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accession-icon GSE1577
T-ALL and T-lymphoblastic lymphoma
  • organism-icon Homo sapiens
  • sample-icon 28 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

T-cell acute lymphoblastic leukemia (T-ALL) and T-cell lymphoblastic lymphoma (T-LL) and are often thought to represent a spectrum of a single disease. The malignant cells in T-ALL and T-LL are morphologically indistinguishable, and they share the expression of common cell surface antigens and cytogenetic characteristics. However, despite these similarities, differences in the predominant sites of disease in T-ALL and T-LL are observed. To determine if underlying biological distinctions may potentially contribute to some of these differences, we analyzed the global gene expression profiles of malignant T-cell precursors in ten T-ALL and nine T-LL using DNA arrays. Ten additional B-precursor ALL bone marrow samples, were used in a separate analysis.

Publication Title

Gene expression profiling reveals intrinsic differences between T-cell acute lymphoblastic leukemia and T-cell lymphoblastic lymphoma.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE34880
Epigenetic reprogramming in relapsed childhood ALL
  • organism-icon Homo sapiens
  • sample-icon 13 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Reversing gene expression signatures in relapsed patient may restore chemosensitivity.

Publication Title

Epigenetic reprogramming reverses the relapse-specific gene expression signature and restores chemosensitivity in childhood B-lymphoblastic leukemia.

Sample Metadata Fields

Specimen part, Disease, Disease stage, Cell line, Treatment

View Samples
accession-icon GSE3912
First bone marrow relapse with or without initial diagnosis
  • organism-icon Homo sapiens
  • sample-icon 113 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Biologic pathways associated with relapse in childhood acute lymphoblastic leukemia: a Children's Oncology Group study.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE3910
35 patients at diagnosis and relapse
  • organism-icon Homo sapiens
  • sample-icon 63 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

35 paired samples from initial diagnosis and first marrow relapse. Genes and pathways differentiating diagnosis and relapse were identified. Potential therapeutic targets were also identified.

Publication Title

Biologic pathways associated with relapse in childhood acute lymphoblastic leukemia: a Children's Oncology Group study.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE28462
Integrated Genomic Analysis of Relapsed Childhood Acute Lymphoblastic Leukemia reveals therapeutic strategies
  • organism-icon Homo sapiens
  • sample-icon 98 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Integrated genomic analysis of relapsed childhood acute lymphoblastic leukemia reveals therapeutic strategies.

Sample Metadata Fields

Specimen part, Disease

View Samples
accession-icon GSE28460
Expression data from ALL diagnosis and relapse pediatric acute lymphoblastic leukemia cases
  • organism-icon Homo sapiens
  • sample-icon 98 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

There is a distinct signature of differentially expressed probes from diagnosis to relapse

Publication Title

Integrated genomic analysis of relapsed childhood acute lymphoblastic leukemia reveals therapeutic strategies.

Sample Metadata Fields

Specimen part, Disease

View Samples
accession-icon SRP009840
Outgrowth of Clones Carrying Mutations in Cytosolic 5’-Nucleotidase II in Childhood Relapsed Acute Lymphoblastic Leukemia
  • organism-icon Homo sapiens
  • sample-icon 20 Downloadable Samples
  • Technology Badge IconIllumina Genome Analyzer IIx

Description

We profiled the transcriptome of matched diagnosis and relapse samples from 10 pediatric B precursor Acute Lymphoblastic Leukemia (ALL) patients using massively parallel sequencing (RNA-Seq) technology to identify novel mutations specific at disease recurrence.

