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1.
J Pineal Res ; 60(2): 142-54, 2016 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-26514342

RESUMO

Peritoneal dissemination of tumor has high mortality and is associated with the loss of epithelial features, acquisition of motile mesenchymal morphology characteristics, and invasive properties by tumor cells. Melatonin is an endogenously produced molecule in all plant species that is known to exert antitumor activity, but to date, its underlying mechanisms and antiperitoneal metastasis efficacy is not well defined. This study determined the antiperitoneal dissemination potential of melatonin in vivo and assessed its association with the inhibition of epithelial-to-mesenchymal transition (EMT) signaling mechanism by endoplasmic reticulum (ER) stress, which may be a major molecular mechanism of melatonin against cancer. The results demonstrate that melatonin inhibited peritoneal metastasis in vivo and activated ER stress in Cignal ERSE Reporter Assay, organelle structure in transmission electron microscopy images, calpain activity, and protein biomarkers like p-elf2α. Moreover, the overexpression of transcription factor C/EBPß in gastric cancer interacted with NFκB and further regulates COX-2 expression. These were dissociated and downregulated by melatonin, as proven by immunofluorescence imaging, immunoprecipitation, EMSA, and ChIP assay. Melatonin or gene silencing of C/EBPß decreased the EMT protein markers (E-cadherin, Snail, and Slug) and Wnt/beta-catenin activity by Topflash activity, and increased ER stress markers. In an animal study, the results of melatonin therapy were consistent with those of in vitro findings and attenuated systemic proangiogenesis factor production. In conclusion, C/EBPß and NFκB inhibition by melatonin may impede both gastric tumor growth and peritoneal dissemination by inducing ER stress and inhibiting EMT.


Assuntos
Proteína beta Intensificadora de Ligação a CCAAT/metabolismo , Calpaína/metabolismo , Estresse do Retículo Endoplasmático/efeitos dos fármacos , Transição Epitelial-Mesenquimal/efeitos dos fármacos , Melatonina/farmacologia , NF-kappa B/metabolismo , Proteínas de Neoplasias/metabolismo , Neoplasias Peritoneais/tratamento farmacológico , Proteólise/efeitos dos fármacos , Transdução de Sinais/efeitos dos fármacos , Neoplasias Gástricas/tratamento farmacológico , Animais , Proteína beta Intensificadora de Ligação a CCAAT/genética , Calpaína/genética , Linhagem Celular Tumoral , Inativação Gênica , Humanos , Camundongos , NF-kappa B/genética , Proteínas de Neoplasias/genética , Neoplasias Peritoneais/genética , Neoplasias Peritoneais/metabolismo , Neoplasias Peritoneais/patologia , Neoplasias Peritoneais/secundário , Neoplasias Gástricas/genética , Neoplasias Gástricas/metabolismo , Neoplasias Gástricas/patologia
2.
BMC Cancer ; 14: 112, 2014 Feb 20.
Artigo em Inglês | MEDLINE | ID: mdl-24555415

RESUMO

BACKGROUND: Resistin, adipocyte-secreting adipokine, may play critical role in modulating cancer pathogenesis. The aim of this study was to investigate the effects of resistin on HCC adhesion to the endothelium, and the mechanism underlying these resistin effects. METHODS: Human SK-Hep1 cells were used to study the effect of resistin on intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) expressions as well as NF-κB activation, and hence cell adhesion to human umbilical vein endothelial cells (HUVECs). 5-Aminoimidazole-4-carboxamide 1-ß-D-ribofuranoside (AICAR), an AMP-activated protein kinase (AMPK) activator, was used to determine the regulatory role of AMPK on HCC adhesion to the endothelium in regard to the resistin effects. RESULTS: Treatment with resistin increased the adhesion of SK-Hep1 cells to HUVECs and concomitantly induced NF-κB activation, as well as ICAM-1 and VCAM-1 expressions in SK-Hep1 cells. Using specific blocking antibodies and siRNAs, we found that resistin-induced SK-Hep1 cell adhesion to HUVECs was through NF-κB-regulated ICAM-1 and VCAM-1 expressions. Moreover, treatment with AICAR demonstrated that AMPK activation in SK-Hep1 cells significantly attenuates the resistin effect on SK-Hep1 cell adhesion to HUVECs. CONCLUSIONS: These results clarify the role of resistin in inducing HCC adhesion to the endothelium and demonstrate the inhibitory effect of AMPK activation under the resistin stimulation. Our findings provide a notion that resistin play an important role to promote HCC metastasis and implicate AMPK may be a therapeutic target to against HCC metastasis.


