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1.
Int J Med Inform ; 157: 104641, 2022 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-34785488

RESUMO

INTRODUCTION: Acute pancreatitis (AP) is a common clinical pancreatic disease. Patients with different severity levels have different clinical outcomes. With the advantages of algorithms, machine learning (ML) has gradually emerged in the field of disease prediction, assisting doctors in decision-making. METHODS: A systematic review was conducted using the PubMed, Web of Science, Scopus, and Embase databases, following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines. Publication time was limited from inception to 29 May 2021. Studies that have used ML to establish predictive tools for AP were eligible for inclusion. Quality assessment of the included studies was conducted in accordance with the IJMEDI checklist. RESULTS: In this systematic review, 24 of 2,913 articles, with a total of 8,327 patients and 47 models, were included. The studies could be divided into five categories: 10 studies (42%) reported severity prediction; 10 studies (42%), complication prediction; 3 studies (13%), mortality prediction; 2 studies (8%), recurrence prediction; and 2 studies (8%), surgery timing prediction. ML showed great accuracy in several prediction tasks. However, most of the included studies were retrospective in nature, conducted at a single centre, based on database data, and lacked external validation. According to the IJMEDI checklist and our scoring criteria, two studies were considered to be of high quality. Most studies had an obvious bias in the quality of data preparation, validation, and deployment dimensions. CONCLUSION: In the prediction tasks for AP, ML has shown great potential in assisting decision-making. However, the existing studies still have some deficiencies in the process of model construction. Future studies need to optimize the deficiencies and further evaluate the comparability of the ML systems and model performance, so as to consequently develop high-quality ML-based models that can be used in clinical practice.

2.
Neoplasma ; 2021 Nov 04.
Artigo em Inglês | MEDLINE | ID: mdl-34734530

RESUMO

Emerin (EMD) plays diverse roles in cellular polarity organization, nuclear stability, and cell motility, however, the biological role of EMD relevant to the migration and invasion of hepatocellular carcinoma (HCC) cells has not yet been illustrated. In the present study, we initially found that the upregulation of EMD in HCC tissues, and EMD expression was negatively correlated with the spontaneous metastatic potential of HCC cell lines. Loss of EMD in HCC cells facilitated cell migration and invasion in vitro and metastasis in vivo. Meanwhile, we demonstrated that EMD knockdown induced EMT but enhanced p21 expression in HCC cells. Notably, silencing of EMD in HCC cells increased the cytoplasmic localization of p21 protein, whereas p21 knockdown partially abrogated the migratory and invasive ability, EMT, and the actin cytoskeleton rearrangement induced by EMD knockdown in HCC cells. Our results indicated a significant role of EMD knockdown in the HCC cell motility and metastasis through upregulating the cytoplasmic p21, unveiling a novel mechanism of cell motility regulation induced by EMD.

3.
Zhongguo Zhong Yao Za Zhi ; 46(12): 2963-2971, 2021 Jun.
Artigo em Chinês | MEDLINE | ID: mdl-34467686

RESUMO

To overview the systematic reviews of Panax notoginseng saponins in the treatment of acute cerebral infarction. CNKI, CBM, Wanfang, VIP, PubMed, Cochrane Library and EMbase databases were retrieved to collect the systematic reviews of the efficacy of P. notoginseng saponins in the treatment of acute cerebral infarction. The retrieval time was from the time of database establishment to January 2021. After two researchers independently screened out the literature and extracted the data, AMSTAR-2 scale was used to evaluate the methodological quality of the included systematic reviews, GRADE system was used to grade the quality of evidences of the outcome indicators, and the efficacy evaluation was summarized. A total of 5 systematic reviews were included. AMSTAR-2 evaluation results showed that 3 items were relatively complete, while 4 items had a poor overall quality. P. notoginseng saponins combined with conventional Western medicine therapy was superior to single conventional therapy in the recovery of neurological function, enhancement of the total effective rate in clinic, and improvement of activities of daily living. GRADE evaluation results showed that the quality of evidence was from low quality to very low quality. In conclusion, in the treatment of acute cerebral infarction, P. notoginseng saponins can improve the clinical efficacy, with a good safety but a not high methodological quality and a low evidence quality. It is suggested that high-quality clinical studies shall be further carried out to provide evidence-based basis for the application of P. notoginseng saponins in the treatment of acute cerebral infarction.