Publication Title

Relapse-specific mutations in NT5C2 in childhood acute lymphoblastic leukemia.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE112780
Multiwalled carbon nanotube-induced pulmonary inflammatory and fibrotic responses and genomic changes following aspiration exposure in mice: A 1-year postexposure study.
  • organism-icon Mus musculus
  • sample-icon 135 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 2.1 ST Array (mogene21st)

Description

Pulmonary exposure to multiwalled carbon nanotubes (MWCNT) induces an inflammatory and rapid fibrotic response, although the long-term signaling mechanisms are unknown. The aim of this study was to examine the effects of 1, 10, 40, or 80 g MWCNT administered by pharyngeal aspiration on bronchoalveolar lavage (BAL) fluid for polymorphonuclear cell (PMN) infiltration, lactate dehydrogenase (LDH) activity, and lung histopathology for inflammatory and fibrotic responses in mouse lungs 1 mo, 6 mo, and 1 yr postexposure. Further, a 120-g crocidolite asbestos group was incorporated as a positive control for comparative purposes. Results showed that MWCNT increased BAL fluid LDH activity and PMN infiltration in a dose-dependent manner at all three postexposure times. Asbestos exposure elevated LDH activity at all 3 postexposure times and PMN infiltration at 1 mo and 6 mo postexposure. Pathological changes in the lung, the presence of MWCNT or asbestos, and fibrosis were noted at 40 and 80 g MWCNT and in asbestos-exposed mice at 1 yr postexposure. To determine potential signaling pathways involved with MWCNT-associated pathological changes in comparison to asbestos, up- and down-regulated gene expression was determined in lung tissue at 1 yr postexposure. Exposure to MWCNT tended to favor those pathways involved in immune responses, specifically T-cell responses, whereas exposure to asbestos tended to favor pathways involved in oxygen species production, electron transport, and cancer. Data indicate that MWCNT are biopersistent in the lung and induce inflammatory and fibrotic pathological alterations similar to those of crocidolite asbestos, but may reach these endpoints by different mechanisms.

Publication Title

Multiwalled carbon nanotube-induced pulmonary inflammatory and fibrotic responses and genomic changes following aspiration exposure in mice: A 1-year postexposure study.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE68790
caArray_EXP-578: Gene Expression Profiles of Pediatric B-Precursor High-Risk Acute Lymphoblastic Leukemia (COG Study AALL0232 - Cohort 1).
  • organism-icon Homo sapiens
  • sample-icon 274 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

This experiment comprises 283 CEL files generated on the Affymetrix U133 Plus 2.0 gene expression microarray platform, using patient peripheral blood and bone marrow samples from the first cohort of patients accrued to Children's Oncology Group Study AALL0232. No clinical covariate data is provided at this time as the clinical study is not yet published. Researchers who would like to request outcome or other covariate data are asked to contact Dr. Cheryl Willman, cwillman@unm.edu, 505.272.5622 (University of New Mexico) and Dr. Steven Hunger, Stephen.Hunger@childrenscolorado.org (Children's Oncology Group and Children's Hospital Colorado) to arrange a collaboration.

Publication Title

Tyrosine kinome sequencing of pediatric acute lymphoblastic leukemia: a report from the Children's Oncology Group TARGET Project.

Sample Metadata Fields

Disease

View Samples
accession-icon GSE75225
Bone marrow-derived monocytes give rise to self-renewing and fully differentiated Kupffer cells
  • organism-icon Mus musculus
  • sample-icon 19 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Self-renewing tissue-resident macrophages are thought to be exclusively derived from embryonic progenitors. However, whether circulating monocytes can also give rise to such macrophages has not been formally investigated. Here we use a new model of diphtheria toxin-mediated depletion of liver-resident Kupffer cells to generate niche availability and show that circulating monocytes engrafted in the liver, gradually adopt the transcriptional profile of their depleted counterparts and become long-lived self-renewing cells. Underlining the physiological relevance of our findings, circulating monocytes also contribute to the expanding pool of macrophages in the liver shortly after birth, when macrophage niches become available during normal organ growth. Thus, like embryonic precursors, monocytes can and do give rise to self-renewing tissue-resident macrophages if the niche is available to them.

Publication Title

Bone marrow-derived monocytes give rise to self-renewing and fully differentiated Kupffer cells.

Sample Metadata Fields

Specimen part

View Samples

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)

fund-icon Fund the CCDL

Developed by the Childhood Cancer Data Lab

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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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