Assuntos
Proteínas Quinases Ativadas por AMP/metabolismo , Carcinoma Hepatocelular/enzimologia , Adesão Celular/fisiologia , Neoplasias Hepáticas/enzimologia , Resistina/fisiologia , Adesão Celular/efeitos dos fármacos , Ativação Enzimática/efeitos dos fármacos , Ativação Enzimática/fisiologia , Células Endoteliais da Veia Umbilical Humana/efeitos dos fármacos , Células Endoteliais da Veia Umbilical Humana/enzimologia , Humanos
3.
ScientificWorldJournal ; 2014: 408613, 2014.
Artigo em Inglês | MEDLINE | ID: mdl-24982948

RESUMO

The demands of precise time/phase synchronization have been increasing recently due to the next generation of telecommunication synchronization. This paper studies the issues that are relevant to distributing accurate time/phase over optical transport network (OTN). Each node and link can introduce asymmetry, which affects the adequate time/phase accuracy over the networks. In order to achieve better accuracy, protocol level full timing support is used (e.g., Telecom-Boundary clock). Due to chromatic dispersion, the use of different wavelengths consequently causes fiber link delay asymmetry. The analytical result indicates that it introduces significant time error (i.e., phase offset) within 0.3397 ns/km in C-band or 0.3943 ns/km in L-band depending on the wavelength spacing. With the proposed scheme in this paper, the fiber link delay asymmetry can be compensated relying on the estimated mean fiber link delay by the Telecom-Boundary clock, while the OTN control plane is responsible for processing the fiber link delay asymmetry to determine the asymmetry compensation in the timing chain.


Assuntos
Telecomunicações/instrumentação , Redes de Comunicação de Computadores/instrumentação , Desenho de Equipamento , Tecnologia de Fibra Óptica/instrumentação
4.
J Cell Physiol ; 227(2): 697-704, 2012 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-21465475

RESUMO

Both the urokinase-type plasminogen activator (uPA) and the uPA receptor (uPAR) play important roles with regard to hepatocellular carcinoma (HCC) progression and metastasis. Notably, the stromal cell-derived factor-1 (SDF-1) is an important chemokine involved in HCC pathology. However, the influence of uPA on SDF-1 expression in human HCC cells remains unknown. We investigated the mechanisms underlying the modulation of SDF-1 expression through uPA stimulation in human HCC SK-Hep-1 cells. SK-Hep-1 cells stimulation with uPA induced increases in the expression and secretion of SDF-1. By using specific inhibitors and small interfering RNA, we have demonstrated that the activation of extracellular signal-related kinase (ERK) and c-Jun-NH(2)-terminal kinase (JNK) pathways are critical for uPA-induced SDF-1 expression. Transcription factor ELISA and chromatin immunoprecipitation assays suggest that uPA increase Sp1- and AP-1-DNA-binding activities in SK-Hep-1 cells. Inhibition of Sp1 and AP-1 activations by specific siRNAs blocked the uPA-induced SDF-1 promoter activity and expression. The effect of uPA on SK-Hep-1 signaling and SDF-1 expression is mediated by uPAR. In summary, our findings serve to elucidate the uPA/uPAR downstream signaling, providing new insight into the function of uPA in HCC cells.


Assuntos
Carcinoma Hepatocelular/metabolismo , Quimiocina CXCL12/metabolismo , Regulação Neoplásica da Expressão Gênica/fisiologia , Neoplasias Hepáticas/metabolismo , Ativador de Plasminogênio Tipo Uroquinase/farmacologia , Linhagem Celular Tumoral , Quimiocina CXCL12/genética , MAP Quinases Reguladas por Sinal Extracelular/genética , MAP Quinases Reguladas por Sinal Extracelular/metabolismo , Regulação Enzimológica da Expressão Gênica/fisiologia , Humanos , MAP Quinase Quinase 4/genética , MAP Quinase Quinase 4/metabolismo , Fosforilação , Regiões Promotoras Genéticas , Interferência de RNA , RNA Interferente Pequeno , Receptores de Ativador de Plasminogênio Tipo Uroquinase/metabolismo , Transdução de Sinais
5.
Pharm Biol ; 50(3): 291-396, 2012 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-22085220

