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1.
Neuroendocrinology ; 2020 Jan 15.
Artigo em Inglês | MEDLINE | ID: mdl-31940636

RESUMO

PURPOSE: To evaluate whether the European Neuroendocrine Tumor Society (ENETS) system or the 8th American Joint Committee on Cancer (AJCC) staging manual are suitable for gastric neuroendocrine carcinomas and/or mixed adenoneuroendocrine carcinomas (G-NECs/MANECs). METHODS: Patients in the a multicentric series with G-NEC/MANEC who underwent curative-intent surgical resection for a primary tumor were included. An optimal staging system was proposed base on analysis of the T and N status and validated by the SEER database. RESULTS: Compared with the ENETS system, the survival curves of the T category and N category in the 8th AJCC system were better separated and distributed in a more balanced way, but the survival curves of T2 vs T3, N0 vs N1, and N3a vs N3b overlapped. For the T category, the 8th AJCC T category was modified by combining T2 and T3, which was consistent with the T category in the 6th AJCC manual for GC. For the N category, the optimal cut-off values of metastatic lymph nodes using X-tile were also similar to those of the N category in the 6th AJCC system. The Kaplan-Meier plots of the 6th AJCC system showed statistically significant differences between individual substages. Compared with the other two classifications, the 6th AJCC system also showed superior prognostic stratification. Similar results were obtained in both multicentric and SEER validation sets. CONCLUSIONS: Compared to the 8th AJCC and ENETS systems, the 6th AJCC staging system for GC is more suitable for G-NEC/MANEC and can be adopted in clinical practice.

2.
Chem Biodivers ; 16(11): e1900400, 2019 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-31482617

RESUMO

The Keap1-Nrf2/ARE signaling pathway is an important defense system against exogenous and endogenous oxidative stress injury. The dysregulation of the signaling pathway is associated with many diseases, such as cancer, diabetes, and respiratory diseases. Over the years, a wide range of natural products has provided sufficient resources for the discovery of potential therapeutic drugs. Among them, polyphenols possess Nrf2 activation, not only inhibit the production of ROS, inhibit Keap1-Nrf2 protein-protein interaction, but also degrade Keap1 and regulate the Nrf2 related pathway. In fact, with the continuous improvement of natural polyphenols separation and purification technology and further studies on the Keap1-Nrf2 molecular mechanism, more and more natural polyphenols monomer components of Nrf2 activators have been gradually discovered. In this view, we summarize the research status of natural polyphenols that have been found with apparent Nrf2 activation and their action modes. On the whole, this review may guide the design of novel Keap1-Nrf2 activator.


Assuntos
Produtos Biológicos/farmacologia , Proteína 1 Associada a ECH Semelhante a Kelch/antagonistas & inibidores , Fator 2 Relacionado a NF-E2/antagonistas & inibidores , Polifenóis/farmacologia , Transdução de Sinais/efeitos dos fármacos , Produtos Biológicos/química , Humanos , Proteína 1 Associada a ECH Semelhante a Kelch/metabolismo , Estrutura Molecular , Fator 2 Relacionado a NF-E2/metabolismo , Polifenóis/química
3.
Cancer Med ; 8(14): 6165-6175, 2019 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-31464101

RESUMO

AIMS: To assess the safety and efficacy of parenchymal-sparing hepatectomy (PSH) as a treatment of colorectal liver metastases (CLM). METHODS: A comprehensive medical literature search was performed. Perioperative and long-term survival outcomes were pooled. Subgroup analysis and meta-regression analysis were performed to identify potential sources of heterogeneity. RESULTS: A total of 18 studies comprising 7081 CLM patients were eligible for this study. The PSH was performed on 3974 (56.1%) patients. We found that the OS (overall survival; hazard ratio [HR] = 1.01, 95% confidence interval [CI]: 0.94-1.08) and RFS (recurrence-free survival; HR = 1.00, 95% CI: 0.94-1.07) were comparable between non-PSH and PSH group. The perioperative outcomes were better in PSH than in non-PSH group. Non-PSH group was significantly associated with longer operative time (standard mean difference [SMD] = 1.17, 95% CI: 0.33-2.00), increased estimated blood loss (SMD = 1.36, 95% CI: 0.64-2.07), higher intraoperative transfusion rate (risk ratio [RR] = 2.27, 95% CI: 1.60-3.23), and more postoperative complications (RR = 1.39, 95% CI: 1.16-1.66). Meta-regression analyses revealed that no variable influenced the association between surgical types and the survival outcomes. CONCLUSIONS: This study shows that PSH is associated with better perioperative outcomes without compromising oncological outcomes. Given the increasing incidence of hepatic parenchyma, the PSH treatment offers a greater opportunity of repeat resection for intrahepatic recurrent tumors. It should be considered as an effective surgical approach for CLM.

