Céu Figueiredo

ORCID: 0000-0001-5247-840X
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About
Contact & Profiles
Research Areas
  • Helicobacter pylori-related gastroenterology studies
  • Gastric Cancer Management and Outcomes
  • Galectins and Cancer Biology
  • Veterinary medicine and infectious diseases
  • Eosinophilic Esophagitis
  • Gastrointestinal disorders and treatments
  • Genetic factors in colorectal cancer
  • Microbial Metabolites in Food Biotechnology
  • Gut microbiota and health
  • Digestive system and related health
  • RNA modifications and cancer
  • Bacteriophages and microbial interactions
  • Glycosylation and Glycoproteins Research
  • Cancer-related gene regulation
  • Colorectal Cancer Screening and Detection
  • Mycobacterium research and diagnosis
  • Cancer-related molecular mechanisms research
  • Wnt/β-catenin signaling in development and cancer
  • Viral gastroenteritis research and epidemiology
  • IL-33, ST2, and ILC Pathways
  • Advanced biosensing and bioanalysis techniques
  • Celiac Disease Research and Management
  • RNA Interference and Gene Delivery
  • Clostridium difficile and Clostridium perfringens research
  • Gastroesophageal reflux and treatments

Universidade do Porto
2016-2025

i3S - Instituto de Investigação e Inovação em Saúde, Universidade do Porto
2016-2025

IPO Porto
2004-2023

Institut de Recherche et d’Innovation
2022

Institute of Molecular Pathology and Pathomorphology
2012-2016

Institut Català d'Oncologia
2011

Faculty (United Kingdom)
2008

DDL Diagnostic Laboratory
1998-2003

Hospital de Santo António
2001

Vanderbilt University
1999-2000

Background: Both Helicobacter pylori genotype and host genetic polymorphisms play a role in determining the clinical consequences of H. infection. We investigated whether there are any combinations bacterial genotypes that particularly associated with occurrence gastric carcinoma. Methods: Genotypic variations virulence-associated genes vacA (s m regions) cagA were determined 221 subjects chronic gastritis 222 patients carcinoma by polymerase chain reaction (PCR)–line probe assay....

10.1093/jnci/94.22.1680 article EN JNCI Journal of the National Cancer Institute 2002-11-20

Gastric carcinoma development is triggered by Helicobacter pylori. Chronic H. pylori infection leads to reduced acid secretion, which may allow the growth of a different gastric bacterial community. This change in microbiome increase aggression mucosa and contribute malignancy. Our aim was evaluate composition microbiota chronic gastritis carcinoma.The retrospectively investigated 54 patients with 81 16S rRNA gene profiling, using next-generation sequencing. Differences microbial two patient...

10.1136/gutjnl-2017-314205 article EN cc-by Gut 2017-11-04

The amount of host DNA, poses a major challenge to metagenome analysis. However, there is no guidance on the levels nor depth sequencing needed acquire meaningful information from whole (WMS). Here, we evaluated impact wide range amounts DNA and depths microbiome taxonomic profiling using WMS. Synthetic samples with increasing were created by spiking mock bacterial community, mouse-derived cell line. Taxonomic analysis revealed that proportions led decreased sensitivity in detecting very low...

10.3389/fmicb.2019.01277 article EN cc-by Frontiers in Microbiology 2019-06-12

ABSTRACT The diversity of the gene encoding vacuolating cytotoxin ( vacA ) Helicobacter pylori was analyzed in 98 isolates obtained from different geographic locations. studies focused on variation previously defined s and m regions , as determined by PCR direct sequencing. Phylogenetic analysis revealed existence four distinct types s-region alleles: aside described s1a, s1b, s2 allelic types, a novel subtype, designated s1c, found. Subtype s1c observed exclusively East Asia appears to be...

10.1128/jcm.36.9.2597-2603.1998 article EN Journal of Clinical Microbiology 1998-09-01

ABSTRACT The present report describes an analysis of two virulence genes Helicobacter pylori . Parts the cagA gene, as well parts from signal (s) and middle (m) regions mosaic vacA were amplified with biotin-labelled PCR primers products subsequently analyzed by a single-step reverse hybridization line probe assay (LiPA). This comprises strip containing multiple specific probes for s region (s1a, s1b, s2 alleles), m (m1 m2 gene. A total 103 H. -positive materials, including cultured...

10.1128/jcm.36.5.1271-1276.1998 article EN Journal of Clinical Microbiology 1998-05-01

There are no established predictive markers of progression gastric preneoplastic lesions. The aim this study was to analyze the relationship between Helicobacter pylori cagA and vacA genotypes lesions.This a follow-up that carried out in province Spain with high risk cancer. A total 312 patients who underwent upper endoscopy biopsy 1988-1994 diagnoses normal mucosa, non-atrophic gastritis (NAG), non-metaplastic multifocal atrophic (MAG), complete or incomplete intestinal metaplasia (IM),...

10.1038/ajg.2011.1 article EN The American Journal of Gastroenterology 2011-02-01

Helicobacter pylori is a major cause of gastric carcinoma. To investigate possible link between bacterial infection and genetic instability the host genome, we examined effect H. on known cellular repair pathways in vitro vivo. Moreover, various types instabilities nuclear mitochondrial DNA (mtDNA) were examined.We observed effects cell line (AGS), C57BL/6 mice, individuals with chronic gastritis. In AGS cells, base excision mismatch (MMR) was analyzed by reverse transcription-PCR, Western...

10.1158/1078-0432.ccr-08-2686 article EN Clinical Cancer Research 2009-04-22

Although salt intake is considered a probable risk factor for gastric cancer, relevant studies have provided heterogeneous results, and the magnitude of association has not been accurately quantified. To quantify cancer in relation to dietary exposure according Helicobacter pylori infection status virulence, smoking, tumour site, histological type, we evaluated 422 cases 649 community controls. Salt was estimated year before onset symptoms through: sodium (estimated by food frequency...

10.1038/sj.bjc.6605993 article EN cc-by-nc-sa British Journal of Cancer 2010-11-16

Chronic Helicobacter pylori infection is recognized as a cause of gastric cancer. H. adhesion to cells mediated by bacterial adhesins such sialic acid–binding adhesin (SabA), which binds the carbohydrate structure sialyl–Lewis x. Sialyl–Lewis x expression in epithelium induced during persistent infection, suggesting that modulates host cell glycosylation patterns for enhanced adhesion. Here, we evaluate changes glycosylation-related gene profile human carcinoma line following infection. We...

10.1172/jci34324 article EN Journal of Clinical Investigation 2008-05-01

H. pylori drug-resistant strains and non-compliance to therapy are the major causes of eradication failure. For some bacterial species it has been demonstrated that fatty acids have a growth inhibitory effect. Our main aim was assess ability docosahexaenoic acid (DHA) inhibit both in vitro mouse model. The effectiveness standard (ST) combination with DHA on recurrence prevention success also investigated. effects were analyzed an dose-response study n vivo We analized colonize mice gastric...

10.1371/journal.pone.0035072 article EN cc-by PLoS ONE 2012-04-17

Helicobacter pylori induces an invasive phenotype in gastric epithelial cells through a mechanism that requires the type IV secretion system and phosphorylation of c-Met. The E-cadherin-catenin complex is major component adherens junctions functions as invasion suppressor. We investigated whether E-cadherin has role H. pylori-induced, c-Met phosphorylation-dependent cell-invasive phenotype.AGS lack are to stimulation were transduced with infected pylori. NCI-N87 cells, which endogenously...

10.1086/604727 article EN The Journal of Infectious Diseases 2009-07-15
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