Helicobacter pylori is a well-recognized bacterium associated with the development of several histopathological lesions in the stomach. The chronic infection produces an inflammatory lesion known as gastritis. This lesion can later progress to more serious lesions such as intestinal metaplasia. Some attempts in the transcriptome of these conditions have been made; these however, have yielded limited information. Given the potential of high-throughput technologies for understanding biological processes altered and in the description of biomarkers of disease, we performed a genome-wide gene expression analysis in gastric biopsies. The aim of this study was to describe the altered molecular mechanism and potential biomarkers of follicular gastritis, chronic gastritis and intestinal metaplasia, through the identification of characteristic gene expression profiles in each histopathological lesion. The exploratory set comprised twenty-one biopsies from patients with follicular gastritis (n=7), chronic gastritis (n=7), and intestinal metaplasia (n=7), which were analyzed by whole-genome gene expression microarrays. The enrichment analyses and functional annotation of genes using computational tools were performed. The bioinformatics data of the same 21 biopsies were validated by real time PCR analysis while 79 FFPE samples were analyzed by immunohistochemistry.
No associated publication
Sex, Age
View SamplesGlioblastomas (GBM) are one of the most frequent and aggressive brain tumors. In these malignancies, progesterone (P4) promotes proliferation, migration, and invasion. The P4 metabolite allopregnanolone (3-THP) similarly promotes cell proliferation in the U87 human GBM cell line.
Allopregnanolone Alters the Gene Expression Profile of Human Glioblastoma Cells.
Specimen part, Cell line, Treatment
View SamplesExperimental in vtiro approach to molecular pathways implicated in Apert Syndromes craniosynostosis through transcriptomics techniques. FGFR2 activation requires a tridimensional configuration between ligand, receptor and heparan sulfate(HS). Mutations in the extracellular region of this receptor affect the balance between proliferation and differentiation of osteoprogenitor cells, leading to craniosynostosis as Apert Syndrome (AS). We postulate that the degradation of HS in periosteal tissue in patients with AS can modify the gene expression profile and modulate cell behavior. Based on previous evidence we propose that the treatment with an enzyme that degrades HS, as Idursulfase, in periosteal tissue of patients with AS, could be affect the formation of the ternary complex (FGF / FGFR / HS), triggering changes in gene profiles expression in several molecular pathways, regarding their basal state with the mutated receptor.
No associated publication
Sex, Specimen part, Disease
View SamplesThe main goal of the research was to find some new biomarkers for the monitoring of the Minimal Residual Disease in Acute Lymphoblastic Leukemia patients.
No associated publication
Sex, Age
View SamplesThis SuperSeries is composed of the SubSeries listed below.
No associated publication
Sex, Specimen part, Cell line, Subject
View SamplesSeveral copy number altered regions (CNA) have been identified in the genome of cervical cancer, especially amplifications of 3q and 5p. However, the contribution of those alterations to cervical carcinogenesis is still a matter of debate, since genome-wide, there is a lack of correlation between CNAs and gene expression. In this study, we investigated whether the CNAs in cell lines (CaLo, CasKi, HeLa, SiHa), at a gene-by-gene level, are related to changes in gene expression. On average 19.2% of the whole genome of cell lines had CNA. However, only 2.4% consisted of minimal recurrent regions (MRR), common to all cell lines. Whereas 3q had just some sparse common gains (13%), 5p was entirely duplicated recurrently. Genome-wide, only 11% of genes located in CNAs changed gene expression. In contrast, the rate increased over 3 fold times in MRRs. Chr 5p was confirmed entirely amplified by FISH. In spite of this, at most 32.9% of the explored genes in 5p (n=202) were de-regulated. In 3q, the rate was just 11.8%. Even in 3q26, which had five MRRs and 38.7% of SNPs was gained recurrently, the rate rose slightly to 13.6% (10 out of 73). Interestingly, up to 16% of de-regulated genes in 5p and 80% in 3q26 were down-regulated, suggesting additional factors are involved in gene repression. The de-regulated genes in 3q and 5p were found in clusters, suggesting local chromatin factors may also influence gene expression. In regions amplified discontinuously, the rate of down-regulated genes rose steadily as the number of amplified SNPs increased (p<0.01, Spearman's correlation). This suggests partial gene amplification as a mechanism of silencing gene expression. Additional genes were identified up- or down-regulated in 5p and 3q, which could be involved in cervical carcinogenesis, especially implicated in apoptosis. Those include CLPTM1L, AHRR, PDCD6 and DAP in 5p and TNFSF10 and ECT2 in 3q. Overall, the gene expression and copy number profiles suggest other factors, like epigenetic or chromatin domains, may influence gene expression within the entirely amplified genome segments. Further studies are needed to elucidate how these mechanisms regulate gene expression.
No associated publication
Sex, Cell line
View SamplesWe analyzed the changes in the spinal cord transcriptome after a spinal cord contusion injury and MSC or OEC transplantation. The cells were injected immediately or 7 days after the injury. The mRNA of the spinal cord injured segment was extracted and analyzed by microarray at 2 and 7 days after cell grafting.
Gene expression changes in the injured spinal cord following transplantation of mesenchymal stem cells or olfactory ensheathing cells.
Treatment
View SamplesAlthough Human papillomavirus infection is the main causal factor for cervical cancer (CC), there is data suggesting genetic factors could modulate the risk and progression of CC. Sibling studies suggest that maternally inherited factors could be involved in CC. To assess whether mitochondrial DNA (mtDNA) polymorphisms are associated to cervical cancer, HPV infection and HPV types, a case-control study was performed in the Mexican mestizo population. The polymorphism of mtDNA D-Loop was investigated in 187 cervical cancer patients and 270 healthy controls. D-loop was amplified from a blood DNA sample and analyzed by sequencing. HPV was detected and typed in cervical scrapes from both groups. mtDNA polymorphisms were compared in the whole samples and stratified by HPV types. The expression of 29 mitochondrial genes was analyzed in a subset of 45 tumor biopsies using the expression microarray ST1.0. The Amerindian haplogroup B2 increased the risk for CC (OR=1.6, 95% CI: 1.05-2.58) and showed an additive effect of 36% over the risk conferred by the HPV (OR=153, 95% CI: 65.4-357.5). The frequency of HPV 16, 18, 31 and 45 in cancer samples was similar in all haplogroups but one (D1). It showed a very low frequency of HPV16, any HPV18 and high frequency of HPVs 31, 45 and other types. Two mtDNA genes (MT-TD, MTTK) could be involved in the increased risk conferred by the haplogroup B2, since they were up-regulated exclusively in B2 tumors (p<0.05, t-test). These findings will contribute to clarify the importance of genetic factors in CC.
The Amerindian mtDNA haplogroup B2 enhances the risk of HPV for cervical cancer: de-regulation of mitochondrial genes may be involved.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Identification of putative TAL effector targets of the citrus canker pathogens shows functional convergence underlying disease development and defense response.
Age, Specimen part, Time
View SamplesThis SuperSeries is composed of the SubSeries listed below.
DIDO as a Switchboard that Regulates Self-Renewal and Differentiation in Embryonic Stem Cells.
Specimen part
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