4.
Am J Transl Res ; 11(4): 2181-2193, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31105827

RESUMO

miR-590-5p functions as an onco-miR or an anti-onco-miR in various types of cancers. However, the exact role of miR-590-5p in liver cancer remains to be elucidated. In the present study, we explored the predictive role of miR-590-5p expression in liver cancer patients. In addition, CCK-8 assay, colony formation assay, and analysis of xenograft tumors were performed to investigate the biological effects of miR-590-5p in liver cancer. A direct target of miR-590-5p was identified based on a luciferase assay and further molecular experiments. Our results demonstrated that miR-590-5p was upregulated in malignant tissues of liver cancer patients and in liver cancer cell lines. miR-590-5p expression was found to be inversely correlated with disease-free survival of liver cancer patients. Furthermore, both in vitro and in vivo experiments showed that miR-590-5p knockdown inhibited the growth of HepG2 and Bel-7404 tumor cells by promoting apoptosis and cell cycle arrest. We also demonstrated that increasing of miR-590-5p in 5-Fu resistant patients and liver cancer cells, and knockdown of miR-590-5p enhances chemosensitivity to 5-Fu in liver cancer. FOXO1 was identified as a direct and necessary target of miR-590-5p during regulating liver cancer growth. Taken together, our findings provide insights into the role of miR-590-5p in liver cancer. Moreover, it is suggested that miR-590-5p can serve as a novel therapeutic target and predictive biomarker for liver cancer.

5.
Gastroenterol Res Pract ; 2019: 1750329, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-30838039

RESUMO

Background: Circulating tumor DNA (ctDNA) derived from tumors is a promising biomarker for monitoring tumor status and evaluating therapeutic effects and prognosis. We studied the plasma human epidermal growth factor receptor 2 (HER2) amplification in gastric cancer (GC) patients by droplet digital PCR (ddPCR) during therapy with trastuzumab. Methods: A total of 12 patients were recruited after surgery. All patients received FOLFOX chemotherapy combined with trastuzumab as a treatment regimen. During the 12 months of the follow-up period, using elongation factor Tu GTP binding domain containing 2 (EFTUD2) as a reference gene, plasma HER2 to EFTUD2 ratios (the HER2 ratio) were determined for each patient every 2 months by ddPCR. Results: The concordance rate of HER2 amplification examined in plasma and formalin-fixed paraffin-embedded (FFPE) samples with ddPCR was 81.4%, with a sensitivity of 76.5% and a specificity of 83.8%. Plasma HER2 ratios were correlated with the primary tumor size (p < 0.01). A significant decrease in the plasma HER2 ratio was found after two months of treatment (p < 0.0001). Nine patients experienced partial response, and three patients had stable disease. Seven patients had progressive disease (PD) during follow-up, and four of them had died. The median progression-free survival (PFS) was 9.8 months. For each patient who developed PD, the plasma HER2 ratio was approximately 2.3-4.1 times higher than the cut-off value at the time of PD, which was the highest during the whole follow-up period. Conclusion: Longitudinal monitoring for the plasma HER2 ratio by ddPCR in the clinical courses of GC patients holds great promise for use as an indicator of tumor progression and treatment efficacy.

6.
Biochem Biophys Res Commun ; 507(1-4): 91-99, 2018 12 09.
Artigo em Inglês | MEDLINE | ID: mdl-30392914

RESUMO

Numerous studies have shown that CMTM family members have a variety of important roles in the occurrence and progression of cancer. CMTM7 has also been reported to be down-regulated in some digestive system tumors, but the expression patterns and pathological role of CMTM7 in gastric cancer remains unclear. In this study, we found that both CMTM7 and SOX10 were significantly down-regulated in gastric cancer tissues compared with paracancerous tissues, and the expression pattern of CMTM7 and SOX10 were strongly correlated (r = 0.6455, p < 0.001). Further, through bioinformatics technology and luciferase assay, we identify that SOX10 can be a transcriptional regulator of CMTM7 to mediate the expression of CMTM7 in gastric cancer. In addition, we found silencing the expression of CMTM7 can increase the proliferation and tumorigenesis of gastric cancer cells in vivo and in vitro. More interestingly, overexpression of SOX10 in cell lines stably silencing CMTM7 expression significantly inhibited the proliferation and tumor growth of gastric cancer. Therefore, our results demonstrate that CMTM7 as a tumor suppressor is down-regulated in gastric cancer, and SOX10 can regulate the proliferation and tumor formation of gastric cancer by regulating the expression of CMTM7.