Assuntos
Panax notoginseng , Saponinas , Atividades Cotidianas , Infarto Cerebral/tratamento farmacológico , Humanos , Revisões Sistemáticas como Assunto
4.
Artigo em Inglês | MEDLINE | ID: mdl-34335808

RESUMO

Objective: To assess the efficacy and safety of PNS on antiplatelet therapy in the treatment of AIS. Methods: We searched 7 literature databases and 2 clinical studies databases for randomized controlled studies (RCTs) evaluating PNS as an adjuvant therapy for AIS. Relevant studies were retrieved and screened, and data were extracted independently by two reviewers. The quality of the included studies was assessed using the Cochrane Risk Assessment Tool. Meta-analysis was carried out with the Rev Man 5.4 software. Results: Of 8267 records identified, 43 RCTs met our inclusion criteria (n = 4170 patients). Patients assigned to PNS with conventional treatments (CTs) had improved functional independence at 90 days compared with those assigned to CTs alone (RR = 1.87, 95% CI = 1.37, to 2.55, P < 0.0001). Patients who received PNS combined with CTs showed significantly high improvements in neurological function among individuals with AIS on the neurologic deficit score (NDS) (MD CSS = -5.71, 95% CI = -9.55 to -1.87, P=0.004; MD NIHSS = -3.94, 95% CI = -5.65 to -2.23, P < 0.00001). The results also showed PNS contributed to a betterment in activities of daily living (ADL) on the Barthel index (MD day 10 BI = 4.86, 95% CI = 2.18, to 7.54, P < 0.00001; MD day 14 BI = 13.92, 95% CI = 11.46 to 16.38, P < 0.00001; MD day 28 BI = 7.16, 95% CI = 0.60, to 13.72, P < 0.00001). In addition, PNS, compared with CTs alone, could significantly improve overall response rate (ORR) (RR NIHSS = 1.20, 95% CI = 1.16, to 1.24, P < 0.00001; RR CSS = 1.15, 95% CI = 1.08, to 1.24, P < 0.0001), hemorheological parameters, maximum platelet aggregation rate (MPAR) (MD = -6.82, 95% CI = -9.62 to -4.02, P < 0.00001), platelet parameters (MD PLT = 4.85, 95% CI = 1.82 to 7.84, P=0.002; MD MPV = -0.79, 95% CI = -1.09 to -0.48, P < 0.00001), and serum CD62P (MD = -0.21, 95% CI = -0.29 to -0.13, P < 0.00001). The incidence of adverse reactions in PNS was lower than that in the control group (RR = 0.62, 95% CI = 0.39 to 0.97, P=0.04). Adverse reactions in the PNS were mild adverse reactions. Conclusion: PNS may be effective and safe in treating AIS on ameliorating neurological deficit, improving activities of daily living function, and enhancing antiplatelet effects. However, more high-quality evidence is needed before it can be recommended for routine antiplatelet therapy in patients with AIS.

5.
Am J Transl Res ; 10(7): 2015-2025, 2018.
Artigo em Inglês | MEDLINE | ID: mdl-30093939

RESUMO

Clinical studies have confirmed that patients with diabetes had an elevated risk of acute pancreatitis (AP) and diabetes was associated with increased severity and mortality in patients with AP. However, these studies failed to prove a cause-and-effect relationship between diabetes and AP. In the present study, we for the first time have evaluated the effects of diabetes on AP by adopting a type 2 diabetes animal model db/db mice and investigated the possible underlying mechanisms. The results showed that in comparison to wide type (WT) mice, db/db mice showed exacerbated pancreatic and pulmonary injuries, elevated serum amylase and lipase levels, increased myeloperoxidase (MPO) expressions in pancreatic and pulmonary tissues as well as increased apoptotic acinar cells after AP induction. Furthermore, we observed that NLRP3 inflammasome in pancreatic tissues was remarkably activated in db/db mice compared with WT mice. In addition, we also found that diabetes could increase the susceptibility of mice to AP. Taken together, our results indicated that diabetes could predispose and aggravate the disease severity of AP potentially via promoting the activation of NLRP3 inflammasome pathway.