RESUMO

CONTEXT: Tournefortia sarmentosa Lam. (Boraginaceae), a Chinese herbal medicine, is commonly used as a detoxicant or anti-inflammatory agent. OBJECTIVE: As acetaminophen (APAP) is a well-known hepatotoxin, we investigated the effect of the aqueous extract of the T. sarmentosa on APAP-induced hepatotoxicity in vivo and in vitro. MATERIALS AND METHODS: Levels of liver function markers serum glutamate oxaloacetate transaminase (SGOT), glutamate pyruvate transaminase (SGPT), and alkaline phosphatase (ALP), inflammatory markers tumor necrosis factor (TNF)-α, interleukin (IL)-1b, and IL-6 in serum, and antioxidant enzymes catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GPx), as well as lipid peroxidation were determined. RESULTS: T. sarmentosa significantly reduced the elevated liver function (SGOT, SGPT, and ALP, p < 0.01) and inflammatory markers (TNF-α, IL-1ß, and IL-6, p < 0.01) in serum of APAP-intoxicated rats. Malondialdehyde level (p < 0.05) and antioxidant enzyme levels (CAT, SOD, and GPx, p < 0.05) were also reduced in APAP-intoxicated rats treated with T. sarmentosa. Incubation of rat hepatocyte cell line clone-9 cells with APAP reduced cell viability and increased the extent of lipid peroxidation. APAP stimulation also reduced the level of glutathione (GSH) and caused reduction in the activities of the antioxidant enzymes, CAT, SOD, and GPx. Pretreatment of hepatocytes with T. sarmentosa aqueous extract before and during APAP stimulation attenuated the extent of lipid peroxidation, increased cell viability and GSH level, and enhanced the activities of antioxidant enzymes. DISCUSSION AND CONCLUSION: These data suggest that the aqueous extract of T. sarmentosa can prevent APAP-induced hepatotoxicity.


Assuntos
Acetaminofen/toxicidade , Boraginaceae/química , Doença Hepática Induzida por Substâncias e Drogas/prevenção & controle , Extratos Vegetais/farmacologia , Analgésicos não Narcóticos/toxicidade , Animais , Antioxidantes/metabolismo , Linhagem Celular , Sobrevivência Celular/efeitos dos fármacos , Doença Hepática Induzida por Substâncias e Drogas/patologia , Hepatócitos/efeitos dos fármacos , Hepatócitos/patologia , Técnicas In Vitro , Peroxidação de Lipídeos/efeitos dos fármacos , Testes de Função Hepática , Masculino , Medicina Tradicional Chinesa , Estresse Oxidativo/efeitos dos fármacos , Ratos , Ratos Wistar
6.
Anticancer Res ; 39(6): 2791-2797, 2019 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-31177115

RESUMO

BACKGROUND/AIM: The aim of this study was to examine the role of caspase-8 rs3834129 polymorphism on colorectal cancer (CRC) risk in Taiwanese CRC patients and healthy controls. MATERIALS AND METHODS: The caspase-8 rs3834129 (-652 6N insertion/deletion) polymorphic genotypes were analyzed in 362 patients with CRC and the same number of age- and gender-matched healthy subjects. The interaction of caspase-8 rs3834129 genotypes with personal behaviors and clinicopathological features were also examined. RESULTS: The percentage of variants ID and DD for caspase-8 rs3834129 genotype were 37.6 and 5.8% in CRC group and 39.0 and 6.6% in the control group, respectively (p for trend=0.7987). The allelic frequency distribution analysis showed that caspase-8 rs3834129 D allele conferred a non-significant lower susceptibility for CRC compared with I allele (OR=0.92, 95%CI=0.74-1.20, p=0.5063). There was no obvious link between caspase-8 rs3834129 genotype and CRC risk among ever-smokers, non-smokers, non-alcohol drinkers or alcohol drinkers. No statistically significant correlation was observed between caspase-8 rs3834129 genotypic distribution and age, gender, tumor size, location or metastasis status. CONCLUSION: Overall, caspase-8 rs3834129 genotypes may not serve as predictors for CRC risk or prognosis.