Assuntos
Quimiocinas/genética , Regulação Neoplásica da Expressão Gênica , Proteínas com Domínio MARVEL/genética , Fatores de Transcrição SOXE/metabolismo , Neoplasias Gástricas/genética , Neoplasias Gástricas/patologia , Animais , Carcinogênese/genética , Carcinogênese/patologia , Linhagem Celular Tumoral , Proliferação de Células/genética , Quimiocinas/metabolismo , Humanos , Proteínas com Domínio MARVEL/metabolismo , Masculino , Camundongos Endogâmicos BALB C , Camundongos Nus , RNA Mensageiro/genética , RNA Mensageiro/metabolismo , Fatores de Transcrição SOXE/genética , Transcrição Genética
7.
Cell Physiol Biochem ; 49(5): 1703-1716, 2018.
Artigo em Inglês | MEDLINE | ID: mdl-30248669

RESUMO

BACKGROUND/AIMS: Colorectal cancer (CRC) is one of leading cancers in both incidence and mortality rate. The 5-year survival rate varies considerably depending on the pathological stage of the tumor. Although prominent progress has been made through screening for survival-associated factors from a certain type of genetic or epigenetic modifications, few attempts have been made to apply a network-based approach in prognostic factor identification, which could prove valuable for a complex, multi-faceted disease such as CRC. METHODS: In this study, a TCGA dataset of 379 CRC patients was subjected to a network-based analysis strategy consisting of multivariate regression, co-expression network and gene regulatory network analyses, and survival analyses. Both genetic and epigenetic aberrations, including those in gene expression and DNA methylation at specific sites, were screened for significant association with patient survival. A prognostic index (PI) integrating all potential prognostic factors was subsequently validated for its prognostic value. RESULTS: A collection of six miRNAs, eleven mRNAs, and nine DNA methylation sites were identified as potential prognostic factors. The low- and high-risk patient groups assigned based on PI level showed significant difference in overall survival (hazard ratio = 1.32, 95% confidence interval 1.29-1.36, p < 0.0001). Patients in the low- and high-risk groups can be further divided into a total of four subgroups, based on pathological staging. In the two high-risk subgroups (PI > 0), there was significant different (Cox p < 0.0001) in OS between the earlier (stages I/II) and later stages (stages III/IV). However, in the two low-risk subgroups (PI < 0), earlier (stages I/II) and later stages (stages III/IV) showed no significant difference in OS (Cox p = 0.185). On the other hand, there were significant differences in OS between the low- and high-risk subgroups when both subgroups were of earlier stages (Cox p < 0.001) or of later stages (Cox p < 0.0001). CONCLUSION: The novel network-based, integrative analysis adopted in this study was efficient in screening for prognostic predictors. Along with PI, the set of 6 miRNAs, 11 mRNAs, and 9 DNA methylation sites could serve as the basis for improved prognosis estimation for CRC patients in future clinical practice.


Assuntos
Neoplasias Colorretais/diagnóstico , Redes Reguladoras de Genes/genética , Idoso , Neoplasias Colorretais/genética , Neoplasias Colorretais/mortalidade , Metilação de DNA , Feminino , Humanos , Estimativa de Kaplan-Meier , Masculino , MicroRNAs/genética , MicroRNAs/metabolismo , Pessoa de Meia-Idade , Estadiamento de Neoplasias , Prognóstico , Modelos de Riscos Proporcionais , RNA Mensageiro/genética , RNA Mensageiro/metabolismo , Risco
8.
BMC Cancer ; 18(1): 676, 2018 Jun 22.
Artigo em Inglês | MEDLINE | ID: mdl-29929476

RESUMO

BACKGROUND: Novel non-invasive biomarkers for gastric cancer (GC) are needed, because the present diagnostic methods for GC are either invasive or insensitive and non-specific in clinic. The presence of stable circulating microRNAs (miRNAs) in plasma suggested a promising role as GC biomarkers. METHODS: Based on the quantitative droplet digital PCR (ddPCR), four miRNAs (miR-21, miR-93, miR-106a and miR-106b) related to the presence of GC were identified in plasma from a training cohort of 147 participants and a validation cohort of 28 participants. RESULTS: All circulating miRNA levels were significantly higher in the plasma of GC patients compared to healthy controls (P < 0.05). Through a combination of four miRNAs by logistic regression model, receiver operating characteristic (ROC) analyses yielded the highest AUC value of 0.887 in discriminating GC patients from healthy volunteers. Furthermore, miR-21, miR-93 and miR-106b levels were significantly related to an advanced TNM stage in GC patients. ROC analyses of the combined miRNA panel also showed the highest AUC value of 0.809 in discriminating GC patients with TNM stage I and II from stage III and IV. Through combining four miRNAs and clinical parameters, a classical random forest model was established in the training stage. In the validation cohort, it correctly discriminated 23 out of 28 samples in the blinded phase (false rate, 17.8%). CONCLUSIONS: Using the ddPCR technique, circulating miR-21, miR-93, miR-106a and miR-106b could be used as diagnostic plasma biomarkers in gastric cancer patients.


