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SRP066619
Homo sapiens
10 Downloadable Samples
IlluminaHiSeq2500
Description
We report gene expression data for human melanoma cell lines using RNAseq. Overall design: RNAseq was performed on 8 melanoma cell lines and one normal human melanocyte cell line. All done as single replicates, except for two biological replicates of A375.
Publication Title
A zebrafish melanoma model reveals emergence of neural crest identity during melanoma initiation.
Sample Metadata Fields
No sample metadata fields
View Samples- Danio rerio
- 2 Downloadable Samples
- IlluminaHiSeq2500
Description
We report gene expression data for FACS sorted zebrafish crestin_1kb:EGFP + cells collected at 15 somite stage (SS). Overall design: crestin_1kb:EGFP + embryos were homogenized, filtered, and sorted using FACS into PBS, collecting ~5,500 EGFP (+) cells and 100K EGFP (-) cells with a single sample for each.
Publication Title
A zebrafish melanoma model reveals emergence of neural crest identity during melanoma initiation.
Sample Metadata Fields
No sample metadata fields
View Samples- Danio rerio
- 4 Downloadable Samples
- IlluminaHiSeq4000
Description
We report high-throughput profiling of gene expression from whole zebrafish ventricles. We profile mRNA in uninjured ventricles and those undergoing regeneration 14 days after genetic ablation. This study provides a framework for understanding transcriptional changes during adult models of regeneration. Overall design: Examination of gene expression in cardiomyocytes under different states of proliferation.
Publication Title
Resolving Heart Regeneration by Replacement Histone Profiling.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 24 Downloadable Samples
- IlluminaHiSeq2500
Description
Cancer metabolism has been actively studied to gain insights into tumorigenic survival mechanisms and susceptibilities. In melanoma, we identify HEXIM1, a transcription elongation regulator, as a novel melanoma suppressor that participates in nucleotide stress regulation. HEXIM1 expression is low in melanoma. Its overexpression suppresses melanoma while its inactivation accelerates tumor onset in vivo. HEXIM1 responds to nucleotide stress. Knockdown of HEXIM1 rescues neural crest and melanoma nucleotide stress phenotypes in vivo. Mechanistically, under nucleotide stress, HEXIM1 is induced to form an inhibitory complex with P-TEFb, the kinase that initiates transcription elongation, to pause transcription at tumorigenic genes. The resulting alteration in gene expression also causes anti-tumorigenic transcripts to bind to and be stabilized by HEXIM1. HEXIM1 therefore plays an important role in inhibiting cancer cell-specific gene transcription while also facilitating anti-cancer gene expression. Our study reveals a novel role for HEXIM1 in coupling nucleotide metabolism with transcriptional regulation in melanoma. Overall design: RNA-seq analysis of human A375 melanoma cells treated with either DMSO or 25 µM A771726 for 0-72 hrs.
Publication Title
Stress from Nucleotide Depletion Activates the Transcriptional Regulator HEXIM1 to Suppress Melanoma.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 12 Downloadable Samples
- IlluminaHiSeq2500
Description
Cancer metabolism has been actively studied to gain insights into tumorigenic survival mechanisms and susceptibilities. In melanoma, we identify HEXIM1, a transcription elongation regulator, as a novel melanoma suppressor that participates in nucleotide stress regulation. HEXIM1 expression is low in melanoma. Its overexpression suppresses melanoma while its inactivation accelerates tumor onset in vivo. HEXIM1 responds to nucleotide stress. Knockdown of HEXIM1 rescues neural crest and melanoma nucleotide stress phenotypes in vivo. Mechanistically, under nucleotide stress, HEXIM1 is induced to form an inhibitory complex with P-TEFb, the kinase that initiates transcription elongation, to pause transcription at tumorigenic genes. The resulting alteration in gene expression also causes anti-tumorigenic transcripts to bind to and be stabilized by HEXIM1. HEXIM1 therefore plays an important role in inhibiting cancer cell-specific gene transcription while also facilitating anti-cancer gene expression. Our study reveals a novel role for HEXIM1 in coupling nucleotide metabolism with transcriptional regulation in melanoma. Overall design: RNA-seq analysis of human Tet-On HEXIM1-inducible A375 melanoma cells treated with either DMSO or 1 µg/mL doxycycline in triplicate for 48 hrs.
Publication Title
Stress from Nucleotide Depletion Activates the Transcriptional Regulator HEXIM1 to Suppress Melanoma.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 6 Downloadable Samples
Affymetrix Human Genome U95 Version 2 Array (hgu95av2)
Description
We show the molecular and functional characterization of a novel population of lineage-negative CD34-negative (Lin- CD34-) hematopoietic stem cells (HSCs) from chronic myelogenous leukemia (CML) patients at diagnosis. Molecular caryotyping and quantitative analysis of BCR/ABL transcript demonstrated that about one third of CD34- was leukemic. CML CD34- cells showed kinetic quiescence and limited clonogenic capacity. However, stroma-dependent cultures and cytokines induced CD34 expression on some HSCs, cell cycling, acquisition of clonogenic activity and increased expression of BCR/ABL transcript. CML CD34- cells showed an engraftment rate in immunodeficient mice similar to that of CD34+ cells. Gene expression profiling revealed the down-regulation of cell cycle arrest genes together with genes involved in antigen presentation and processing, while the expression of angiogenic factors was strongly up-regulated when compared to normal counterparts. Flow cytometry analysis confirmed the significant down-regulation of HLA class I and II molecules in CML CD34-cells. Increasing doses of imatinib mesilate (IM) did not affect fusion transcript levels, BCR-ABL kinase activity and the clonogenic efficiency of CML CD34- cells as compared to leukemic CD34+cells.