Assuntos
Caspase 8/genética , Neoplasias Colorretais/genética , Estudos de Associação Genética/métodos , Técnicas de Genotipagem/métodos , Polimorfismo de Nucleotídeo Único , Estudos de Casos e Controles , Feminino , Frequência do Gene , Predisposição Genética para Doença , Genótipo , Humanos , Masculino , Prognóstico , Taiwan
7.
Cancer Genomics Proteomics ; 15(3): 207-212, 2018.
Artigo em Inglês | MEDLINE | ID: mdl-29695403

RESUMO

BACKGROUND/AIM: Matrix metalloproteinases (MMPs) play important roles in inflammation and carcinogenesis, but the genotypic role of MMP-7 has never been investigated in colorectal cancer (CRC) among the Taiwanese. Therefore, in this study we aimed to evaluate the contribution of MMP-7 genotypes to the risk of CRC in Taiwan. MATERIALS AND METHODS: In this case-control study, MMP-7 A-181G and C-153T promoter genotypes were determined and their association with CRC risk were investigated among 362 CRC patients and 362 age- and gender-matched healthy controls. In addition, the interaction of MMP-7 genotypes and personal behaviors were also examined. RESULTS: The percentages of variant AG and GG for MMP-7 A-181G genotypes were 10.5% and 1.7% in the CRC group and 11.9% and 2.2% in the control group, respectively (p for trend=0.7145). The allelic frequency distribution analysis showed that the variant G allele of MMP-7 A-181G conferred a slight but non-significant decreased CRC susceptibility to the wild-type C allele (odds ratio (OR)=0.86, 95% confidence interval (CI)=0.64-1.31, p=0.37). Taiwanese all harbour the CC genotype at MMP-7 C-153T. As for the gene-lifestyle interaction, there were no obvious joint effects of MMP-7 A-181G genotype on the risk of CRC among ever smoker, alcohol drinker, non-smoker or non-drinker subgroups. No statistically significant correlation was observed between MMP-7 A-181G genotypic distributions and age, gender, tumor size, location or metastasis status. CONCLUSION: The genotypes of MMP-7 A-181G may play an indirect role in determining personal susceptibility to CRC and prognosis. The further genotyping work on MMP-7 and other genes (such as other MMPs, oncogenes and tumor suppression genes) on CRC susceptibility and prognosis, should be taken into consideration spontaneously in the precision medicine era.


Assuntos
Neoplasias Colorretais/genética , Predisposição Genética para Doença , Metaloproteinase 7 da Matriz/genética , Polimorfismo de Nucleotídeo Único , Consumo de Bebidas Alcoólicas , Estudos de Casos e Controles , Neoplasias Colorretais/epidemiologia , Feminino , Genótipo , Humanos , Masculino , Pessoa de Meia-Idade , Prognóstico , Regiões Promotoras Genéticas , Fatores de Risco , Fumar , Taiwan/epidemiologia
8.
Anticancer Res ; 38(10): 5671-5677, 2018 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-30275186

RESUMO

BACKGROUND/AIM: Matrix metalloproteinase-7 (MMP-7) plays an important role in metastasis behavior of cancer cells, and overexpression of MMP-7 has been associated with poor prognosis in non-small cell lung cancer. However, the contribution of various genotypes of MMP-7 has not yet been investigated in lung cancer in Taiwan. Therefore, this study aimed to investigate the association of MMP-7 genotypes with lung cancer risk among the Taiwanese. MATERIALS AND METHODS: In this hospital-based case-control study, genotypes and distributions at two promoter sites of MMP-7, A-181G and C-153T, were determined, and their association with lung cancer risk in Taiwan was evaluated among 358 lung cancer patients and 716 age- and gender-matched healthy control individuals. In addition, the interaction of MMP-7 genotypes and smoking status were also examined. RESULTS: The percentages of variant AG and GG at MMP-7 A-181G in the lung cancer group were similar to the control group (12.8% and 2.3% vs. 11.3% and 1.5%, respectively; ptrend=0.5294). The allelic frequency distribution analysis showed that the variant G allele at MMP-7 A-181G conferred non-significant elevated lung cancer risk compared to the wild-type A allele [odds ratio (OR)=1.18, 95% confidence interval (CI)=0.85-1.66, p=0.2289]. As for the genotypes of MMP-7 C-153T, all the studied Taiwanese population was of CC genotype. Furthermore, there was no obvious joint effect of MMP-7 A-181G genotype and smoking status on the lung cancer risk. No statistically significant correlation was observed between MMP-7 A-181G genotype distributions and gender. CONCLUSION: There was no evidence that the genotypes of MMP-7 A-181G may act as a biomarker in determining personal susceptibility to lung cancer in Taiwan.