Assuntos
Biomarcadores Tumorais/sangue , MicroRNA Circulante/sangue , Reação em Cadeia da Polimerase/métodos , Neoplasias Gástricas/diagnóstico , Adulto , Idoso , Área Sob a Curva , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Curva ROC , Sensibilidade e Especificidade , Neoplasias Gástricas/sangue
9.
J Cell Biochem ; 119(8): 7091-7104, 2018 08.
Artigo em Inglês | MEDLINE | ID: mdl-29738066

RESUMO

Emerging evidence has identified that long non-coding RNAs (lncRNAs) may play an important role in the pathogenesis of many cancer types, including colorectal cancer (CRC). However, the role of PlncRNA-1 in CRC remains unclear. The aim of our present study was to investigate the potential functions of PlncRNA-1 in CRC and to identify the underlying mechanisms of action. We demonstrated that up-regulated PlncRNA-1 in CRC tissues and cells promoted cell proliferation by accelerating cell cycle process and inhibiting cell apoptosis in vitro, enhanced tumor growth and matastasis in vivo and was associated with cell migration and invasion, EMT process of CRC cells. In addition, PlncRNA-1 was a target of miR-204 and enhanced the expression of an endogenous miR-204 target, MMP9 in CRC cells. Furthermore, we found that PlncRNA-1 activates Wnt/ß-catenin pathway through the miR-204 in CRC cells. These results suggest that the PlncRNA-1/miR-204/ Wnt/ß-catenin regulatory network may shed light on tumorigenesis in CRC.


Assuntos
Proliferação de Células , Neoplasias Colorretais/metabolismo , Neoplasias Hepáticas/metabolismo , Neoplasias Hepáticas/secundário , RNA Longo não Codificante/metabolismo , RNA Neoplásico/metabolismo , Neoplasias Colorretais/genética , Neoplasias Colorretais/patologia , Feminino , Células HCT116 , Humanos , Neoplasias Hepáticas/genética , Masculino , MicroRNAs/genética , MicroRNAs/metabolismo , Pessoa de Meia-Idade , Metástase Neoplásica , RNA Longo não Codificante/genética , RNA Neoplásico/genética , Via de Sinalização Wnt
10.
Clin Exp Pharmacol Physiol ; 45(7): 729-741, 2018 07.
Artigo em Inglês | MEDLINE | ID: mdl-29542167

RESUMO

MicroRNA-21-3p (miR-21-3p), the passenger strand of pre-mir-21, has been found to be high-expressing in various cancers and to be associated with tumour malignancy, which is proposed as a novel focus in malignant tumours. Colorectal cancer (CRC), currently known as one of the most prevalent malignancy, is a leading cause of cancer death. This study aimed to investigate the key role of miR-21-3p in CRC by inhibiting its expression using transfection with miR-21-3p inhibitors into human CRC HCT116 cells. Results showed that the expression of miR-21-3p was higher than other CRC cells used in the study including Lovo, HT29, Colo320 and SW480 cells, inhibition of which suppressed the proliferation and induced cell cycle arrest in HCT116 cells. Besides, transfection with miR-21-3p inhibitors also attenuated cell migration and invasion, and induced apoptosis as well. Moreover, luciferase assay confirmed RBPMS as a direct target of miR-21-3p in HCT116 cells. Further, miR-21-3p inhibitors increased the nuclear accumulation of Smad4 and reduced phosphorylation of ERK. Interestingly, we found that silence of RBPMS using RNA interference (siRNA) not only elevated the cell viability but also increased the phosphorylation of ERK and reversed the nuclear accumulation of Smad4 induced by miR-21-3p inhibitors in HCT116 cells. Data suggest that inhibition of miR-21-3p suppresses cell proliferation, invasion as well as migration and induces apoptosis by directly targeting RBPMS through Smad4/ERK signalling pathway in HCT116 cells. Our study demonstrates miR-21-3p as a potent target for suppressing tumour progression of CRC which may have implications in CRC therapy in the future.


Assuntos
Apoptose/genética , Neoplasias Colorretais/patologia , MAP Quinases Reguladas por Sinal Extracelular/metabolismo , Sistema de Sinalização das MAP Quinases/genética , MicroRNAs/genética , Proteínas de Ligação a RNA/genética , Proteína Smad4/metabolismo , Movimento Celular/genética , Proliferação de Células/genética , Células HCT116 , Humanos , Invasividade Neoplásica
11.
Neoplasia ; 18(4): 242-52, 2016 04.
Artigo em Inglês | MEDLINE | ID: mdl-27108387

RESUMO

Helicobacter pylori infection is the strongest risk factor for development of gastric cancer. Host cellular stress responses, including inflammatory and immune responses, have been reported highly linked to H. pylori-induced carcinogenesis. However, whether mitochondrial regulation and metabolic reprogramming, which are potently associated with various cancers, play a role in H. pylori-induced gastric carcinogenesis is largely unknown. Here we revealed that Lon protease (Lonp1), which is a key inductive of mitochondrial unfolded protein response (UPR(mt)) and is required to maintain the mitochondrial quality, was greatly induced in H. pylori infected gastric epithelial cells. Importantly, we uncovered that knockdown of Lonp1 expression significantly diminished the metabolic switch to glycolysis and gastric cell proliferation associated with low multiplicity of H. pylori infection. In addition, Lonp1 overexpression in gastric epithelial cells also promoted glycolytic switch and cell overgrowth, suggesting H. pylori effect is Lonp1 dependent. We further demonstrated that H. pylori induced Lonp1 expression and cell overgrowth, at least partially, via HIF-1α regulation. Collectively, our results concluded the relevance of Lonp1 for cell proliferation and identified Lonp1 as a key regulator of metabolic reprogramming in H. pylori-induced gastric carcinogenesis.


