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accession-icon GSE85577
Expression of rat hepatocytic progenitor cells with and without hepatic Thy1-positive cells in retrorsine/partial hepatectomy treated rats models.
  • organism-icon Rattus norvegicus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Gene 2.0 ST Array (ragene20st)

Description

We found that the transplantation of Thy1+ cells transiently increased the liver mass by expanding resident small hepatocy-like progenitor cells(SHPCs).

Publication Title

Transplantation of Thy1<sup>+</sup> Cells Accelerates Liver Regeneration by Enhancing the Growth of Small Hepatocyte-Like Progenitor Cells via IL17RB Signaling.

Sample Metadata Fields

Specimen part

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accession-icon GSE157142
MUTYH is associated with hepatocarcinogenesis in a NASH model mouse
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.0 ST Array (mogene20st)

Description

Mice with MUTYH-null allele (Mutyh+/-, Mutyh-/-) were fed a high-fat/high-cholesterol (HFHC) diet or HFHC + high iron diet. The incidence of liver tumors and histological features of the liver were compared.

Publication Title

MUTYH is associated with hepatocarcinogenesis in a non-alcoholic steatohepatitis mouse model.

Sample Metadata Fields

Specimen part, Disease, Treatment

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accession-icon GSE35512
Identification of targets specifically regulated by a 'super hybrid p53'
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

p63, like its homologue, the tumor suppressor p53, is also able to induce apoptosis in several cancer cell types. p53 family proteins are composed of three characteristic domains which are: 1) an N-terminal transactivation domain (TAD); 2) a central DNA-binding domain (DBD); and 3) an oligomerization domain (OD). In this study, we constructed recombinant adenoviruses containing hybrid genes composed of fragments of p53 and TAp63 genes by connecting coding sequences of their three functional domains. The potency of tumor growth suppression of these hybrid molecules was evaluated using in vitro and in vivo models. One of the p53-p63 hybrid molecules, p63-53O, was observed to be the most potent activator of human cancer cells to apoptosis when compared to the p53, TAp63 or several alternative p53-p63 hybrid molecules. p63-53O hybrid is composed of TAD and DBD of TAp63 and OD of p53. In an effort to identify specific targets regulated by pro-apoptotic hybrid p63-53O, we next performed Affymetrix Genechip analysis and compared expression patterns in a human osteosarcoma cell line Saos-2 transfected separately with Ad-p53, Ad-TAp63 and Ad-p63-53O.

Publication Title

A novel approach to cancer treatment using structural hybrids of the p53 gene family.

Sample Metadata Fields

Cell line

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accession-icon GSE13504
Identification of targets specifically regulated by TAp73
  • organism-icon Homo sapiens
  • sample-icon 3 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The p53 family consists of three members, p53, p73, and p63. These proteins share a high degree of amino-acid sequence similarity and major functional domains. The p53 gene, the first member of the family to be identified, is the most frequent target gene for genetic alterations in human cancers. In contrast, p73 and p63 are mainly involved in normal development and differentiation. These differences among the p53 family are likely to depend on activation or repression of different sets of target genes. In this study, to identify targets specifically regulated by p73, we performed microarray analysis and compared expression patterns in a human steosarcoma cell line Saos-2 infected separately with p53 and TAp73beta expressing adenovirus.

Publication Title

p53 family members regulate the expression of the apolipoprotein D gene.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE94809
Overcoming AXL Activation and EpithelialMesenchymal Transition is Critical in Conquering ALK-positive NonSmall Cell Lung Cancer
  • organism-icon Homo sapiens
  • sample-icon 1 Downloadable Sample
  • Technology Badge Icon Affymetrix Human Gene 2.0 ST Array (hugene20st)

