsenic exposure. On the southwest coast of Taiwan, high arsenic levels in artesian well water have been documented, and various diseases associated with arsenic exposure have been found to be prevalent in this area. We report two pathologically confirmed cases of MCC in patients who had histories of long-term ingestion of arsenic from drinking water. The tumors were on the anterior chest wall, an area less exposed to the sun, in both cases. The literature on the dose-response relationship between arsenic exposure and MCC is limited. We estimated that the total arsenic ingested by these two cases was around 14.7 and 2.6 gm, respectively. We also tried to assess the cancer risk on the basis of the estimated doses of arsenic exposure and the cancer risk model developed by the U.S. Environmental Protection Agency (EPA). The estimated lifetime target cancer risk was 1.3 x 10(-2) in Case 1 and 2.3 x 10(-3) in Case 2. Both are much higher than the 10(-6) upper limit on lifetime cancer risk put forth by the U.S. EPA health protection standard. We believe that arsenic intoxication played an important role in the carcinogenic process of MCC in our cases.

Aged↗

Prognostic implications of Fas-ligand expression in nasopharyngeal carcinoma.

BACKGROUND: In nasopharyngeal carcinoma (NPC), Fas-ligand (Fas-L)-mediated apoptosis might contribute to the immune privilege of tumors. In some cancers, dysregulation of Fas-L protein in tumors might lead to disease progression. The purpose of this study was to evaluate the correlations between Fas-L expression and the clinical outcomes in patients with NPC. METHODS: We recruited 78 patients with primary NPC, classified clinical stages according to the 1997 American Joint Committee on Cancer staging system, and assessed Fas-L with immunohistochemical methods. RESULTS: Forty-one (53%) of 78 patients were Fas-L-positive. The prevalence was 0%, 57%, 58%, and 82% from stages I to IV, respectively (p <.001). Fas-L expression was associated with the N classification (p=.05) but not the T classification. Patients with positive Fas-L expression had a lower rate of disease-free survival and overall survival (p=.01 for all log-rank tests). CONCLUSION: Patients with NPC with Fas-L-positive tumors had higher clinical stages and lymph node metastasis at diagnosis and poorer disease-free survival and overall survival; therefore, Fas-L expression may be a potential biomarker of prognosis.

Adolescent↗

Increased risk of developing hepatocellular carcinoma associated with carriage of the TNF2 allele of the -308 tumor necrosis factor-alpha promoter gene.

BACKGROUND AND AIMS: Tumor necrosis factor-alpha (TNF-alpha) is a cytokine that may act as an endogenous tumor promoter. A genetic polymorphism of TNF-alpha at position -308 of the promoter region, which includes TNF1 (-308G) and TNF2 (-308A) alleles, has been found to be associated with susceptibility to various types of cancer. We conducted a study to evaluate the association between this polymorphism and hepatocellular carcinoma (HCC). METHODS: We recruited 74 HCC patients and 289 healthy controls, and determined their -308 TNF-alpha promoter genotypes through polymerase chain reaction followed by electrophoresis. RESULTS: Carriage of the TNF2 allele was associated with an increased risk of HCC (odds ratio [OR] = 3.5; 95% confidence interval [CI]:[2.1, 6.0]), and a trend toward a significant increase in the risk of developing HCC was observed from TNF1/TNF1, TNF1/TNF2, to TNF2/TNF2 genotypes (p < 0.01). After adjustment for gender, age, and markers of hepatitis B and C, the OR of developing HCC associated with TNF2 allele carriage was 5.3 (95% CI: [2.3, 12.1]; p < 0.01) CONCLUSIONS: Carriage of the TNF2 allele is a significant predictor of HCC independent of hepatitis B and C, and therefore it may be used as a biomarker for susceptibility to HCC.

Adult↗

Hepatic angiosarcoma presenting as hepatic rupture in a patient with long-term ingestion of arsenic.

Hepatic angiosarcoma (HAS) is a rare primary mesenchymal malignancy of liver with close association to arsenic intoxication. Although the southwest coastal area of Taiwan is well known for its prevalence of arsenic intoxication from drinking well water, few cases of HAS associated with arsenic ingestion have been reported. We report a case of HAS complicated by spontaneous hepatic rupture in a 68-year-old female farmer who presented with acute onset of abdominal pain and shock. The arsenic level in her drinking water had been found to be 0.12 ppm at her childhood home and 0.005 ppm at her residence from age 21 to 68 years. The total ingested arsenic was estimated to be 1.9 g, and the latent period was about 25 years with a weighted mean exposure of 0.12 mg/day. We also reviewed data collected by the National Cancer Registry Program from 1981 to 1999 and identified 25 additional reported cases. The median age of these patients was 55 years, and the male-to-female ratio was 1.9 (17:9). Whereas no case was found during this period in the blackfoot disease (BFD) endemic area, a hyperendemic area of arsenic intoxication in Taiwan, this case demonstrates the existence of cases of HAS associated with exposure to high levels of arsenic near the BFD area in Taiwan.

Adult↗

Modelling the wedge shape for the virtual wedge.

We present a method to model the virtual wedge shape in a 3D treatment planning system as a physical wedge. The virtual wedge shape was determined using the measured dose profile of the virtual wedge at a chosen reference depth. The differences between the calculated and the measured dose profiles for the virtual wedge were within 0.5% at the reference depth, and within 2.5% at other depths. This method provides a fast and accurate way to implement the virtual wedge into our planning system for any wedge angles. This method is also applicable to model the physical wedge shapes with comparable good results.