Assuntos
Proteases Dependentes de ATP/metabolismo , Transformação Celular Neoplásica/metabolismo , Infecções por Helicobacter/complicações , Infecções por Helicobacter/microbiologia , Helicobacter pylori , Proteínas Mitocondriais/metabolismo , Neoplasias Gástricas/etiologia , Neoplasias Gástricas/metabolismo , Proteases Dependentes de ATP/genética , Animais , Proliferação de Células , Células Cultivadas , Análise por Conglomerados , Células Epiteliais/metabolismo , Células Epiteliais/microbiologia , Mucosa Gástrica/metabolismo , Mucosa Gástrica/microbiologia , Mucosa Gástrica/patologia , Perfilação da Expressão Gênica , Regulação da Expressão Gênica , Glicólise , Humanos , Subunidade alfa do Fator 1 Induzível por Hipóxia/metabolismo , Camundongos , Mitocôndrias/metabolismo , Proteínas Mitocondriais/genética , Modelos Biológicos
12.
PLoS One ; 9(10): e109169, 2014.
Artigo em Inglês | MEDLINE | ID: mdl-25360631

RESUMO

LIN28B is involved in "stemness" and tumourigenesis by negatively regulating the maturation of let-7 microRNA family members. In this study, we showed that LIN28B expression promotes migration and recurrence of colon cancer. Immunohistochemistry and reverse-transcription polymerase chain reactions were performed to detect LIN28B expression in colon cancer tissue microarrays, paraffin-embedded surgical resected tissues and cancer cells. Loss-of-function, migration and proliferation analyses were performed to delineate the potential roles of LIN28B in colon cancer. LIN28B was upregulated in colon cancer tissue compared to normal mucosa, and its overexpression correlated with reduced patient survival and increased tumour recurrence. LIN28B suppression inhibited the migration of SW480 colon cancer cells and facilitated the cytotoxicity induced by oxaliplatin in SW480 and HCT116 colon cancer cells. In conclusion, LIN28B overexpression contributes to colon tumourigenesis, and LIN28B may serve as a diagnostic tool and therapeutic target for colon cancer.


Assuntos
Neoplasias do Colo/mortalidade , Neoplasias do Colo/patologia , Proteínas de Ligação a RNA/metabolismo , Antineoplásicos/farmacologia , Linhagem Celular Tumoral , Movimento Celular , Neoplasias do Colo/metabolismo , Neoplasias do Colo/cirurgia , Feminino , Células HCT116/efeitos dos fármacos , Células HCT116/patologia , Humanos , Mucosa Intestinal/metabolismo , Masculino , Pessoa de Meia-Idade , Recidiva Local de Neoplasia , Compostos Organoplatínicos/farmacologia , Oxaliplatina , Proteínas de Ligação a RNA/genética , Valores de Referência , Análise Serial de Tecidos , Regulação para Cima
13.
Sichuan Da Xue Xue Bao Yi Xue Ban ; 43(2): 266-70, 2012 Mar.
Artigo em Chinês | MEDLINE | ID: mdl-22650046

RESUMO

OBJECTIVES: To investigate the optimal condition of bromodeoxyuridine (BrdU) labeling for bone marrow mesenchymal stem cells (BMSCs) in vitro and the feasibility of in vivo tracing of BrdU-labeling BMSCs. METHODS: BMSCs were isolated from Wistar rats and were in vitro routinely cultured. The third passage BMSCs was used for identification of special surface antigens by immunohistochemical methods. The purified BMSCs were incubated with BrdU at different concentrations for different incubating time to investigate optimal BrdU concentration and incubating time for cell labeling. The cell labeling index of BrdU was calculated with immunohistochemical analysis. BMSCs labeled BrdU were injected into damaged gastric mucosa of rats by micro injector. The colonization of BMSCs labeled BrdU in gastric mucosa was viewed. RESULTS: After purification and proliferation, the primary cultured BMSCs were uniformly long spindle-shapped form and formed cell colony, which showed the characteristics of stem cell. Immunocytochemistry showed BMSCs were positive for CD44 and CD90, while negative for CD14, CD45. The labeling rate of BrdU increased with the labeling time lasting and reached its height at 48 h. After incubating 48 and 72 hours, the labeling rate of BrdU with a concentration of 10 micromol/L was higher than that of BrdU with a concentration of 5 micromol/L (P < 0.05) and similar with that of BrdU with a concentration of 15 micromol/L (P > 0.05). In addition, the BrdU labeling could be detected after five consecutive passages and the labeling time could keep 21 d. The pathological observation demonstrated that BrdU-labeled BMSCs could colonize the damaged gastric mucosa with normal morphologic characteristics during observation period. CONCLUSION: BrdU labeling might be a feasible method for dynamic observation of the migration, growth and differentiation of migrating BMSCs in colonizing sites.


