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GSE62877
Homo sapiens
23 Downloadable Samples
Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)
Description
Werner syndrome (WS) is a human adult progeroid syndrome caused by loss-of-function mutations in the WRN RECQ helicase gene. We analyzed mRNA and miRNA expression in fibroblasts from WS patients and in fibroblasts depleted of WRN protein in order to determine the role of WRN in transcription regulation, and to identify genes and miRNAs that might drive WS disease pathogenesis. Genes altered in WS cells participate in cellular growth, proliferation and survival; in tRNA charging and in oncogenic signaling; and in connective tissue and developmental networks. Genes down-regulated in WS cells were highly enriched in Gquadruplex (G4) DNA motifs, indicating G4 motifs are physiologic substrates for WRN. In contrast, there was a remarkable, coordinate up-regulation of nearly all of the cytoplasmic tRNA synthetases and of genes associated with the senescence-associated secretory phenotype (SASP). These results identify canonical pathways that may drive the pathogenesis of Werner syndrome and associated disease risks.
Publication Title
The Werner syndrome RECQ helicase targets G4 DNA in human cells to modulate transcription.
Sample Metadata Fields
Sex, Age, Specimen part, Cell line
View Samples- Rattus norvegicus
- 32 Downloadable Samples
- Affymetrix Rat Gene 1.1 ST Array (ragene11st)
Description
Obesity is a chronic, complex and multifactorial disease that has reached pandemia levels and is becoming a serious health problem. Intestinal microbiota is considered a main factor that affects body weight and fat mass, which points toward a critical role in the development of obesity. In this sense, probiotic bacteria might modulate the intestinal microbiota and the mucosal-associated lymphoid tissue. The aim of this study was to investigate the effects of L. paracasei, L. rhamnosus and B. breve feeding on the intestinal mucosa gene expression in a genetic animal model of obesity.
Publication Title
Adamdec1, Ednrb and Ptgs1/Cox1, inflammation genes upregulated in the intestinal mucosa of obese rats, are downregulated by three probiotic strains.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 25 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Background: Chronic myeloid leukemia (CML) is a malignant clonal disorder of the hematopoietic system caused by the expression of the BCR/ABL fusion oncogene. It is well known that CML cells are genetically unstable. However, the mechanisms by which these cells acquire genetic alterations are poorly understood. Imatinib mesylate (IM) is the standard therapy for newly diagnosed CML patients. IM targets the oncogenic kinase activity of BCR-ABL. Objective: To study the gene expression profile of BM hematopoietic cells in the same patients with CML before and one month after imatinib therapy. Methods: Samples from patients with CML were analyzed using Affymetrix GeneChip Expression Arrays. Results: A total of 594 differentially expressed genes, most of which (393 genes) were downregulated, as a result of imatinib therapy were observed. Conclusions: The blockade of oncoprotein Bcr-abl by imatinib could cause a decrease in the expression of key DNA repair genes, and cells try to restore the normal gene expression levels required for cell proliferation and chromosomal integrity.
Publication Title
Imatinib therapy of chronic myeloid leukemia restores the expression levels of key genes for DNA damage and cell-cycle progression.
Sample Metadata Fields
Age, Specimen part
View Samples- Rattus norvegicus
- 18 Downloadable Samples
- Affymetrix Rat Gene 1.0 ST Array (ragene10st)
Description
CDKN1B (p27) was formally established as a tumor suppressor gene (tsg) following the identification of inactivating germline mutations in rats (MENX syndrome) and patients (MEN4 syndrome) developing multiple neuroendocrine tumors (NETs). MENX-affected rats are homozygous for the predisposing p27 mutation, suggesting a canonical tsg function. In contrast, mice heterozygous for a defective Cdkn1b allele are already predisposed to tumor formation (haploinsufficiency). We here report that heterozygous mutant rats (p27+/mut) develop the same NETs seen in the homozygous (p27mut/mut) animals but with slower progression. In the tumors of p27+/mut rats, the wild-type allele is neither lost nor silenced, implying that p27 is haploinsufficient for tumor suppression also in this model.
