Downregulation of decreases survival gene expression, promotes apoptosis and affects the cell cycle of gastric cancer cells.

Background: Chronic inflammation due to () infection promotes gastric carcinogenesis. Tumour necrosis factor-α (TNF-α), a key mediator of inflammation, induces cell survival or apoptosis by binding to two receptors (TNFR1 and TNFR2). TNFR1 can induce both survival and apoptosis, while TNFR2 results only in cell survival.

Hydrogen peroxide and Helicobacter pylori extract treatment combined with APE1 knockdown induce DNA damage, G2/M arrest and cell death in gastric cancer cell line.

Chronic inflammation resulting from Helicobacter pylori (H. pylori) infection, the major risk factor for gastric cancer, results in increased release of reactive oxygen species (ROS), promoting oxidative stress and DNA damage. APE1 endonuclease, a key component of the base excision repair (BER) pathway, is responsible for the repair of damage induced by ROS.

Characterization and strong risk association of to polymorphism and and their influence on mRNA expression in gastric cancer.

Background: Toll-like receptor-2 () is responsible for recognizing () and activating the immune response. Polymorphisms in may modulate gastric carcinogenesis.

Aim: To evaluate whether the (rs3804099) and - (rs111200466) polymorphisms contribute to gastric carcinogenesis in the Brazilian population, and to determine the influence of both polymorphisms and infection on mRNA expression.

Toll-like receptor 9 polymorphisms and influence gene expression and risk of gastric carcinogenesis in the Brazilian population.

Background: Toll-like receptors (TLRs) are the first line of host defense, and are involved in () recognition and activation of both inflammatory and carcinogenic processes. The presence of single nucleotide polymorphisms (SNPs) in genes that activate the immune response may modulate the risk of precancerous lesions and gastric cancer (GC). Among them, Toll-like receptor 9 (TLR9) polymorphisms have emerged with a risk factor of infectious diseases and cancer, however the studies are still inconclusive.

Fusobacterium nucleatum tumor DNA levels are associated with survival in colorectal cancer patients.

There is increasing evidence indicating a role for Fusobacterium nucleatum (F. nucleatum) in colorectal cancer (CRC) development and prognosis. This study evaluated F.

Upregulation of the and genes and miRNAs involved in DNA damage response and repair in gastric cancer.

Gastric cancer remains one of the leading causes of cancer-related death worldwide, and most of the cases are associated with infection. This bacterium promotes the production of reactive oxygen species (ROS), which cause DNA damage in gastric epithelial cells. In this study, we evaluated the expression of important genes involved in the recognition of DNA damage (, , and ) and ROS-induced damage repair () and the expression of some miRNAs (miR-15a, miR-21, miR-24, miR-421 and miR-605) that target genes involved in the DNA damage response (DDR) in 31 fresh tissues of gastric cancer.

Erratum to "Epidemiological and Clinical-Pathological Aspects of Infection in Brazilian Children and Adults".

[This corrects the article DOI: 10.1155/2018/8454125.].

Up-regulation of tumor necrosis factor-α pathway survival genes and of the receptor TNFR2 in gastric cancer.

Background: Gastric carcinogenesis can be induced by chronic inflammation triggered by () infection. Tumor necrosis factor (TNF)-α and its receptors (TNFR1 and TNFR2) regulate important cellular processes, such as apoptosis and cell survival, and the disruption of which can lead to cancer. This signaling pathway is also modulated by microRNAs (miRNAs), altering gene expression.

Relationship between , inflammatory mediators and microRNAs in colorectal carcinogenesis.

Aim: To examine the effect of () on the microenvironment of colonic neoplasms and the expression of inflammatory mediators and microRNAs (miRNAs).

Methods: Levels of DNA, cytokine gene mRNA (, , , , , and ), and potentially interacting miRNAs (miR-21-3p, miR-22-3p, miR-28-5p, miR-34a-5p, miR-135b-5p) were measured by quantitative polymerase chain reaction (qPCR) TaqMan assays in DNA and/or RNA extracted from the disease and adjacent normal fresh tissues of 27 colorectal adenoma (CRA) and 43 colorectal cancer (CRC) patients. mutations were detected by direct sequencing and microsatellite instability (MSI) status by multiplex PCR.

Epidemiological and Clinical-Pathological Aspects of Infection in Brazilian Children and Adults.