6.
Pancreatology ; 18(3): 263-268, 2018 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-29477252

RESUMO

OBJECTIVE: The aim of this study was to investigate the prevalence and risk factors of fatty pancreas in Yangzhou, China. METHODS: This was a cross-sectional study. Initially, 2093 subjects were included in the study. After the exclusion of 865 subjects based on incomplete information, a total of 1228 subjects were selected for further analysis. The subjects were stratified into two groups (the fatty pancreas group and the non-fatty pancreas group) based on the results. Anthropometric and biochemical findings were compared between the groups. RESULTS: Among the 2093 study subjects, 56 (2.7%) had fatty pancreas. Overall, 53 out of 1228 subjects were diagnosed with fatty pancreas and included into the fatty pancreas group. Univariate analysis showed significant differences in age and the prevalence of general obesity, central obesity, alcohol consumption, metabolic syndrome and fatty liver between the two groups (all p < 0.01). The fatty pancreas group had higher levels of aspartate aminotransferase, alanine aminotransferase, serum uric acid, fasting blood glucose, total cholesterol, triglycerides and low-density lipoprotein, and lower levels of high-density lipoprotein than did the non-fatty pancreas group (all p < 0.05). Multivariate logistic regression analysis showed that age (p = 0.007), central obesity (p = 0.002) and fatty liver (p = 0.006) were independent risk factors for fatty pancreas, with odds ratios (ORs) of 1.034 (95% confidence interval (CI): 1.009-1.059), 5.364 (95% CI: 1.890-15.227), and 2.666 (95% CI: 1.332-5.338), respectively. CONCLUSION: The prevalence of fatty pancreas in the examined population is approximately 2.7%. Increased age, central obesity and fatty liver disease are independent risk factors for fatty pancreas.


Assuntos
Pancreatopatias/epidemiologia , Adulto , Fatores Etários , Idoso , Alcoolismo/complicações , Alcoolismo/epidemiologia , China/epidemiologia , Estudos Transversais , Fígado Gorduroso/complicações , Fígado Gorduroso/epidemiologia , Feminino , Humanos , Masculino , Síndrome Metabólica/complicações , Síndrome Metabólica/epidemiologia , Pessoa de Meia-Idade , Obesidade/complicações , Obesidade/epidemiologia , Testes de Função Pancreática , Prevalência , Fatores de Risco
7.
Cancer Med ; 7(3): 796-808, 2018 03.
Artigo em Inglês | MEDLINE | ID: mdl-29446253

RESUMO

Surgical results for intrahepatic cholangiocarcinoma (ICC) remain unsatisfactory due to the high rate of recurrence. Here, we investigated that the expression and roles of tripartite motif-containing protein 44 (TRIM44) in human ICCs. Firstly, TRIM44 expression was analyzed in several kinds of cancers by referring to public Oncomine database, and the expressions of TRIM44 mRNA and protein were tested in ICC and corresponding paratumorous tissues. Secondly, functions and mechanisms of TRIM44 in ICC cells were further evaluated by TRIM44 interference and cDNA transfection. Finally, the prognostic role of TRIM44 was assessed by Kaplan-Meier and Cox regression. We found that TRIM44 expression was upregulated in ICC tissues compared with corresponding paratumorous tissues, which were consistent with the results from the public cancer database. Knockdown of TRIM44 repressed the invasion and migration of ICC cells, while increased the ICC cell apoptosis. Additionally, high level of TRIM44 was shown to induce ICC cell epithelial to mesenchymal transition (EMT). Mechanistically, a high level of TRIM44 was found to activate MAPK signaling, and a MEK inhibitor, AZD6244, reversed cell EMT and apoptosis endowed by TRIM44 overexpression. Clinically, TRIM44 expression was positively associated with large tumor size (P = 0.035), lymphatic metastasis (P = 0.008) and poor tumor differentiation (P = 0.036). Importantly, patients in TRIM44high group had shorter overall survival and higher cumulative rate of recurrence than patients in TRIM44low group. Our results suggest elevated TRIM44 promotes ICC development by inducing cell EMT and apoptosis resistance, and TRIM44 is a valuable prognostic biomarker and promising therapeutic target of ICC.