Description

Anaplastic lymphoma kinase tyrosine kinase inhibitors (ALK-TKIs) induce a dramatic response in nonsmall cell lung cancer (NSCLC) patients with the ALK fusion gene. However, acquired resistance to ALK-TKIs in lung cancer cells remains an inevitable problem: ALK secondary mutations and bypass pathways have been reported as major resistance mechanisms. In this study, we aimed to discover a novel mechanism of acquired resistance to ALK-TKIs and a strategy to conquer ALK-positive lung cancer. We established three types of ALK-TKI (crizotinib, alectinib and ceritinib)resistant H2228 non-small cell lung cancer cell lines by high exposure and stepwise methods. We found these cells showed a loss of ALK signaling, overexpressed AXL with epithelialmesenchymal transition (EMT), and had cancer stem celllike properties. Similarly, we demonstrated that TGF-1 treated H2228 cells also showed AXL overexpression with EMT features and ALK-TKIresistance. The AXL inhibitor, R428, or HSP90 inhibitor, ganetespib, were effective in reversing ALK-TKIresistance and EMT changes in both ALK-TKIresistant and TGF-1exposed H2228 cells. Progression-free survival of ALK-positive NSCLC patients with AXL overexpression was shorter than that of patients who underwent crizotinib therapy and showed low AXL expression. Thus, we found ALK signaling-independent AXL overexpression and EMT features were commonly involved in intrinsic and acquired resistance to first and second generation ALK-TKIs. This suggests AXL and HSP90 inhibitors may be promising therapeutic drugs to overcome tumor cells in ALK-positive NSCLC patients.

Publication Title

No associated publication

Sample Metadata Fields

Cell line

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accession-icon SRP178159
Clinical study of human mesenchymal stem cells on the treatment of severe liver disease
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 4000

Description

we aimed to explore the potential therapeutic effects of human mesenchymal stem cell on severe liver disease

Publication Title

No associated publication

Sample Metadata Fields

Sex, Specimen part, Cell line

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accession-icon SRP131607
Compare RNA expression of Old Fibroblast to RNA expression of Young Fbroblast
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

Analyze of RNA expression of Old Fibroblast and Young Fibroblast. Compare RNA expression of Old Fibroblast to RNA expression of Young Fbroblast

Publication Title

No associated publication

Sample Metadata Fields

Sex, Specimen part

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accession-icon SRP131659
Compare RNA expression of UVA fibroblast to sham fibroblast
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

we analysis of sham fibroblast and UVA fibroblast RNA expression using RNA sequencing and compare RNA expression.

Publication Title

No associated publication

Sample Metadata Fields

Sex, Specimen part

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accession-icon SRP188485
miR-25 knock out mice kidney RNA sequencing
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 4000

Description

We generate miR-25 KO mice by Cas-9 technology, and run 5 month kidney RNA sequencing.

Publication Title

No associated publication

Sample Metadata Fields

Sex, Specimen part, Cell line

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accession-icon SRP129355
Gene expression change affected by Sirt1 depletion and ionizing radiation in adult neural stem cells
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Adult neural stem cells derived from wild type and Sirt1 conditional knockout mice were treated with or without X-ray, the total RNA extracted from these cells were used for RNA sequencing.

Publication Title

No associated publication

Sample Metadata Fields

Sex, Age, Specimen part, Cell line

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refine.bio is a repository of uniformly processed and normalized, ready-to-use transcriptome data from publicly available sources. refine.bio is a project of the Childhood Cancer Data Lab (CCDL)

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Cite refine.bio

Casey S. Greene, Dongbo Hu, Richard W. W. Jones, Stephanie Liu, David S. Mejia, Rob Patro, Stephen R. Piccolo, Ariel Rodriguez Romero, Hirak Sarkar, Candace L. Savonen, Jaclyn N. Taroni, William E. Vauclain, Deepashree Venkatesh Prasad, Kurt G. Wheeler. refine.bio: a resource of uniformly processed publicly available gene expression datasets.
URL: https://www.refine.bio

Note that the contributor list is in alphabetical order as we prepare a manuscript for submission.

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