Assuntos
Bromodesoxiuridina , Movimento Celular , Transplante de Células-Tronco Mesenquimais , Células-Tronco Mesenquimais/citologia , Animais , Células da Medula Óssea/citologia , Diferenciação Celular , Células Cultivadas , Feminino , Masculino , Ratos , Coloração e Rotulagem/métodos
14.
Cancer Epidemiol ; 34(1): 66-72, 2010 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-20061204

RESUMO

BACKGROUND: Studies investigating the association between genetic polymorphism of glutathione S-transferase T1 (GSTT1) and risk of colorectal cancer have reported conflicting results. In order to clarify the effect of GSTT1 polymorphism on the risk of developing colorectal cancer, we carried out a meta-analysis using published data to obtain more precise estimates of risk. METHODS: Electronic searches of PubMed and EMBASE were conducted to select studies for this meta-analysis. Papers were included if they were observational studies investigating the association between GSTT1 polymorphism and colorectal cancer risk. The principal outcome measure was the odds ratio (OR) with 95% confidence interval (CI) for the risk of colorectal cancer associated with GSTT1 null genotype. RESULTS: We identified 30 eligible studies, which included 7635 cases and 12,911 controls. The combined results based on all studies showed that there was a statistically significant link between GSTT1 null genotype and colorectal cancer risk (OR=1.20, 95% CI=1.03-1.40). In the analysis of ethnic groups, we observed distinct differences associated with GSTT1 null genotype, the pooled odds ratios for the GSTT1 polymorphism were 1.32 in Caucasians (95% CI=1.09-1.58) and 1.03 in Asians (95% CI=0.81-1.32). As far as concerned the interaction between GSTT1 genotype and colorectal cancer risk in relation to smoking history, there was no increase in risk for smokers or nonsmokers with the GSTT1 null genotype (smokers: OR=1.13, 95% CI=0.80-1.60, nonsmokers: OR=0.99, 95% CI=0.71-1.38). When stratifying by the location of colorectal cancer, we found that there was a statistically significant link in rectal cancer (OR=1.50, 95% CI=1.09-2.07), but not in colon cancer (OR=1.33, 95% CI=0.94-1.88). No associations could be detected between null GSTT1 polymorphism and age, sex, tumor stage and differentiation. CONCLUSION: Our current study demonstrates that GSTT1 null genotype is associated with an increased risk of colorectal cancer, specifically, among Caucasians.


Assuntos
Neoplasias Colorretais/genética , Glutationa Transferase/genética , Polimorfismo Genético , Idoso , Neoplasias Colorretais/epidemiologia , Humanos , Masculino , Pessoa de Meia-Idade , Fatores de Risco
15.
Dig Dis Sci ; 55(7): 1831-8, 2010 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-19960261

RESUMO

PURPOSE: Studies investigating the association between genetic polymorphism of glutathione S-transferase T1 (GSTT1) and gastric cancer risk have reported conflicting results. Therefore, we conducted this meta-analysis to provide more precise evidence. METHODS: We searched the databases Medline, PubMed, Embase, and China National Knowledge Infrastructure up to July 30, 2009. Thirty-six studies with 4,357 gastric cancer cases and 9,796 controls were selected. Odds ratio (OR) and 95% confidence intervals (CI) were calculated based on fixed- and random-effects models. RESULTS: The combined results based on all studies showed there was a significant link between GSTT1 null genotype and gastric cancer risk (OR = 1.14, 95%CI = 1.01-1.28). In subgroup analysis stratified on the basis of ethnic group, we also observed positive association between GSTT1 polymorphism and gastric cancer risk among Caucasians (non-Europeans + non-Americans), but not among East Asians. When stratifying by control source, the overall ORs for population- and hospital-based studies were 1.09 (95%CI = 0.94-1.28) and 1.17 (95%CI = 1.03-1.34), respectively. Subjects with both GSTM1 and GSTT1 negative genotypes had increased gastric cancer risk compared with those who had nonnull genotypes of both GST genes. Subgroup analyses for Helicobacter pylori infection and smoking habit did not reveal any significant association between GSTT1 polymorphism and gastric cancer development. CONCLUSIONS: This meta-analysis suggests that GSTT1 gene polymorphism may be not associated with increased gastric cancer risk among Europeans, Americans, and East Asians. More large-scale studies based on the same racial group are needed.