Assuntos
Neoplasias dos Ductos Biliares/genética , Neoplasias dos Ductos Biliares/metabolismo , Proteínas de Transporte/metabolismo , Colangiocarcinoma/genética , Colangiocarcinoma/metabolismo , Transição Epitelial-Mesenquimal/genética , Quinases de Proteína Quinase Ativadas por Mitógeno , Neoplasias dos Ductos Biliares/patologia , Proteínas de Transporte/genética , Colangiocarcinoma/patologia , Progressão da Doença , Feminino , Humanos , Peptídeos e Proteínas de Sinalização Intracelular , Masculino , Pessoa de Meia-Idade , Prognóstico , Transfecção , Proteínas com Motivo Tripartido
8.
BMC Gastroenterol ; 16: 24, 2016 Feb 25.
Artigo em Inglês | MEDLINE | ID: mdl-26912038

RESUMO

BACKGROUND: Pseudoachalasia is a rare disorder whose presentation strongly resembles idiopathic achalasia. CASE PRESENTATION: Here, we present a case of a 42-year-old female patient with esophageal leiomyoma who was initially diagnosed with achalasia. On endoscopical investigation, however, it became apparent that she had pseudoachalasia as consequence of a leiomyoma at the esophagogastric junction (EGJ). The condition was successfully treated through submucosal tunneling endoscopic resection. CONCLUSION: This case suggests that submucosal tunneling endoscopic resection is a therapeutic u option for the treatment of pseudoachalasia caused by leiomyoma of EGJ.


Assuntos
Neoplasias Esofágicas/cirurgia , Junção Esofagogástrica/cirurgia , Leiomioma/cirurgia , Adulto , Sulfato de Bário , Diagnóstico Diferencial , Endoscopia do Sistema Digestório/métodos , Acalasia Esofágica/diagnóstico , Neoplasias Esofágicas/diagnóstico , Esôfago/diagnóstico por imagem , Feminino , Humanos , Leiomioma/diagnóstico , Manometria , Radiografia
9.
Asian Pac J Cancer Prev ; 14(11): 6487-91, 2014 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-24377555

RESUMO

To investigate the cognition of medical professionals when following screening guidelines for colorectal cancer (CRC) and barriers to CRC screening. Between February 2012 and December 2012, an anonymous survey with 19-questions based on several CRC screening guidelines was randomly administered to gastroenterologists, oncologists, general surgeons, and general practitioners in Jiangsu, a developed area in China where the incidence of CRC is relatively high. The average cognitive score was 26.4% among 924 respondents. Gastroenterologists and oncologists had higher scores compared with others (p<0.01 and p<0.01, respectively); doctor of medicine (M.D.) with or without doctor of philosophy (Ph.D.) or holders with bachelor of medical science (BMS) achieved higher scores than other lower degree holders (P<0.05). More importantly, doctors who finished CRC related education in the past year achieved higher scores than the others (p<0.001). The most commonly listed barriers to referring high-risk patients for CRC screening were "anxiety about colonoscopy without anesthesia", "lack of awareness of the current guidelines" and "lack of insurance reimbursement. " Lack of cognition was detected among doctors when following CRC screening guidelines for high-risk populations. Educational programs should be recommended to improve their cognition and reduce barriers to CRC screening.


