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accession-icon GSE8835
Chronic lymphocytic leukemia cells induce changes in gene expression of CD4 and CD8 T cells.
  • organism-icon Homo sapiens
  • sample-icon 66 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

To examine the impact of tumors on the immune system, we compared global gene expression profiles of peripheral blood T cells from previously untreated patients with B cell chronic lymphocytic leukemia (CLL) with those from age-matched healthy donors. Although the cells analyzed were not part of the malignant clone, analysis revealed differentially expressed genes, mainly involved in cell differentiation in CD4 cells and defects in cytoskeleton formation, vesicle trafficking, and cytotoxicity in CD8 cells of the CLL patients. In coculture experiments using CLL cells and T cells from healthy allogeneic donors, similar defects developed in both CD4 and CD8 cells. These changes were induced only with direct contact and were not cytokine mediated. Identification of the specific pathways perturbed in the T cells of cancer-bearing patients will allow us to assess steps to repair these defects, which will likely be required to enhance antitumor immunity.

Publication Title

Chronic lymphocytic leukemia cells induce changes in gene expression of CD4 and CD8 T cells.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE28896
Dexamethasone and lenalidomide have distinct functional effects on erythropoiesis
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix HT Human Genome U133A Array (hthgu133a)

Description

We explored the effects of dexamethasone and lenalidomide, individually and in combination, on the differentiation of primary human bone marrow progenitor cells in vitro. Both agents promote erythropoiesis, increasing the absolute number of erythroid cells produced from normal CD34+ cells and from CD34+ cells with the types of ribosome dysfunction found in DBA and del(5q) MDS. However, the drugs had distinct effects on the production of erythroid progenitor colonies; dexamethasone selectively increased the number burst-forming units-erythroid (BFU-E), while lenalidomide specifically increased colony-forming units-erythroid (CFU-E). Use of the drugs in combination demonstrates that their effects are not redundant.

Publication Title

Dexamethasone and lenalidomide have distinct functional effects on erythropoiesis.

Sample Metadata Fields

Specimen part, Treatment

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accession-icon SRP156903
Acute activation of ER-RAC1 P29S in melanocytes
  • organism-icon Mus musculus
  • sample-icon 18 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2500

Description

We studied the effects of acute activation of the melanoma oncogene RAC1 P29S using a tamoxifen-inducible ER-fusion protein system in mouse melanocytes Overall design: An ER-RAC1 P29S fusion protein was stably expressed in the spontaneously immortalized mouse melanocyte cell line melan-a. The fusion protein was activated by treatment with 500 nM 4OH-tamoxifen. RNA was isolated and sequenced at 0 h, 4 h and 40 h post-treatment. The gene expression profiles at 4 h and 40 h were compared to the 0 h time-point. To control for effects induced by 4OH-tamoxifen independent from ER-RAC1 P29S, we performed the same experiment in melan-a cells transduced with an empty vector.

Publication Title

RAC1<sup>P29S</sup> Induces a Mesenchymal Phenotypic Switch via Serum Response Factor to Promote Melanoma Development and Therapy Resistance.

Sample Metadata Fields

Subject

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accession-icon SRP156888
Endogenous RAC1 P29S in mouse melanoma
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 4000

Description

We studied the effects of endogenous expression of the melanoma oncogene RAC1 P29S in BRAF V600E;PTEN hemizygous mouse melanomas. Overall design: Transgenic mice with a conditional knock-in of the P29S mutation in the endogenous Rac1 locus were generated and crossed onto C57BL/6J, Tyr-CreER;BrafCA/wt;Ptenfl/wt mice. Melanomas were induced by topical 4OH-tamoxifen. We compared the gene expression profile in whole tumour lysates from Tyr-CreER+/-;Ptenfl/wt;BrafCA/wt;Rac1LSL-P29S/wt mice versus Tyr-CreER+/-;Ptenfl/wt;BrafCA/wt;Rac1wt/wt mice (n = 6 tumours from 5-6 animals per group).

Publication Title

RAC1<sup>P29S</sup> Induces a Mesenchymal Phenotypic Switch via Serum Response Factor to Promote Melanoma Development and Therapy Resistance.