Biophysical Phenomena↗

Skin tumor-promoting potential and systemic effects of pentachlorophenol and its major metabolite tetrachlorohydroquinone in CD-1 Mice.

The mouse skin carcinogenesis model provides a conceptual framework to study the carcinogenesis process. It has been used extensively to assess whether a chemical or physical agent carries a carcinogenic hazard to humans and to define the mechanism involved with the carcinogenic effects. We conducted a study to evaluate whether the tumor-promoting activity of pentachlorophenol (PCP) is mainly from its major metabolite tetrachlorohydroquinone (TCHQ). We applied the mouse skin model to CD-1 mice and the results showed that PCP and TCHQ are much weaker promoters than 12-O-tetradecanoylphorbol-13-acetate (TPA) in mouse skin during a 25-wk experiment. Both PCP and TCHQ could induce mice skin epidermal hyperplasia and proliferating cell nuclear antigen (PCNA) labeling index in the epidermis. However, TCHQ caused a more significant induction of epidermal hyperplasia and PCNA positive cells than PCP. Topical application of PCP, but not TCHQ, induced significant organ enlargement and lymphoma in mice, whereas short-term treatment of TCHQ increased tumor necrosis factor-alpha (TNF-alpha) gene expression in mouse skin. We did not observe a significant association between the carcinogenic process and serum TNF-alpha or interleukin-1 beta (IL-1 beta) levels in mice.

9,10-Dimethyl-1,2-benzanthracene↗

Nutritional predictors of survival in terminally ill cancer patients.

BACKGROUND AND PURPOSE: Malnutrition can affect the prognosis of terminally ill patients, but over-treatment of malnutrition can worsen patients' quality of life. Decisions on nutrition and the supply of fluids to terminally ill patients are complex, and the identification of useful clinical indicators is needed. This study evaluated the relationships between various nutritional indices and survival of terminally ill cancer patients. METHODS: We recruited terminally ill patients from a teaching hospital between February 2000 and January 2001. All of the 145 candidates were cancer patients, 109 (75%) of whom agreed to participate. Nutritional assessments including physical examination, anthropometric measurements, and biochemical profiles were performed on admission. RESULTS: Univariate analyses showed that triceps skin-fold thickness (TSF) and midarm muscle circumference were significant predictors of survival. Poor survival was associated with prealbumin </= 100 mg/L (hazard ratio [HR], 1.5; 95% confidence interval [CI], 1.1 to 2.3; p = 0.03), asparate transaminase (AST) > 45 U/L (HR, 1.6; 95% CI, 1.1 to 2.3; p = 0.03), alkaline phosphatase > 120 U/L (HR, 1.6; 95% CI, 1.1 to 2.5; p = 0.02), creatinine > 1.4 mg/dL (HR, 1.9; 95% CI, 1.2 to 3.2; p = 0.01), and blood urea nitrogen (BUN) > 20 mg/dL (HR, 1.9; 95% CI, 1.3 to 2.8; p < 0.01) at admission. Multivariate analyses found that TSF < 25% of the nomogram (HR, 2.9; 95% CI, 1.6 to 5.3; p < 0.01), prealbumin </= 100 mg/L (HR, 2.2; 95% CI, 1.4 to 3.5; p < 0.01), AST > 45 U/L (HR, 2.0; 95% CI, 1.3 to 3.2; p = 0.01), and BUN > 20 mg/dL (HR, 2.8; 95% CI, 1.7 to 4.5; p < 0.01) were independent predictors of poor survival. CONCLUSIONS: This study found that nutritional status was associated with the survival of terminally ill cancer patients. Both TSF and prealbumin appeared to be useful predictors that may help set strategies to improve palliative care. Because predictors of survival are not necessarily factors that actually influence survival, further studies should be conducted to evaluate the usefulness of these prognostic indicators in clinical practice.

Adult↗

Lipid peroxidation and cell death mechanisms in pulmonary epithelial cells induced by peroxynitrite and nitric oxide.

Nitric oxide (NO) is an environmental pollutant found in smog and cigarette smoke. Recently, NO has been discovered to act as a molecular messenger, mediating various physiological functions. However, when an excess of NO is present, cytotoxic and mutagenic effects can also be induced. The reaction of NO with superoxide results in the formation of peroxynitrite (ONOO(-)), which decomposes into the hydroxyl radical and nitrogen dioxide. Both of them are potent oxidant species that may initiate and propagate lipid peroxidation. In the present study, we examined the effects of NO and ONOO(-) on the induction of lipid peroxidation and cell death mechanisms in rats and in A549 pulmonary epithelial cells. The results showed that ONOO(-) is able to induce lipid peroxidation in pulmonary epithelial cells in a dose-dependent manner. 8-Epi-prostaglandin F(2)(alpha) can serve as a good biomarker of lipid peroxidation both in vitro and in vivo. Postmitotic apoptosis was found in A549 cells exposed to NO, whereas ONOO(-) induced cell death more characteristic of necrosis than apoptosis. Apoptosis that occurred in cells may be related to the dysfunction of mitochondria, the release of cytochrome c into cytosol, and the activation of caspase-9. The relationship between caspase activation and the cleavage of other death substrates during postmitotic apoptosis in A549 cells needs further investigation.

Animals↗