Publication Title
Characterization of neuroendocrine tumors in heterozygous mutant MENX rats: a novel model of invasive medullary thyroid carcinoma.
Sample Metadata Fields
Age
View Samples- Mus musculus
- 15 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
Robles-Valero et al. report a tumor suppression role for the otherwise oncogenic Vav1 Rho GEF. This paradoxical action is mediated by the catalysis-independent buffering of Notch1 signaling in immature T cells.
Publication Title
A Paradoxical Tumor-Suppressor Role for the Rac1 Exchange Factor Vav1 in T Cell Acute Lymphoblastic Leukemia.
Sample Metadata Fields
Specimen part, Treatment
View Samples- Rattus norvegicus
- 13 Downloadable Samples
- Affymetrix Rat Gene 1.0 ST Array (ragene10st)
Description
As overwhelming evidence coming from transgenic mouse models but also from MEN4 patients seem to suggest that loss or inactivation of a single p27 allele plays an important role in neuroendocrine tumorigenesis, we decided to perform a detailed analysis of the phenotype of rats heterozygous for the MENX-associated germline Cdkn1b mutation. We here show that the reduction to a single functional p27 allele predisposes MENX heterozygous rats to the development of neuroendocrine malignancies.
Publication Title
Characterization of neuroendocrine tumors in heterozygous mutant MENX rats: a novel model of invasive medullary thyroid carcinoma.
Sample Metadata Fields
Sex, Age, Specimen part
View Samples- Rattus norvegicus
- 11 Downloadable Samples
- Affymetrix Rat Gene 1.0 ST Array (ragene10st)
Description
As overwhelming evidence coming from transgenic mouse models but also from MEN4 patients seem to suggest that loss or inactivation of a single p27 allele plays an important role in neuroendocrine tumorigenesis, we decided to perform a detailed analysis of the phenotype of rats heterozygous for the MENX-associated germline Cdkn1b mutation.
Publication Title
Characterization of neuroendocrine tumors in heterozygous mutant MENX rats: a novel model of invasive medullary thyroid carcinoma.
Sample Metadata Fields
Sex, Age, Specimen part
View Samples- Homo sapiens
- 6 Downloadable Samples
- Affymetrix Clariom S Human array (clariomshuman)
Description
MiR-1246 was found to promote tumorigenesis and metastasis in sevearl cancer types. In the context of tumor microenvironment, tumor-associated macrophages are a central part typically correlated with poor prognosis.
Publication Title
Mutant p53 cancers reprogram macrophages to tumor supporting macrophages via exosomal miR-1246.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 110 Downloadable Samples
- Affymetrix HT Human Genome U133A Array (hthgu133a)
Description
Gene expression profiling of 111 colon tissues from tumors and adjacent noncancerous tissues.
Publication Title
Germline variation in NCF4, an innate immunity gene, is associated with an increased risk of colorectal cancer.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 35 Downloadable Samples
- Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)
Description
Bloom syndrome is a rare autosomal recessive genetic instability and cancer predisposition syndrome caused by loss of function mutations in the BLM RECQ helicase gene. To ask if some of the distinctive pathological features of Bloom syndrome might reflect altered gene expression, we analyzed global mRNA and miRNA expression in fibroblasts from 16 patients and 15 matched normal controls, and in control primary diploid fibroblasts depleted of the BLM protein. We document significant differential expression of both protein-coding genes and miRNAs with well-characterized cancer associations in BLM-deficient cells. Differences in expression correlated significantly with G4 motifs, which are associated with potential to form G-quadruplex structures. These results indicate that BLM helicase may modulate gene expression by regulating the in vivo stability of G-quadruplex structures, and identify sets of genes and miRNAs whose expression, when altered, may drive the pathogenesis of Bloom syndrome and associated cancers.
Publication Title
Regulation of gene expression by the BLM helicase correlates with the presence of G-quadruplex DNA motifs.
Sample Metadata Fields
Sex, Age, Specimen part, Cell line
View Samples