Assuntos
Carcinoma Pulmonar de Células não Pequenas/genética , Predisposição Genética para Doença , Neoplasias Pulmonares/genética , Metaloproteinase 7 da Matriz/genética , Polimorfismo de Nucleotídeo Único , Regiões Promotoras Genéticas , Adenocarcinoma/genética , Adenocarcinoma/patologia , Idoso , Biomarcadores Tumorais/genética , Carcinoma Pulmonar de Células não Pequenas/patologia , Carcinoma de Células Escamosas/genética , Carcinoma de Células Escamosas/patologia , Estudos de Casos e Controles , Feminino , Seguimentos , Genótipo , Humanos , Neoplasias Pulmonares/patologia , Masculino , Pessoa de Meia-Idade , Prognóstico , Fatores de Risco , Taxa de Sobrevida
9.
In Vivo ; 32(3): 487-491, 2018.
Artigo em Inglês | MEDLINE | ID: mdl-29695550

RESUMO

BACKGROUND/AIM: The family of matrix metalloproteinases (MMPs) are responsible for the homeostasis of extracellular matrix components and their genetic polymorphisms may be associated with cancer susceptibility. The serum levels of MMP-1 have been reported to be lower in breast cancer patients than healthy subjects. In the current study, we aimed at investigating the contribution of a polymorphism in the promoter region of MMP-1 to breast cancer in Taiwan. MATERIALS AND METHODS: The MMP-1 rs1799705 polymorphic genotypes were genotyped among 1,232 breast cancer patients and 1,232 healthy controls by the typical polymerase chain reaction-restriction fragment length polymorphism methodology. RESULTS: The percentages of 2G/2G, 1G/2G, and 1G/1G for MMP1 -1607 genotypes were 35.4, 40.6 and 24.0% in the breast cancer group and 34.1, 43.6, and 22.3% in the healthy control group (p trend=0.3025), respectively. The odds ratios (ORs) after adjusting for age, smoking and alcohol drinking status for those carrying 1G/2G and 1G/1G genotypes at MMP1 -1607 were 0.93 (95%CI=0.76-1.11, p=0.2390) and 1.01 (95%CI=0.77-1.23, p=0.7377), respectively, compared to those carrying the wild-type 2G/2G genotype. Supporting this finding, the adjusted OR for those carrying the 1G allele at MMP-1 -1607 was 1.03 (95%CI=0.91-1.18, p=0.8860), compared to those carrying the wild-type 2G allele. Our findings suggest that the polymorphic genotypes at MMP1 promoter -1607 investigated in the current study, may not play a major role in determining cancer susceptibility to breast cancer in Taiwan. Other early diagnostic and predictive markers are urgently needed for personalized and precise breast cancer detection and therapy.


Assuntos
Neoplasias da Mama/genética , Predisposição Genética para Doença , Metaloproteinase 1 da Matriz/genética , Polimorfismo de Nucleotídeo Único , Regiões Promotoras Genéticas , Adulto , Idoso , Alelos , Neoplasias da Mama/patologia , Estudos de Casos e Controles , Feminino , Frequência do Gene , Estudos de Associação Genética , Genótipo , Humanos , Estilo de Vida , Pessoa de Meia-Idade , Razão de Chances , Medição de Risco , Fatores de Risco , Taiwan , Adulto Jovem
10.
Cancer Genomics Proteomics ; 15(5): 405-411, 2018.
Artigo em Inglês | MEDLINE | ID: mdl-30194081

