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accession-icon GSE57797
Expression data from the subclones of Lewis Lung Carcinoma (LLC) cells
  • organism-icon Mus musculus
  • sample-icon 23 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Medium conditioned by LLC cells stimulates thermogenic gene expression when added onto primary adipocytes. We generated single cell colonies from parental LLC cells. Media conditioned by the subclones stimulated thermogenic gene expression in primary adipocytes at varying degrees.

Publication Title

Tumour-derived PTH-related protein triggers adipose tissue browning and cancer cachexia.

Sample Metadata Fields

Specimen part

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accession-icon GSE74082
PTH and PTHrP treatment of primary adipocytes
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Parathyroid hormone (PTH) and PTH-related protein (PTHrP) are involved in cachexia associated with chronic kidney disease and cancer respectively. Tumor-derived PTHrP triggers adipose tissue browning and thereby leads to wasting of fat tissue in tumor-bearing mice. Similarly, elevated in 5/6 nephrectomized mice, PTH stimulates adipose tissue browning and wasting. Mice lacking the PTH/PTHrP receptor in their fat tissue are resistant to wasting of both adipose tissue and skeletal muscle. Therefore, the PTH/PTHrP signaling in adipocytes should activate various pathways that contribute to hypermetabolism and muscle wasting.

Publication Title

PTH/PTHrP Receptor Mediates Cachexia in Models of Kidney Failure and Cancer.

Sample Metadata Fields

Sex, Specimen part

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accession-icon GSE38467
Transcriptional perturbations caused by tumor virus proteins
  • organism-icon Homo sapiens
  • sample-icon 448 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Genotypic differences greatly influence susceptibility and resistance to disease. Understanding genotype-phenotype relationships requires that phenotypes be viewed as manifestations of network properties, rather than simply as the result of individual genomic variations. Genome sequencing efforts have identified numerous germline mutations associated with cancer predisposition and large numbers of somatic genomic alterations. However, it remains challenging to distinguish between background, or passenger and causal, or driver cancer mutations in these datasets. Human viruses intrinsically depend on their host cell during the course of infection and can elicit pathological phenotypes similar to those arising from mutations. To test the hypothesis that genomic variations and tumour viruses may cause cancer via related mechanisms, we systematically examined host interactome and transcriptome network perturbations caused by DNA tumour virus proteins. The resulting integrated viral perturbation data reflects rewiring of the host cell networks, and highlights pathways that go awry in cancer, such as Notch signalling and apoptosis. We show that systematic analyses of host targets of viral proteins can identify cancer genes with a success rate on par with their identification through functional genomics and large-scale cataloguing of tumour mutations. These complementary approaches together result in increased specificity for cancer gene identification. Combining systems-level studies of pathogen-encoded gene products with genomic approaches will facilitate prioritization of cancer-causing driver genes so as to advance understanding of the genetic basis of human cancer.

Publication Title

Interpreting cancer genomes using systematic host network perturbations by tumour virus proteins.

Sample Metadata Fields

Cell line

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accession-icon GSE61578
Gene Expression and HD-SNP6.0 data from Primary Testicular (PTL), Primary Central Nervous System Lymphoma (PCNSL) and Primary Mediastinal B-cell Lymphoma (PMLBCL)
  • organism-icon Homo sapiens
  • sample-icon 39 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

We obtained gene expression data and HD-SNP6.0 copy number data from PTL, PCNSL and PMLBCL samples and performed an integrative analysis on them. RNA was whole genome amplified using Nugen.

Publication Title

Targetable genetic features of primary testicular and primary central nervous system lymphomas.

Sample Metadata Fields

Disease, Disease stage

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accession-icon GSE31048
Expression data from normal B cells and chronic lymphocytic leukemia B cells -- with/without treatment of Wnt3a
  • organism-icon Homo sapiens
  • sample-icon 220 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Wnt pathway is dysregulated in CLL-We characterized Wnt pathway gene expression in normal B and CLL-B cells and identified Wnt targets in normal B and CLL-B cells through this data set.

Publication Title

Somatic mutation as a mechanism of Wnt/β-catenin pathway activation in CLL.

Sample Metadata Fields

Specimen part

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accession-icon GSE50006
Expression data from chronic lymphocytic leukemia (CLL) tumors and sorted CD19pos B cells from healthy donors
  • organism-icon Homo sapiens
  • sample-icon 217 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

As part of a large study regarding the epigenetics of CLL we also acquired 3UTR expression arrays.

Publication Title

No associated publication

Sample Metadata Fields

Specimen part

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accession-icon GSE97284
Gene expression profiling of laser capture microdissected prostate specimens
  • organism-icon Homo sapiens
  • sample-icon 188 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

We performed gene expression profiling of laser capture microdissected normal non-neoplastic prostate (cystoprostatectomies) epithelial tissue and compared it to non-transformed and neoplastic low and high grade prostate epithelial tissue from radical prostatectomies, each with its immediately surrounding stroma.

Publication Title

Stromal and epithelial transcriptional map of initiation progression and metastatic potential of human prostate cancer.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE45630
Time course gene expression profiling of five diffuse large B-cell lymphoma cell lines following JQ1 treatment
  • organism-icon Homo sapiens
  • sample-icon 180 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

To understand the molecular curcuits perturbed by BET bromodoman inhibtion we obtained gene expression profiling of five DLBCL cell lines, SU-DHL6, OCI-Ly1, OCI-Ly4, Toledo and HBL-1, which were treated with either 500nM JQ1 or DMSO for 0,2,6,12,24 and 48hr.

Publication Title

Discovery and characterization of super-enhancer-associated dependencies in diffuse large B cell lymphoma.

Sample Metadata Fields

Specimen part, Cell line, Treatment, Time

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accession-icon GSE39754
Gene Expression profiling of Multiple Myeloma
  • organism-icon Homo sapiens
  • sample-icon 175 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)

Description

Gene Expression profiling of 170 newly diagnosed Multiple Myeloma patients

Publication Title

A small molecule inhibitor of ubiquitin-specific protease-7 induces apoptosis in multiple myeloma cells and overcomes bortezomib resistance.

Sample Metadata Fields

Disease

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accession-icon GSE69034
Expression data from chronic lymphocytic leukemia (CLL) cells
  • organism-icon Homo sapiens
  • sample-icon 146 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

We compared gene expression profiles of CLL patients with and without MYD88 L265P mutations, taking into consideration IGHV mutation status.

Publication Title

No associated publication

Sample Metadata Fields

Specimen part

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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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