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accession-icon GSE150409
Expression data from murine lymphatic endothelial cells with angiotensin II treated
  • organism-icon Mus musculus
  • sample-icon 15 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Clariom S Array (clariomsmouse)

Description

Proliferation and migration of lymphatic endothelial cells (LECs) are essential for lymphatic vessel growth (also known as lymphangiogenesis), which plays a critical role in regulating the tissue fluid balance and immune cell trafficking in physiological and pathological conditions.

Publication Title

Angiotensin II Stimulates the Proliferation and Migration of Lymphatic Endothelial Cells Through Angiotensin Type 1 Receptors.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon GSE24046
Viable Mice Produced from 3-factor Induced Pluripoent Stem (iPS) Cells through Tetraploid Complementation
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Ectopic expression of four transcription factors including Oct4, Sox2, Klf4 and c-Myc in differentiated fibroblast cells could reset the cell fate of fibroblast cells to pluripotent state. Subsequently, fully pluripotency of these so-called induced pluripotent stem cells (iPSCs) has been demonstrated as viable mice could be generated autonomously from iPS cells through tetraploid blastocyst complementation. Moreover, the generation of human and patient-specific iPS cells have raised the possibility of utilizing iPS cells clinically. However, the utilization of c-Myc in iPS cells induction greatly increased the incidence of tumorigenecity in the iPS-chimeric mice and also might hinder the clinical application of human iPS cells in the future. Fortunately, c-Myc has been recently found dispensable for iPS induction even though the iPS induction efficiency is greatly reduced in the absence of c-Myc. However, it remains unknown if these three factors-induced iPS cells are fully pluripotent. In the present study, we have successfully demonstrated that 3-factor iPS cells could also be fully pluripotent as viable mice could be generated from 3-factor iPS cells autonomously via tetraploid complementation and moreover, our data indicated that the pluripotency regulatory mechanism in 3-factor iPS cells might be distinct from 4-factor iPS cells.

Publication Title

Viable mice produced from three-factor induced pluripotent stem (iPS) cells through tetraploid complementation.

Sample Metadata Fields

Specimen part

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accession-icon GSE17004
Inducible iPS Cells Support Full-term Development of Tetraploid BlastocystComplemented Embryos
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Differentiated somatic cells can be reprogrammed into induced pluripotent stem (iPS) cells by forced expression of four transcription factorsOct4, Sox2, Klf4, and c-Myc. However, it remains undetermined whether the reprogrammed iPS cells are fully pluripotent, resembling normal embryonic stem (ES) cells, given that no iPS cell lines have been shown to possess the capability to autonomously generate full-term mice after injection into tetraploid blastocysts. Here, we provide evidence demonstrating that iPS cells induced by the four transcription factors can be fully pluripotent and that full-term mice can be produced from complemented tetraploid blastocysts. This work serves as a proof of principle that iPS cells can generate full term embryos by tetraploid complementation.

Publication Title

iPS cells can support full-term development of tetraploid blastocyst-complemented embryos.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE54091
Docetaxel-loaded solid lipid nanoparticles suppress breast cancer cells growth with reduced myelosuppression toxicity
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Docetaxel is an adjuvant chemotherapy drug widely used to treat multiple solid tumors, however its toxicity and side-effect limits its clinical efficacy. Herein, the docetaxel-loaded solid lipid nanoparticles (DSNs) were developed to reduce systemic toxicity while still keeping its anti-cancer activity. To evaluate its anti-cancer activity and toxicity and understand the molecular mechanisms of DSNs, different cellular, molecular and whole genome transcription analysis approaches were utilized. The DSNs showed lower cytotoxicity compared with the commercial formulation of docetaxel-Taxotere and induced more apoptosis at 24 h treatment in vitro. It can cause the treated cancer cells arrested at G2/M phase in a dose-depend manner as Taxotere. The DSNs can also suppress tumor growth very effectively in a murine breast cancer model. Systemic analysis of gene expression profiles by microarray and the following verification experiments suggested that both DSNs and Taxotere regulate expression of series genes and these genes functions involved in DNA replication, DNA damage response, cell proliferation, apoptosis and cell cycle regulation. Some of these genes expressed differentially at protein level although their transcription level was similar under TAX and DSNs treatment. Moreover, DSNs improved main side-effect of Taxotere by greatly lowering myelosuppression toxicity to bone marrow cells from mice. Taken together, our results expound the anti-tumor efficacy and the potential working mechanisms of DSNs in its anti-cancer activity and toxicity, which provide a theoretical foundation to develop and apply more efficient docetaxel formulation to treat cancer patients.