RESUMO

BACKGROUND/AIM: The genomic role of human mouse double minute 2 (MDM2) in colorectal cancer (CRC) is unclear, therefore, our study aimed to evaluate the contribution of MDM2 genotype to the risk of CRC in Taiwan. MATERIALS AND METHODS: In this case-control study, MDM2 SNP309 T to G (rs2279744) genotypes were determined and their association with CRC risk were investigated among 362 patients with CRC and 362 age- and gender-matched healthy controls in central Taiwan. In addition, the interaction of MDM2 SNP309 genotypes with personal behaviors and clinicopathological features were also examined. RESULTS: The percentage of variant GG for the MDM2 SNP309 genotype was 30.9% in the CRC group and 24.0% in the control group, respectively (odds ratio (OR)=1.78, 95% confidence interval (CI)=1.25-2.86, p=0.0057). The allelic frequency distribution analysis showed that the variant G allele of MDM2 SNP309 conferred a significantly increased susceptibility to CRC compared with the wild-type T allele (OR=1.32, 95% CI=1.14-1.69, p=0.0062). As for the gene-lifestyle interaction, there was an obvious joint effect of MDM2 SNP309 GG genotype on the risk of CRC among ever-smokers and non-alcohol drinkers, but not non-smoker or alcohol drinker subgroups. No statistically significant correlation was observed between MDM2 SNP309 genotypic distributions and age, gender, tumor size, location or metastasis status. CONCLUSION: The genotypes of MDM2 SNP309 may allow forr early detection of and predictor for CRC risk, especially among smokers and non-alcohol drinkers, but not for prognosis. The combined effects of MDM2 SNP309 and other genes (such as matrix metalloproteinases) on CRC susceptibility and prognosis, should also be taken into consideration in the era of precision medicine.


Assuntos
Neoplasias Colorretais/genética , Estudos de Associação Genética , Predisposição Genética para Doença , Proteínas Proto-Oncogênicas c-mdm2/genética , Consumo de Bebidas Alcoólicas/patologia , Animais , Neoplasias Colorretais/patologia , Detecção Precoce de Câncer , Feminino , Frequência do Gene , Genótipo , Humanos , Masculino , Metaloproteinases da Matriz/genética , Camundongos , Polimorfismo de Nucleotídeo Único , Medicina de Precisão , Prognóstico , Fatores de Risco , Taiwan
11.
Cancer Genomics Proteomics ; 14(2): 119-125, 2017.
Artigo em Inglês | MEDLINE | ID: mdl-28387651

RESUMO

BACKGROUND/AIM: Metalloproteinases (MMPs) are a family of proteases which have been shown to be overexpressed in various types of cancers. However, the contribution of MMP1 genotype to hepatocellular carcinoma (HCC) has not been well studied. This study aimed to evaluate the contribution of MMP1 promoter 1607 genotype to the risk of HCC in Taiwan, where HCC incidence is relatively high in the world. MATERIALS AND METHODS: In this case-control study, MMP1 genotype and its interaction with consumption of cigarettes and alcohol in determining HCC risk was investigated among 298 HCC patients and 889 age- and gender-matched healthy controls. RESULTS: The percentages of ever smokers and ever alcohol drinkers were much higher in the case group than in the control group. The percentages of 2G/2G, 1G/2G and 1G/1G for MMP1 promoter 1607 genotype were 37.2%, 38.3% and 24.5% in the HCC group and 34.8%, 44.0% and 21.2% in the control group, respectively (p for trend=0.2048). The allelic frequency distribution analysis showed the variant 1G allele of MMP1 promoter 1607 conferred similar HCC susceptibility as the wild-type 2G allele (odds ratio (OR)=1.01, 95% confidence interval (CI)=0.84-1.22, p=0.8735). As for the gene-lifestyle interaction, there was an obvious protective effect of MMP1 promoter 1607 1G allele on the risk of HCC among non-smokers, but not non-smokers, even alcohol drinkers or non-drinkers. CONCLUSION: The 1G allele of MMP1 promoter 1607 may have a protective effect on HCC risk for non-smokers in Taiwan and further validations are needed in other population groups.


Assuntos
Carcinoma Hepatocelular/genética , Predisposição Genética para Doença/genética , Neoplasias Hepáticas/genética , Metaloproteinase 1 da Matriz/genética , Polimorfismo de Nucleotídeo Único , Regiões Promotoras Genéticas/genética , Consumo de Bebidas Alcoólicas , Alelos , Povo Asiático/genética , Carcinoma Hepatocelular/etnologia , Estudos de Casos e Controles , Feminino , Frequência do Gene , Predisposição Genética para Doença/etnologia , Genótipo , Humanos , Neoplasias Hepáticas/etnologia , Modelos Logísticos , Masculino , Pessoa de Meia-Idade , Razão de Chances , Fatores de Risco , Fumar , Taiwan
15.
Anticancer Res ; 36(4): 1657-63, 2016 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-27069143