Assuntos
Cognição , Neoplasias Colorretais/psicologia , Detecção Precoce de Câncer , Fidelidade a Diretrizes , Pesquisas sobre Serviços de Saúde , Padrões de Prática Médica/estatística & dados numéricos , Idoso , China/epidemiologia , Colonoscopia , Neoplasias Colorretais/diagnóstico , Neoplasias Colorretais/epidemiologia , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Sangue Oculto , Prognóstico , Fatores de Risco , Inquéritos e Questionários
10.
PLoS One ; 8(5): e63777, 2013.
Artigo em Inglês | MEDLINE | ID: mdl-23723999

RESUMO

Regulatory T cell (Treg)-mediated immunosuppression represents one of the crucial tumor immune evasion mechanisms and is a main obstacle for successful tumor immunotherapy. Hypoxia, a common feature of solid tumors, has been associated with potentiated immunosuppression, decreased therapeutic response, malignant progression and local invasion. Unfortunately, the link between hypoxia and Treg-mediated immune tolerance in gastric cancer remains poorly understood. In our study, Tregs and hypoxia inducible factor-1α were found to be positively correlated with each other and were increased with the tumor progression. A subsequent in vitro study indicated that supernatants derived from gastric cancer cells under hypoxic condition, could induce the expression of Foxp3 via TGF-ß1. These findings confirmed the crucial role of Tregs as a therapeutic target in gastric cancer therapy and provided helpful thoughts for the design of immunotherapy for gastric cancer in the future.


Assuntos
Hipóxia , Tolerância Imunológica , Neoplasias Gástricas/imunologia , Neoplasias Gástricas/metabolismo , Linfócitos T Reguladores/imunologia , Linfócitos T Reguladores/metabolismo , Fator de Crescimento Transformador beta1/metabolismo , Adulto , Idoso , Linhagem Celular Tumoral , Feminino , Fatores de Transcrição Forkhead/metabolismo , Humanos , Subunidade alfa do Fator 1 Induzível por Hipóxia/metabolismo , Masculino , Pessoa de Meia-Idade , Estadiamento de Neoplasias , Neoplasias Gástricas/mortalidade , Neoplasias Gástricas/patologia , Neoplasias Gástricas/cirurgia
11.
World J Gastroenterol ; 19(13): 2080-6, 2013 Apr 07.
Artigo em Inglês | MEDLINE | ID: mdl-23599628

RESUMO

AIM: To compare synchronous laparoscopic cholecystectomy (LC) combined with endoscopic sphincterotomy (EST) and sequential LC combined with EST for treating cholecystocholedocholithiasis. METHODS: A total of 150 patients were included and retrospectively studied. Among these, 70 were selected for the synchronous operation, in which the scheme was endoscopic retrograde cholangiopancreatography combined with EST during LC. The other 80 patients were selected for the sequential operation, in which the scheme involved first cutting the papillary muscle under endoscopy and then performing LC. The indexes in the two groups, including the operation time, the success rate, the incidence of complications, and the length of the hospital stay, were observed. RESULTS: There were no significant differences between the groups in terms of the numbers of patients, sex distribution, age, American Society of Anesthesiologists score, serum bilirubin, γ-glutamyl transpeptidase, mean diameter of common bile duct stones, and previous medical and surgical history (P = 0.54, P = 0.18, P = 0.52, P = 0.22, P = 0.32, P = 0.42, P = 0.68, P = 0.70, P = 0.47 and P = 0.57). There was no significant difference in the surgical operation time between the two groups (112.1 ± 30.8 min vs 104.9 ± 18.2 min). Compared with the sequential operation group, the incidence of pancreatitis was lower (1.4% vs 6.3%), the incidence of hyperamylasemia (1.4% vs 10.0%, P < 0.05) was significantly reduced, and the length of the hospital stay was significantly shortened in the synchronous operation group (3 d vs 4.5 d, P < 0.001). CONCLUSION: For treatment of cholecystocholedocholithiasis, synchronous LC combined with EST reduces incidence of complications, decreases length of hospital stay, simplifies the surgical procedure, and reduces operation time.