Publication Title
Molecular and functional analysis of the stem cell compartment of chronic myelogenous leukemia reveals the presence of a CD34- cell population with intrinsic resistance to imatinib.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 6633 Downloadable Samples
- Affymetrix Human Genome U133A 2.0 Array (hgu133a2), Affymetrix HT Human Genome U133A Array (hthgu133a)
Description
To identify patterns of drug-induced gene modulation that occur across different cell types, we measured gene expression changes across NCI-60 cell lines after exposure to 15 anticancer agents. The results were integrated into a database and set of interactive analysis tools, the NCI Transcriptional Pharmacodynamics Workbench (NCI TPW), intended to allow exploration of gene expression modulation, including by molecular pathway, drug target, and association with drug sensitivity. We identified common transcriptional responses across drugs and cell types and uncovered cell signaling pathway–specific gene expression changes associated with drug sensitivity. We also demonstrated the value of this tool for investigating clinically relevant molecular hypotheses, utilizing the NCI TPW to assess drug-induced expression changes in genes associated with immune function and epithelial-mesenchymal transition, and to identify candidate biomarkers for drug activity. The NCI TPW provides a comprehensive resource to facilitate understanding of tumor cell characteristics that define sensitivity to anticancer drugs.
Publication Title
The NCI Transcriptional Pharmacodynamics Workbench: A Tool to Examine Dynamic Expression Profiling of Therapeutic Response in the NCI-60 Cell Line Panel.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 538 Downloadable Samples
Affymetrix HT Human Genome U133A Array (hthgu133a), Affymetrix Human Genome U133A 2.0 Array (hgu133a2)
Description
To identify patterns of drug-induced gene modulation that occur across different cell types, we measured gene expression changes across NCI-60 cell lines after exposure to 15 anticancer agents. The results were integrated into a database and set of interactive analysis tools, the NCI Transcriptional Pharmacodynamics Workbench (NCI TPW), intended to allow exploration of gene expression modulation, including by molecular pathway, drug target, and association with drug sensitivity. We identified common transcriptional responses across drugs and cell types and uncovered cell signaling pathwayspecific gene expression changes associated with drug sensitivity. We also demonstrated the value of this tool for investigating clinically relevant molecular hypotheses, utilizing the NCI TPW to assess drug-induced expression changes in genes associated with immune function and epithelial-mesenchymal transition, and to identify candidate biomarkers for drug activity. The NCI TPW provides a comprehensive resource to facilitate understanding of tumor cell characteristics that define sensitivity to anticancer drugs.
Publication Title
The NCI Transcriptional Pharmacodynamics Workbench: A Tool to Examine Dynamic Expression Profiling of Therapeutic Response in the NCI-60 Cell Line Panel.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 534 Downloadable Samples
- Affymetrix HT Human Genome U133A Array (hthgu133a), Affymetrix Human Genome U133A 2.0 Array (hgu133a2)
Description
To identify patterns of drug-induced gene modulation that occur across different cell types, we measured gene expression changes across NCI-60 cell lines after exposure to 15 anticancer agents. The results were integrated into a database and set of interactive analysis tools, the NCI Transcriptional Pharmacodynamics Workbench (NCI TPW), intended to allow exploration of gene expression modulation, including by molecular pathway, drug target, and association with drug sensitivity. We identified common transcriptional responses across drugs and cell types and uncovered cell signaling pathwayspecific gene expression changes associated with drug sensitivity. We also demonstrated the value of this tool for investigating clinically relevant molecular hypotheses, utilizing the NCI TPW to assess drug-induced expression changes in genes associated with immune function and epithelial-mesenchymal transition, and to identify candidate biomarkers for drug activity. The NCI TPW provides a comprehensive resource to facilitate understanding of tumor cell characteristics that define sensitivity to anticancer drugs.
Publication Title
The NCI Transcriptional Pharmacodynamics Workbench: A Tool to Examine Dynamic Expression Profiling of Therapeutic Response in the NCI-60 Cell Line Panel.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 526 Downloadable Samples
- Affymetrix HT Human Genome U133A Array (hthgu133a), Affymetrix Human Genome U133A 2.0 Array (hgu133a2)
Description
To identify patterns of drug-induced gene modulation that occur across different cell types, we measured gene expression changes across NCI-60 cell lines after exposure to 15 anticancer agents. The results were integrated into a database and set of interactive analysis tools, the NCI Transcriptional Pharmacodynamics Workbench (NCI TPW), intended to allow exploration of gene expression modulation, including by molecular pathway, drug target, and association with drug sensitivity. We identified common transcriptional responses across drugs and cell types and uncovered cell signaling pathwayspecific gene expression changes associated with drug sensitivity. We also demonstrated the value of this tool for investigating clinically relevant molecular hypotheses, utilizing the NCI TPW to assess drug-induced expression changes in genes associated with immune function and epithelial-mesenchymal transition, and to identify candidate biomarkers for drug activity. The NCI TPW provides a comprehensive resource to facilitate understanding of tumor cell characteristics that define sensitivity to anticancer drugs.
Publication Title
The NCI Transcriptional Pharmacodynamics Workbench: A Tool to Examine Dynamic Expression Profiling of Therapeutic Response in the NCI-60 Cell Line Panel.
Sample Metadata Fields
Specimen part
View Samples