RESUMO

BACKGROUND/AIM: It has been previously proposed that genetic variations on DNA repair genes confer susceptibility to cancer and the DNA repair gene Xeroderma Pigmentosum Group D (XPD) is thought to play the role of a helicase during excision repair and transcription. We investigated three genotypes of XPD, at promoter -114 (rs3810366), Asp312Asn (rs1799793) and Lys751Gln (rs13181), regarding their association with colorectal cancer susceptibility in a Taiwanese population. MATERIALS AND METHODS: In total, 362 patients with colorectal cancer and 362 gender- and age-matched healthy controls were genotyped by polymerase chain reaction-based restriction fragment length polymorphism (PCR-RFLP), and their XPD genotypes' association with colorectal cancer risk was investigated. RESULTS: The genotypes of XPD Asp312Asn (p=0.2493), Lys751Gln (p=0.7547) and promoter -114 (p=0.8702), were not associated with susceptibility for colorectal cancer. The Chi-square test revealed that the variant alleles of XPD Asp312Asn, Lys751Gln and promoter -114 was not associated with susceptibility for colorectal cancer either [p=0.1330, 0.3888 and 0.8740; odds ratio (OR)=1.20, 0.83 and 0.98; 95% confidence interval (95%CI)=0.95-1.52, 0.54-1.27 and 0.80-1.21, respectively]. The risk of A/G and A/A genotypes have no association with cancer risk among non-alcohol drinkers (OR=1.24, 95%, CI=0.90-1.72, p=0.2103) or alcohol drinkers (OR=1.51, 95% CI=0.64-3.55, p=0.4648). There exists no obvious contribution of XPD genotypes to tumor size (p=0.3531), location (p=0.3006) and lymph node metastasis (p=0.1061). CONCLUSION: Asp312Asn, Lys751Gln and promoter -114 of the XPD gene were not found to be adequate predictive markers for colorectal cancer risk in Taiwan.


Assuntos
Neoplasias Colorretais/genética , Reparo do DNA/genética , Predisposição Genética para Doença/genética , Polimorfismo de Fragmento de Restrição/genética , Proteína Grupo D do Xeroderma Pigmentoso/genética , Alelos , Estudos de Casos e Controles , Feminino , Genótipo , Humanos , Masculino , Pessoa de Meia-Idade , Regiões Promotoras Genéticas/genética , Fatores de Risco , Taiwan
16.
Anticancer Res ; 35(10): 5417-23, 2015 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-26408704

RESUMO

AIM: Hepatocellular carcinoma (HCC), the fifth most common cancer worldwide, has high prevalence and mortality rates in Taiwan. Tumor necrosis factor-α (TNFα), an important proinflammatory cytokine, is involved in multiple physiological and pathogenic phenomena that lead to the destruction and dysregulation of tissues. The present study aimed to evaluate the contribution of TNFA genotype, together with cigarette smoking and alcohol drinking lifestyle to the risk of HCC. MATERIALS AND METHODS: In this hospital-based case-control study, association of TNFA single-nucleotide polymorphisms -1031T/C, -863C/A, -857T/C, -308G/A and +489A/G, with HCC risk were examined in 298 patients with HCC and 889 age- and gender-matched healthy controls. RESULTS: The percentages of AA, AG and GG TNFA -308G/A were 6.4%, 18.1% and 75.5% in the HCC patient group and 2.0%, 16.0% and 82.0% in the non-cancer control group, respectively. The AA and AG genotypes were associated with 3.42- and 1.23-fold higher odds of HCC than the GG genotype (95% confidence interval=1.76-6.63 and 0.87-1.74, respectively). No such significant difference was found for other polymorphic sites. We further stratified the populations by gender, cigarette smoking and alcohol drinking status to investigate their combined contributions with TNFA -308G/A genotype to HCC risk. The results showed that the AA and AG genotypes of TNFA -308G/A increased HCC susceptibility which was obvious among males, smokers, and alcohol drinkers, but not females, non-smokers, or non-drinkers (p=0.0003, 0.0003, 0.0014, 0.6127, 0.7442 and 0.3010, respectively). CONCLUSION: Our results suggest that the AA and AG polymorphism of TNFA -308G/A genotypes associated with HCC risk in Taiwan, particularly among males, smokers and alcohol drinkers.