Assuntos
Colecistectomia Laparoscópica/métodos , Coledocolitíase/cirurgia , Adulto , Idoso , Angiografia/métodos , Colangiopancreatografia Retrógrada Endoscópica/métodos , Coledocolitíase/terapia , Feminino , Seguimentos , Hospitalização , Humanos , Incidência , Tempo de Internação , Masculino , Pessoa de Meia-Idade , Estudos Retrospectivos , Esfinterotomia Endoscópica/métodos , Resultado do Tratamento
12.
Dig Dis Sci ; 58(6): 1627-35, 2013 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-23306848

RESUMO

BACKGROUND: The integrin α6 subunit is part of the integrin α6ß1 and α6ß4 complexes, which are known to mediate the invasion of carcinoma cells. However, the precise role of integrin α6 in intrahepatic cholangiocarcinoma (ICC) has not yet been addressed. METHODS: Twenty cases of ICCs and matched nontumor samples were used to analyze integrin α6 expression by immunohistochemistry. After the expression of integrin α6 was determined by RT-PCR and Western blot in ICC cells, we regulated the expression of integrin α6 in ICC cells with specific vshRNA-integrin α6, and assessed the role of integrin α6 in the proliferation and metastasis/invasion of ICC cells. Finally, the involved mechanisms and clinical significance were further investigated. RESULTS: The expression of integrin α6 in ICC tissues was much higher than that in nontumor samples, and the high level of integrin α6 was detected in ICC cells compared with normal liver cells and HepG2 cells. After the down-regulation of integrin α6 in HCCC-9810 cells, we showed that the ability of ICC cells to metastasize and invade was much decreased in vitro, and cell proliferation was inhibited significantly. Further study indicated high expression of integrin α6 enhanced the activation of ERK1/2 and AKT signals in ICC cells and the inhibition of ERK1/2 down-regulated ICC cell proliferation, while the inhibition of AKT markedly impaired ICC cell metastasis and invasion. Integrin α6 overexpression was significantly correlated with larger tumors, multiple nodular, microvascular/bile duct invasion, and lymphatic metastasis (p < 0.05). The postoperative 5-year overall survival (OS) rate in patients with integrin α6(low) was higher than that of the integrin α6(high) group. CONCLUSIONS: Overexpression of integrin α6 is associated with a migratory and invasive phenotype of ICC, and integrin α6 may be used as molecular target for therapy of ICC.


Assuntos
Neoplasias dos Ductos Biliares/metabolismo , Ductos Biliares Intra-Hepáticos/metabolismo , Biomarcadores Tumorais/metabolismo , Colangiocarcinoma/metabolismo , Integrina alfa6/metabolismo , Adulto , Idoso , Idoso de 80 Anos ou mais , Neoplasias dos Ductos Biliares/mortalidade , Neoplasias dos Ductos Biliares/patologia , Ductos Biliares Intra-Hepáticos/patologia , Western Blotting , Estudos de Casos e Controles , Linhagem Celular Tumoral , Colangiocarcinoma/mortalidade , Colangiocarcinoma/patologia , Feminino , Humanos , Imuno-Histoquímica , Metástase Linfática , Masculino , Pessoa de Meia-Idade , Invasividade Neoplásica , Metástase Neoplásica , Fenótipo , Reação em Cadeia da Polimerase Via Transcriptase Reversa , Análise de Sobrevida , Regulação para Cima
13.
Asian Pac J Cancer Prev ; 14(12): 7613-9, 2013.
Artigo em Inglês | MEDLINE | ID: mdl-24460342