Aim: To evaluate the prevalence and risk factors of infection in the pediatric and adult population seen at a public hospital in São José do Rio Preto, SP, Brazil.

Methods: This is a retrospective study that evaluated 2406 medical records of children, adolescents, and adults with dyspeptic symptoms who underwent upper gastrointestinal endoscopy. diagnosis and demographic and clinical-pathological features were recorded.

Annexin A1 peptide is able to induce an anti-parasitic effect in human placental explants infected by Toxoplasma gondii.

This study was conducted to investigate annexin A1 (ANXA1) functions in human placental explants infected with Toxoplasma gondii (T. gondii). We examined the first and third trimester placental explants infected with T.

, and polymorphisms in sporadic colorectal neoplasms.

Aim: To investigate the contribution of polymorphisms in the , and genes on sporadic colorectal cancer (SCRC) risk.

Methods: Six hundred forty-one individuals (227 patients with SCRC and 400 controls) were enrolled in the study. The variables analyzed were age, gender, tobacco and alcohol consumption, and clinical and histopathological tumor parameters.

Interaction between inflammatory mediators and miRNAs in Helicobacter pylori infection.

Helicobacter pylori cause chronic inflammation favouring gastric carcinogenesis, and its eradication may prevent malignant transformation. We evaluated whether H. pylori infection and its eradication modify the expression of inflammatory mediators in patients with chronic gastritis.

TLR2 and TLR4 polymorphisms influence mRNA and protein expression in colorectal cancer.

Aim: To evaluate the effect of promoter region polymorphisms of toll-like receptor (TLR)2-196 to -174del and TLR4-1607T/C (rs10759932) on mRNA and protein expression in tumor tissue and of TLR4+896A/G (rs4986790) on colorectal cancer (CRC) risk.

Methods: The TLR2-196 to -174del polymorphism was investigated using allele-specific polymerase chain reaction (PCR) and the TLR4-1607T/C and TLR4+896A/G by PCR-restriction fragment length polymorphism (RFLP). We genotyped 434 DNA samples from 194 CRC patients and 240 healthy individuals.

Influence of functional polymorphisms in TNF-α, IL-8, and IL-10 cytokine genes on mRNA expression levels and risk of gastric cancer.

Functional polymorphisms in promoter regions can produce changes in the affinity of transcription factors, thus altering the messenger ribonucleic acid (mRNA) expression levels of inflammatory cytokines associated with the risk of cancer development. The goal of this study was to evaluate the influence that polymorphisms in the cytokine genes known as TNF-α-308 G/A (rs1800629), TNF-α-857 C/T (rs1799724), IL-8-251 T/A (rs4073), IL-8-845 T/C (rs2227532), and IL-10-592 C/A (rs1800872) have on changes to mRNA expression levels and on the risks of chronic gastritis (CG) and gastric cancer (GC). A sample of 723 individuals was genotyped using the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) technique.

Effect of Helicobacter pylori eradication on TLR2 and TLR4 expression in patients with gastric lesions.

Objective: Helicobacter pylori (Hp) is recognized by TLR4 and TLR2 receptors, which trigger the activation of genes involved in the host immune response. Thus, we evaluated the effect of eradication therapy on TLR2 and TLR4 mRNA and protein expression in H. pylori-infected chronic gastritis patients (CG-Hp+) and 3 months after treatment.

Deregulation of annexin-A1 and galectin-1 expression in precancerous gastric lesions: intestinal metaplasia and gastric ulcer.

Objective: Annexin-A1 (ANXA1/AnxA1) and galectin-1 (LGALS1/Gal-1) are mediators that play an important role in the inflammatory response and are also associated with carcinogenesis. We investigated mRNA and protein expression in precancerous gastric lesions that participate in the progression cascade to gastric cancer, such as intestinal metaplasia (IM) and gastric ulcer (GU).

Methods: Quantitative real-time PCR (qPCR) and immunohistochemical techniques were used to analyze the relative quantification levels (RQ) of ANXA1 and LGALS1 mRNA and protein expression, respectively.

Helicobacter pylori infection: host immune response, implications on gene expression and microRNAs.

Helicobacter pylori (H. pylori) infection is the most common bacterial infection worldwide. Persistent infection of the gastric mucosa leads to inflammatory processes and may remain silent for decades or progress causing more severe diseases, such as gastric adenocarcinoma.

Expression of annexin-A1 and galectin-1 anti-inflammatory proteins and mRNA in chronic gastritis and gastric cancer.