Assuntos
Predisposição Genética para Doença/epidemiologia , Glutationa Transferase/genética , Polimorfismo Genético , Neoplasias Gástricas/epidemiologia , Neoplasias Gástricas/genética , Ásia/epidemiologia , Grupo com Ancestrais do Continente Asiático/genética , Estudos de Casos e Controles , Europa (Continente)/epidemiologia , Grupo com Ancestrais do Continente Europeu/genética , Feminino , Regulação Neoplásica da Expressão Gênica , Humanos , Incidência , Masculino , Prognóstico , Medição de Risco , Neoplasias Gástricas/patologia , Análise de Sobrevida , Estados Unidos/epidemiologia
16.
Dig Dis Sci ; 55(6): 1533-9, 2010 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-19672710

RESUMO

PURPOSE: Studies investigating the association between aspirin use and gastric cancer risk have reported conflicting results. The objective of this study was to quantitatively summarize the evidence for such a relationship. RESULTS: Two investigators independently searched the Medline, PubMed, Embase, and Academic Search Premier (EBSCO) databases. Fourteen studies with a total number of 5,640 gastric cancer cases were identified. Most of the study populations were Caucasian. The combined results based on all studies showed there was no statistically significant difference between aspirin use and gastric cancer risk (odds ratio (OR) = 0.80, 95% confidence intervals (CI) = 0.54-1.19). When stratifying by study designs and gender, results were similar except for cohort and randomized controlled trial (RCT) studies (OR = 0.72, 95% CI = 0.62-0.84). When stratifying by location and Helicobacter pylori (H. pylori) infection, we observed there were lower risks in noncardia gastric cancer (OR = 0.62, 95% CI = 0.55-0.69) and H. pylori-infected individuals (OR = 0.62, 95% CI = 0.42-0.90) for aspirin users. Among Caucasians, there were lower risks for noncardia gastric cancer (OR = 0.73, 95% CI = 0.62-0.87) and H. pylori-infected individuals (OR = 0.62, 95% CI = 0.42-0.90) also. CONCLUSIONS: This meta-analysis indicated that regular use of aspirin may be associated with reduced risk of noncardia gastric cancer, especially among Caucasians; for H. pylori-infected subjects the result was similar.


Assuntos
Anti-Inflamatórios não Esteroides/uso terapêutico , Anticarcinógenos/uso terapêutico , Aspirina/uso terapêutico , Neoplasias Gástricas/prevenção & controle , Anti-Inflamatórios não Esteroides/efeitos adversos , Anticarcinógenos/efeitos adversos , Aspirina/efeitos adversos , Distribuição de Qui-Quadrado , Grupo com Ancestrais do Continente Europeu , Medicina Baseada em Evidências , Feminino , Infecções por Helicobacter/microbiologia , Helicobacter pylori/patogenicidade , Humanos , Masculino , Razão de Chances , Medição de Risco , Fatores de Risco , Neoplasias Gástricas/etnologia , Neoplasias Gástricas/etiologia , Neoplasias Gástricas/microbiologia
17.
Sichuan Da Xue Xue Bao Yi Xue Ban ; 40(4): 719-23, 2009 Jul.
Artigo em Chinês | MEDLINE | ID: mdl-19764582

RESUMO

OBJECTIVE: To explore a suitable method for isolation, purification and multiplication of bone marrow mesenchymal stem cells (BMSCs). METHODS: Density gradient centrifugation and adherence separation methods were applied for isolation of BMSCs from Wistar rats. The cells were cultured and proliferated in culture medium containing calf serum (CS), fetal bovine serum (FBS), free of serum or different volume fraction of FBS. The characteristic and the morphology of BMSCs were observed under inverted microscope every day. The growth curves were draw and the surface antigen of BMSCs were detected by immunocytochemistry technique. The microstructure was observed by transmission electron microscope (TEM). RESULTS: The pure primary cells can be procured by density gradient centrifugation. But the primary cells cultured by adherence separation methods demonstrated higher cytoactive, more rapid proliferation, earlier colony confluence and shorter time for passage than that cultured by density gradient centrifugation method. The cells by adherence separation methods were essentially purified at passage 4. Both CS and FBS can promote the growth and proliferation of BMSCs, but the colony forming efficacy of cells (46.50%) cultured in medium containing 0.12 volume fraction FBS was the highest. The cells surface markers CD44, CD90 were positive and CD14, CD45 were negative. BMSCs were observed by TEM and possessed the characteristic of stem cells. Conclusion BMSCs with high quality and activity can be obtained with adherence separation by suitable method and culture conditions. L-DMEM medium containing 0.12 volume fraction FBS showed more profitable for the growth and proliferation of BMSCs.


Assuntos
Células da Medula Óssea/citologia , Técnicas de Cultura de Células , Proliferação de Células , Separação Celular/métodos , Células-Tronco Mesenquimais/citologia , Animais , Células Cultivadas , Feminino , Masculino , Ratos , Ratos Wistar
18.
Artigo em Chinês | MEDLINE | ID: mdl-19594028

RESUMO

OBJECTIVE: To investigate the effect of BMSCs on the repair of digestive tract injury and its mechanisms. METHODS: Recent literature on the effect of BMSCs on the repair of digestive tract injury was reviewed. RESULTS: BMSCs had the potency of self-replication, proliferation and multipotential differentiation, which played an important role in the repair of digestive tract injury. The probable mechanisms included: BMSCs' ability of migrating to the injured tissue and inhibiting the host immune response; BMSCs' dedifferentiation and redifferentiation; BMSCs' direct differentiation into the epithelial cells or the stem cells of digestive tract; BMSCs' fusion with the stem cells or the mature epithelial cells of digestive tract; BMSCs' participation in the reconstruction of injured microenvironment. CONCLUSION: BMSCs participates in the repair of digestive tract injury and has a bright future in the treatment of digestive system disease.