RESUMO

BACKGROUND AND AIMS: Helicobacter pylori infection may be associated with an increased risk of colorectal carcinoma. However, as most studies on this subject were relatively small in size and differed at least partially in their designs, their results remain controversial. In this study, we aimed to carry out a meta-analysis to evaluate the potential association of H. pylori infection with colorectal adenoma and adenocarcinoma risk, covering all of the different testing methods. METHODS: We conducted a search in PubMed, Medline, EBSCO, High Wire Press, OVID, and EMBASE covering all published papers up to March 2013. According to the established inclusion criteria, essential data were then extracted from the included studies and further analyzed by a systematic meta-analysis. Odds ratios were employed to evaluate the relationship between H. pylori infection and the risk of colorectal neoplasms. RESULTS: Twenty-two studies were included, and the odds ratio for the association between H. pylori infection and colorectal cancer was 1.49 (95% confidence interval 1.30-1.72). No statistically significant heterogeneity was observed. Publication bias was ruled out. CONCLUSION: The pooled data suggest H. pylori infection indeed increases the risk of colorectal adenoma and adenocarcinoma.


Assuntos
Adenocarcinoma/etiologia , Adenoma/etiologia , Neoplasias Colorretais/etiologia , Infecções por Helicobacter/complicações , Helicobacter pylori/patogenicidade , Testes Sorológicos/métodos , Infecções por Helicobacter/virologia , Humanos , Prognóstico , Fatores de Risco
14.
Mol Carcinog ; 48(7): 626-32, 2009 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-19058298

RESUMO

Interleukin 2 (IL2) is a typical Th1 cytokine, and interleukin 4 (IL4) is an inducible Th2 cytokine. These cytokines are critical mediators of the Th1/Th2 balance and apoptosis potential and involved in the process of inflammation-mediated carcinogenesis in human organs, including the gastrointestinal tract. Therefore, we tested the hypothesis that functional variants in IL2 and IL4 were associated with risk of gastric cancer by genotyping two promoter polymorphisms in IL2 G-330T (rs2069762) and IL4 T-168C (rs2070874) in a case-control study of 1045 patients with incident gastric cancer and 1100 cancer-free controls in a high-risk Han Chinese population. We found that, compared with the IL4 -168TT genotype, heterozygous -168TC and combined -168TC/CC genotypes were associated with a significantly decreased gastric cancer risk [adjusted odds ratio (OR) = 0.81, 95% confidence interval (CI) = 0.67-0.98 for -168TC; OR = 0.83, 95% CI = 0.69-1.00 for -168TC/CC, respectively]. Furthermore, this significant protective effect was more evident for gastric cardia cancer patients (adjusted OR = 0.73, 95% CI = 0.56-0.95 for -168TC/CC vs. -168TT). For IL2 G-330T, subjects carrying GT/TT genotypes also had a significantly reduced risk of gastric cardia cancer (adjusted OR = 0.68, 95% CI = 0.46-0.99), compared with those carrying the GG genotype. Our results indicate that IL4 T-168C and IL2 G-330T promoter polymorphisms may contribute to the etiology of gastric cardia cancer in Chinese populations.


Assuntos
Predisposição Genética para Doença , Interleucina-2/genética , Interleucina-4/genética , Polimorfismo Genético , Regiões Promotoras Genéticas , Neoplasias Gástricas/genética , Sequência de Bases , Estudos de Casos e Controles , China , Primers do DNA , Feminino , Humanos , Masculino , Pessoa de Meia-Idade
15.
Zhonghua Zhong Liu Za Zhi ; 30(9): 668-71, 2008 Sep.
Artigo em Chinês | MEDLINE | ID: mdl-19173907