Objective: The anti-inflammatory proteins annexin-A1 and galectin-1 have been associated with tumor progression. This scenario prompted us to investigate the relationship between the gene and protein expression of annexin-A1 (ANXA1/AnxA1) and galectin-1 (LGALS1/Gal-1) in an inflammatory gastric lesion as chronic gastritis (CG) and gastric adenocarcinoma (GA) and its association with H. pylori infection.

Profiles of gene polymorphisms in cytokines and Toll-like receptors with higher risk for gastric cancer.

Background: Chronic inflammation and gastric carcinogenesis show a close association, so gene polymorphisms that modify the intensity of the inflammatory response may contribute to variations in gastric cancer risk.

Aims: The purpose of this study was to investigate the combined effect of the pro- and anti-inflammatory cytokines and toll-like receptors polymorphisms on the chronic gastritis and gastric cancer risk in a Brazilian population sample.

Methods: We evaluated 669 DNA samples (200 of gastric cancer [GC], 229 of chronic gastritis [CG], and 240 of healthy individuals [C]).

Alterations of the TP53 gene in gastric and esophageal carcinogenesis.

TP53 genes is one of more important tumor suppressor gene, which acts as a potent transcription factor with fundamental role in the maintenance of genetic stability. The development of esophageal and gastric cancers is a multistep process resulting in successive accumulation of genetic alterations that culminates in the malignant transformation. Thus, this study highlights the participation of the main genetic alterations of the TP53 gene in esophageal and gastric carcinogenesis.

Biologic and genetics aspects of chagas disease at endemic areas.

The etiologic agent of Chagas Disease is the Trypanosoma cruzi, transmitted through blood-sucking insect vectors of the Triatominae subfamily, representing one of the most serious public health concerns in Latin America. There are geographic variations in the prevalence of clinical forms and morbidity of Chagas disease, likely due to genetic variation of the T. cruzi and the host genetic and environmental features.

Polymorphisms of the TLR2 and TLR4 genes are associated with risk of gastric cancer in a Brazilian population.

Aim: To investigate toll-like receptor 2 (TLR2) -196 to -174 del, and TLR4 (+896A/G rs4986790 and +1196C/T rs4986791) polymorphisms at risk of chronic gastritis and gastric cancer in a Brazilian population and association of gastric lesions with risk factors such as smoking, alcohol intake and Helicobacter pylori infection.

Methods: In this case-control study, polymorphism at TLR2 -196 to -174 del was investigated by using the allele-specific polymerase chain reaction (PCR) method, while the PCR-restriction fragment length polymorphism technique was carried out to identify the TLR4 (rs4986790 and rs4986791) genotypes in 607 Brazilian individuals (208 with chronic gastritis-CG, 174 with gastric cancer-GC and 225 controls -C).

Results: The single nucleotide polymorphisms TLR4+1196C/T was not associated with risk of chronic gastritis or gastric cancer and the homozygous genotypes TLR4+896GG and TLR4+1196TT were absent in the studied population.

Gene mutations and polymorphisms of TP53 and FHIT in chronic esophagitis and esophageal carcinoma.

Aim: The aim of this study was to investigate genetic changes of the TP53 (tumor protein p53) and FHIT (fragile histidine triad) genes in precursor lesion such as chronic esophagitis (CE) and in esophageal squamous cell carcinoma (ESCC).

Materials And Methods: PCR-Single Strand Conformation Polymorphism (SSCP) analysis and DNA sequencing in 30 CE and 10 ESCC specimens were performed.

Results: DNA sequencing indicated two novel mutations in the TP53 exons 5 (codon 147) and 6 (codon 197) in 2/9 SSCP positive cases of ESCC, but no mutation was found in the CE.

Expression of ki-67 antigen and caspase-3 protein in benign lesions and esophageal carcinoma.

Background: The present study aimed to evaluate apoptosis and cell proliferation alterations in esophageal benign lesions in comparison to esophageal carcinomas.

Materials And Methods: Immunohistochemistry was performed for caspase-3 protein (CPP32) and Ki-67 antigen expression in the esophageal mucosa from patients with Chagas disease (CD) with and without megaesophagus (CM), chronic esophagitis (CE), esophageal carcinoma (ESCC) and in normal mucosa (NM).

Results: The Ki-67 labeling index (LI) was similar in all groups (range: 30%-48%), having no statistically significant difference among the groups.