Assuntos
Células da Medula Óssea/fisiologia , Trato Gastrointestinal/patologia , Células-Tronco/patologia , Células da Medula Óssea/citologia , Diferenciação Celular , Células-Tronco/citologia , Cicatrização
19.
Eur J Cancer ; 45(16): 2867-73, 2009 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-19427197

RESUMO

The relationship between excess body weight and gastric cancer risk has not been well studied to date. We therefore carried out a systematic review and meta-analysis of published cohort studies to evaluate the association between excess body weight and gastric cancer risk. An electronic search of the MEDLINE, PubMed, EMBASE and Academic Search Premier (EBSCO) databases, which contain articles published from 1950 onwards, was conducted in order to select studies for this meta-analysis. Ten studies with a total number of 9492 gastric cancer cases and a studied population of 3,097,794 were identified. Overall, excess body weight [body mass index (BMI)25] was associated with an increased risk of gastric cancer [odds ratio (OR)=1.22; 95% confidence intervals (CIs)=1.06-1.41]. Specifically, a stratified analysis showed that excess body weight was associated with an increased risk of cardia gastric cancer [overweight and obese (BMI 25), OR=1.55, 95% CIs=1.31-1.84] and gastric cancer among non-Asians (overweight and obese, OR=1.24, 95% CIs=1.14-1.36); however, the stratified analysis also showed that there was no statistically significant link between excess body weight and gastric cancer in the following subgroups: males (overweight and obese, OR=1.22, 95% CIs=0.96-1.55), females (overweight and obese, OR=1.13, 95% CIs=0.65-1.94), non-cardia gastric cancer (overweight and obese, OR=1.18, 95% CIs=0.96-1.45) and Asians (overweight and obese, OR=1.17, 95% CIs=0.88-1.56). The combined results of this meta-analysis, however, do indicate that overweight and obesity are associated with an increased risk of gastric cancer. The strength of the association also increases with increasing BMI.


Assuntos
Sobrepeso/complicações , Neoplasias Gástricas/etiologia , Ásia/etnologia , Índice de Massa Corporal , Estudos de Coortes , Feminino , Humanos , Masculino , Obesidade/complicações , Obesidade/etnologia , Sobrepeso/etnologia , Fatores de Risco , Neoplasias Gástricas/etnologia
20.
Sichuan Da Xue Xue Bao Yi Xue Ban ; 40(1): 44-7, 2009 Jan.
Artigo em Chinês | MEDLINE | ID: mdl-19292042

RESUMO

OBJECTIVE: To investigate the expression of glucose transporter 1 (Glut1) in human breast cancer and its relationship to proliferating cell nuclear antigen (PCNA) protein, other tumor biomarkers and clinical pathologic factors. METHODS: Imunohistochemical staining (SP) was applied to measure the expression of Glut1 and PCNA in 20 cases of human breast fibroadenoma, 20 cases of usual hyperplasia and 80 cases of breast carcinoma. RESULTS: Glut1 was not found expressing in breast fibroadenoma and hyperplastic lesions. In contrast, the total positive rate of Glut1 in breast carcinoma was 58.8% (47/80); that in the ductal carcinoma in situ (DCIS) was 45.0% (9/20), that in the well-differentiated invasive carcinoma was 50.0% (15/30) and that in the poorly differentiated was 76.7% (23/30). The total positive rate of PCNA in breast carcinoma was 75% (60/80), that in DCIS was 65% (13/20) and that in invasive carcinoma was 78.3% (47/60). There was a positive correlation between Glut1 and PCNA level (r = 0.742, P (< 0.01). CONCLUSION: The overexpression of Glut1 play important roles in carcinogenesis and progression of breast carcinoma and closely correlate with cell proliferation of breast carcinoma, may suggest different therapeutic approaches or the need for closer follow-up, and be wished to become a new target for treatment of breast carcinoma.


Assuntos
Neoplasias da Mama/metabolismo , Carcinoma Ductal de Mama/metabolismo , Transportador de Glucose Tipo 1/metabolismo , Neoplasias da Mama/patologia , Carcinoma Ductal/metabolismo , Carcinoma Ductal/patologia , Carcinoma Ductal de Mama/patologia , Proliferação de Células , Feminino , Transportador de Glucose Tipo 1/genética , Humanos , Antígeno Nuclear de Célula em Proliferação/genética , Antígeno Nuclear de Célula em Proliferação/metabolismo
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