Sample Metadata Fields

Cell line, Subject

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accession-icon GSE42547
Annexin A2 Modulates Radiation-Sensitive Transcriptional Programming and Cell Fate
  • organism-icon Mus musculus
  • sample-icon 47 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

Whole genome expression profiling in the presence and absence of annexin A2 [shRNA] identified fundamentally altered transcriptional programming that changes the radioresponsive transcriptome.

Publication Title

Annexin A2 modulates radiation-sensitive transcriptional programming and cell fate.

Sample Metadata Fields

Treatment, Time

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accession-icon GSE27928
Characterization of gene expression of tumor infiltrating T cells (TILs) in previously untreated patients with follicular lymphoma (FL) compared with those of tonsils
  • organism-icon Homo sapiens
  • sample-icon 35 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

It has been shown that tumor infiltrating immune cells have a profound impact on the outcome of FL. To find mechanisms whereby TILs are altered gene expession analysis of highly pure TILs were performed.

Publication Title

Follicular lymphoma cells induce changes in T-cell gene expression and function: potential impact on survival and risk of transformation.

Sample Metadata Fields

Specimen part, Subject

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accession-icon E-MEXP-2072
Transcription profiling of mouse leukemia initiation cells of SALL4B transgenic strains and their control counterparts
  • organism-icon Mus musculus
  • sample-icon 20 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

To compare the gene expression profiles of leukemia initiation cells of SALL4B transgenic mice and their control counterparts.

Publication Title

A SALL4/MLL/HOXA9 pathway in murine and human myeloid leukemogenesis.

Sample Metadata Fields

Specimen part, Disease

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accession-icon GSE76790
Cellular reactions to long-term volatile organic compound (VOC) exposures.
  • organism-icon Homo sapiens
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

A549 cells were grown at air liquid interphase (ALI) and exposed to airborne formaldehyde for three days. An exposure platform was developed for this purpose, which provided the volatile analyte in a humidified atmosphere. The platform was composed of a reference and an exposure chamber.

Publication Title

Cellular reactions to long-term volatile organic compound (VOC) exposures.

Sample Metadata Fields

Cell line

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accession-icon GSE40155
Expression data from RUNX1(41-214)-expressing and Runx1-knockout mice KSL cells
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430A 2.0 Array (mouse430a2)

Description

Mutations of RUNX1 are detected in patients with myelodysplastic syndrome (MDS). In particular, C-terminal truncation mutations lack a transcription regulatory domain and have increased DNA binding through the runt homology domain (RHD). The expression of the RHD, RUNX1(41-214), in mouse hematopoietic cells induced progression to MDS and acute myeloid leukemia (AML). Analysis of pre-myelodysplastic animals revealed expansion of c-Kit+Sca-1+Lin- (KSL) cells and skewed differentiation to myeloid at the expense of the lymphoid lineage. These abnormalities correlate with the phenotype of Runx1-deficient animals, as expected given the reported dominant-negative role of C-terminal mutations over the full-length RUNX1. However, MDS is not observed in Runx1-deficient animals. Gene expression profiling revealed that RUNX1(41-214) KSLs have an overlapping yet distinct gene expression profile from Runx1-deficient animals. Moreover, an unexpected parallel was observed between the hematopoietic phenotype of RUNX1(41-214) and aged animals. Genes deregulated in RUNX1(41-214), but not in Runx1-deficient animals, were inversely correlated with the aging gene signature of hematopoietic stem cells (HSC), suggesting that disruption of the expression of genes related to normal aging by RUNX1 mutations contributes to development of MDS. The data presented here provide insights into the mechanisms of development of MDS in HSCs by C-terminal mutations of RUNX1.

Publication Title

Expression of the runt homology domain of RUNX1 disrupts homeostasis of hematopoietic stem cells and induces progression to myelodysplastic syndrome.

Sample Metadata Fields

Specimen part

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accession-icon GSE43401
MYBL2 Is a Sub-haploinsufficient Tumor Suppressor Gene in Myeloid Malignancy
  • organism-icon Homo sapiens
  • sample-icon 43 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

MYBL2 is a sub-haploinsufficient tumor suppressor gene in myeloid malignancy.

Sample Metadata Fields

Specimen part, Disease, Disease stage

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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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