Assuntos
Consumo de Bebidas Alcoólicas/efeitos adversos , Carcinoma Hepatocelular/genética , Neoplasias Hepáticas/genética , Polimorfismo de Nucleotídeo Único , Fumar/efeitos adversos , Fator de Necrose Tumoral alfa/genética , Povo Asiático/genética , Carcinoma Hepatocelular/etiologia , Estudos de Casos e Controles , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Fatores Sexuais , Taiwan
17.
Cardiovasc Intervent Radiol ; 33(1): 196-200, 2010 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-19730938

RESUMO

Transarterial chemoembolization has been widely used to treat unresectable hepatocellular carcinoma. Various complications have been reported, but they have not included acute myocardial infarction. Acute myocardial infarction results mainly from coronary artery occlusion by plaques that are vulnerable to rupture or from coronary spasm, embolization, or dissection of the coronary artery. It is associated with significant morbidity and mortality. We present a case report that describes a patient with hepatocellular carcinoma who underwent transarterial chemoembolization and died subsequently of acute myocardial infarction. To our knowledge, there has been no previous report of this complication induced by transarterial chemoembolization for hepatocellular carcinoma. This case illustrates the need to be aware of acute myocardial infarction when transarterial chemoembolization is planned for the treatment of hepatocellular carcinoma, especially in patients with underlying coronary artery disease.


Assuntos
Carcinoma Hepatocelular/terapia , Quimioembolização Terapêutica/efeitos adversos , Neoplasias Hepáticas/terapia , Infarto do Miocárdio/etiologia , Arteriopatias Oclusivas/complicações , Arteriopatias Oclusivas/diagnóstico por imagem , Carcinoma Hepatocelular/complicações , Carcinoma Hepatocelular/diagnóstico , Quimioembolização Terapêutica/métodos , Colecistite/complicações , Doença das Coronárias/complicações , Diabetes Mellitus Tipo 2/complicações , Doxorrubicina/administração & dosagem , Evolução Fatal , Artéria Hepática/diagnóstico por imagem , Hepatite B Crônica/complicações , Humanos , Óleo Iodado/administração & dosagem , Neoplasias Hepáticas/complicações , Neoplasias Hepáticas/diagnóstico , Masculino , Pessoa de Meia-Idade , Infarto do Miocárdio/diagnóstico , Radiografia
18.
J Gastroenterol Hepatol ; 21(2): 413-9, 2006 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-16509867

RESUMO

BACKGROUND AND AIM: To compare the efficacy and safety of endoscopic variceal ligation (EVL) with propranolol in prophylaxis on the rate of first esophageal variceal bleeding in patients with cirrhosis. METHODS: A prospective, randomized trial was conducted in 100 cirrhotic patients with no history of previous upper gastrointestinal bleeding and with esophageal varices endoscopically judged to be at high risk of hemorrhage. The end-points of the study were bleeding and death. RESULTS: Life-table curves showed that prophylactic EVL and propranolol were similarly effective for primary prophylaxis of variceal bleeding (11/50 [22%]vs 12/50 [24%]; P = 0.68) and overall mortality (14/50 [28%]vs 12/50 [24%]; P = 0.49). The 2-year cumulative bleeding rate was 18% (9/50) in the EVL group and 16% (8/50) in the propranolol group. The 2-year cumulative mortality rate was 28% (14/50) in the EVL group and 24% (12/50) in the propranolol group. Comparison of Kaplan-Meier estimates of the time to death of both groups showed no significant difference in mortality in both groups (P = 0.86). Patients undergoing EVL had few treatment failures and died mainly of hepatic failure. In the propranolol group, the mean daily dosage of the drug was 68.2 +/- 32.8 mg, which was sufficient to reduce the pulse rate by 25%. 20% of patients withdrew from propranolol treatment due to adverse events. CONCLUSIONS: Prophylaxis EVL is as effective and as safe as treatment with propranolol in decreasing the incidence of first variceal bleeding and death in cirrhotic patients with high-risk esophageal varices.


Assuntos
Antagonistas Adrenérgicos beta/uso terapêutico , Endoscopia Gastrointestinal , Varizes Esofágicas e Gástricas/terapia , Hemorragia Gastrointestinal/prevenção & controle , Cirrose Hepática/complicações , Propranolol/uso terapêutico , Varizes Esofágicas e Gástricas/complicações , Feminino , Seguimentos , Hemorragia Gastrointestinal/etiologia , Hemorragia Gastrointestinal/mortalidade , Humanos , Ligadura/métodos , Masculino , Pessoa de Meia-Idade , Estudos Prospectivos , Fatores de Risco , Taxa de Sobrevida , Resultado do Tratamento
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