RESUMO

OBJECTIVE: To investigate the correlation of Helicobactor pylori (Hp) infection with the expression of COX-2, EGFR and VEGF in human gastric carcinoma. METHODS: The expression of COX-2, EGFR and VEGF was detected by immunohistochemistry in samples of 61 gastric cancers and 20 cancer-adjacent tissues. Western blotting was performed in samples of 10 gastric cancers and corresponding cancer-adjacent tissues. Hp infection was detected in 47 patients by fast urea enzyme test and (13)C breath test. RESULTS: The results of immunohistochemistry showed that the positive expressions of COX-2, EGFR and VEGF in gastric carcinoma were 59.02%, 36.07% and 60.66%, respectively, significantly higher than that in the normal mucosa (25.00%, 0 and 30.00%, respectively). There was a positive correlation between the expression of COX-2, EGFR and VEGF and gastric carcinoma. The expression of COX-2 and EGFR was 75.76% and 45.45% in the gastric carcinomas with Hp infection, significantly higher than that in those without (28.57% and 14.29%). The protein expression of COX-2, EGFR and VEGF detected by Western blot in gastric carcinomas was also significantly higher than that in normal mucosa. CONCLUSION: COX-2, EGFR and VEGF are overexpressed in gastric carcinoma, and there is a positive correlation among them. Hp infection may upregulate the expression of COX-2 and EGFR in gastric cancer tissues.


Assuntos
Ciclo-Oxigenase 2/metabolismo , Receptores ErbB/metabolismo , Infecções por Helicobacter/metabolismo , Neoplasias Gástricas/metabolismo , Fator A de Crescimento do Endotélio Vascular/metabolismo , Idoso , Western Blotting , Feminino , Mucosa Gástrica/metabolismo , Regulação Neoplásica da Expressão Gênica , Infecções por Helicobacter/microbiologia , Helicobacter pylori , Humanos , Imuno-Histoquímica , Masculino , Pessoa de Meia-Idade , Neoplasias Gástricas/microbiologia , Regulação para Cima
16.
Exp Oncol ; 27(2): 108-13, 2005 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-15995627

RESUMO

AIM: 1) To evaluate the effect of prostaglandin E2 (PGE2) on the regulation of vascular endothelial growth factor (VEGF) expression in gastric MKN28 cells, and 2) to investigate the role of the epidermal growth factor receptor (EGFR) signal transduction pathway in any effect exerted by PGE2 on VEGF expression. METHODS: MKN28 cells were incubated with the vehicle (control) or with PGE2 in the presence or absence of AG1478, a selective inhibitor of EGFR tyrosine kinase, or PD098059, a selective inhibitor of the kinase responsible for ERK2 phosphorylation (mitogen-activated protein (MAP)/extracellular signal-regulated kinase (ERK)). Real-time quantitative polymerase chain reaction and Western blot analysis were used to evaluate VEGF mRNA and protein expression. The activity of EGFR and ERK2 was measured by Western blot analysis. RESULTS: PGE2 significantly up-regulated VEGF mRNA and protein expression and increased the activation of EGFR and ERK2. Incubation of MKN28 cells with AG1478 significantly reduced PGE2-induced EGFR activity, ERK2 activity, and VEGF mRNA and protein expression. Meanwhile, incubation of MKN28 with PD098059 reduced PGE2-induced ERK2 activity and VEGF mRNA and protein expression, but had no effect on EGFR activity. CONCLUSION: Our data suggested that PGE2 up-regulates VEGF expression in gastric cancer cells via transactivation of EGFR-MAPK signaling pathways, which may be mechanisms underlying the contribution of COX-2 to tumor angiogenesis in gastric cancer.


Assuntos
Dinoprostona/farmacologia , Receptores ErbB/metabolismo , Ocitócicos/farmacologia , Transdução de Sinais , Neoplasias Gástricas/metabolismo , Fator A de Crescimento do Endotélio Vascular/metabolismo , Proteínas Quinases Dependentes de Cálcio-Calmodulina/antagonistas & inibidores , Inibidores Enzimáticos/farmacologia , Flavonoides/farmacologia , Humanos , Imunoprecipitação , Proteína Quinase 1 Ativada por Mitógeno/antagonistas & inibidores , Proteína Quinase 1 Ativada por Mitógeno/metabolismo , Fosforilação/efeitos dos fármacos , Quinazolinas , RNA Mensageiro/genética , RNA Mensageiro/metabolismo , Neoplasias Gástricas/genética , Ativação Transcricional , Células Tumorais Cultivadas , Tirfostinas/farmacologia , Regulação para Cima , Fator A de Crescimento do Endotélio Vascular/genética
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