Publication Title

Docetaxel-loaded solid lipid nanoparticles suppress breast cancer cells growth with reduced myelosuppression toxicity.

Sample Metadata Fields

Specimen part

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accession-icon GSE103056
Ovaries of PNA mice and controls
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

To investigate the etiology of the hyperandrogenic phenotype of polycystic ovary syndrome (PCOS), a prenatally androgenized (PNA) mouse model was validated and used for microarray analysis.

Publication Title

No associated publication

Sample Metadata Fields

Sex, Specimen part, Treatment

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accession-icon GSE78933
Expression data from melanosis coli (MC)
  • organism-icon Homo sapiens
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Transcriptome Array 2.0 (hta20)

Description

There is still a big debate about the correlation between melanosis coli (MC) and carcinoma. We used HTA2.0 to investigate the expression changes of lncRNAs and mRNAs in human colonic mucosa with or without MC and try to investigate MC from gene aspect, eventually to demonstrate whether theres a certain correlation between MC and carcinoma.

Publication Title

No associated publication

Sample Metadata Fields

Specimen part

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accession-icon GSE77517
Genome-wide evaluation of change in lncRNA expression in non-functioning pituitary adenoma using formalin-fixed and paraffin-embedded tissue specimens
  • organism-icon Homo sapiens
  • sample-icon 20 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Transcriptome Array 2.0 (hta20)

Description

Long noncoding RNAs (lncRNAs) have been implicated in the formation of many different types of tumors. However, expression profiles and potential functions of lncRNAs in non-functioning pituitary adenomas (NFPAs) have not been systematically evaluated.

Publication Title

No associated publication

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon GSE100340
Expression data from MDS patients with der(1;7)(q10;p10)
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Gene expression profiling was significantly different between der(1;7)(q10;p10) and -7/7q- patients by cluster analysis. There were total 1628 dysregulated genes in both der(1;7)(q10;p10) and -7/del(7q) cohorts.

Publication Title

High frequency of RUNX1 mutation in myelodysplastic syndrome patients with whole-arm translocation of der(1;7)(q10;p10).

Sample Metadata Fields

Specimen part

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accession-icon GSE107382
Gene expression data from retina of Babl/c mouse under white LED light exposure
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

The widely used white light-emitting diodes (LED) deliver higher levels of blue light than do conventional domestic light sources. The high intensity of blue component is the main source of concern about the health risks of LED with respect to their light-toxicity to the retina. White LED light with higher correlated color temperature (CCT) is more likely to cause retinal injury in mice, significantly reducing the number of ONL nuclei, however apoptosis pathway may not be the only mechanism.

Publication Title

No associated publication

Sample Metadata Fields

Specimen part

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accession-icon GSE41326
Expression data from HepG2 cells before and after RNF43 knockdown
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

It has been demonstrated that Ring finger protein 43 (RNF43) is overexpressed in colorectal cancer and mediates cancer cell proliferation. We found that RNF43 was frequently overexpressed in HCC, and knockdown of RNF43 could induce apoptosis and inhibit proliferation, invasion, colony formation and xenograft growth of HCC cells. Suggesting that RNF43 is involved in tumorigenesis and progression of HCC.

Publication Title

Reversing effect of ring finger protein 43 inhibition on malignant phenotypes of human hepatocellular carcinoma.

Sample Metadata Fields

Cell line, Treatment

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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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