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accession-icon SRP067026
The role of PRMT5/WDR77 complex in promoting breast cancer oncogenesis [RNA-Seq]
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconIlluminaGenomeAnalyzer

Description

Comprehensive RNA-seq experiments in control and PRMT5 and WDR77 shRNA infected cells delineate the role of PRMT5/WDR77 complex in promoting breast cancer oncogenesis Overall design: RNA-seq was used to measure gene expression levels in scrambled control, PRMT5 and WDR77 short hairpin RNA (shRNA) infected human breast cancer cells

Publication Title

The PRMT5/WDR77 complex regulates alternative splicing through ZNF326 in breast cancer.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP067025
The role of PRMT5/WDR77 complex in promoting breast cancer oncogenesis [RNA-Seq_HPTB]
  • organism-icon Homo sapiens
  • sample-icon 2 Downloadable Samples
  • Technology Badge IconIlluminaGenomeAnalyzer

Description

Comprehensive RNA-seq experiments in DMSO and HPTB (inhibitor of PRMT5) treated cells delineate the role of PRMT5 complex in promoting breast cancer oncogenesis Overall design: RNA-seq was used to measure gene expression levels in DMSO and HPTB (inhibitor of PRMT5) treated human breast cancer cells

Publication Title

The PRMT5/WDR77 complex regulates alternative splicing through ZNF326 in breast cancer.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon SRP058717
The lncRNA LUST promotes CCICs self-renewal stimulating the wnt/b-catenin signaling activation [RNA-Seq]
  • organism-icon Homo sapiens
  • sample-icon 3 Downloadable Samples
  • Technology Badge IconIlluminaGenomeAnalyzer

Description

Comprehensive RNA-seq experiments in CD24bright/CD44bright (CCICs), CD24dim/CD44dim (more differentiated counterpart) cells and colonospheres delineate the role of the lncRNA LUST in promoting CCICs self-renewal. Overall design: RNA-Seq study from HT-29 CD44bright/CD24bright and CD24dim/CD44dim sorted cells subpopulation

Publication Title

RBM5-AS1 Is Critical for Self-Renewal of Colon Cancer Stem-like Cells.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE15830
Identification of potential transcripts involved in chicken PGCs development
  • organism-icon Gallus gallus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Chicken Genome Array (chicken)

Description

From the transcriptomics analysis, this study focused on the genes expressed in PGCs during germline development in early embryogenesis of chickens.

Publication Title

MicroRNA-mediated posttranscriptional regulation is required for maintaining undifferentiated properties of blastoderm and primordial germ cells in chickens.

Sample Metadata Fields

Specimen part

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accession-icon GSE38168
Identification of transcripts predominantly expressed in cultured chicken primordial germ cells and embryonic fibroblasts.
  • organism-icon Gallus gallus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Chicken Genome Array (chicken)

Description

The present investigation was to identify the signaling and metabolic pathways of expressed genes by microarray comparison between Primordial Germ Cells (PGCs) and their somatic counterpart, chicken embryonic fibroblasts (CEFs).

Publication Title

Gene pathways and cell cycle-related genes in cultured avian primordial germ cells.

Sample Metadata Fields

Specimen part

View Samples
accession-icon SRP095426
OTX2 activity at distal regulatory elements shapes the chromatin landscape of Group 3 medulloblastoma [RNA-seq]
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

Medulloblastoma is the most frequent malignant pediatric brain tumor and is divided into at least four subgroups known as Wnt, SHH, Group 3 and Group 4. Here we characterized gene regulation mechanisms in the most aggressive subtype, Group 3 tumors, through genome-wide chromatin and expression profiling. Our results show that most active distal sites in these tumors are occupied by the transcription factor OTX2. Highly active OTX2 bound enhancers are often arranged as clusters of adjacent peaks and are also bound by the transcription factor NEUROD1. These sites are responsive to OTX2 and NEUROD1 knockdown and could also be generated de novo upon ectopic OTX2 expression in primary cells, showing that OTX2 cooperates with NEUROD1 and plays a major role in maintaining and possibly establishing regulatory elements as a pioneer factor. Among OTX2 target genes we identified the kinase NEK2, whose knockdown and pharmacological inhibition decreased cell viability. Our studies thus show that OTX2 controls the regulatory landscape of Group 3 medulloblastoma through cooperative activity at enhancer elements and contributes to the expression of critical target genes. Overall design: Primary Group 3 Medulloblastomas tumor samples were analyzed by RNA-seq. Group 3 medulloblastoma cell line (D341) was analyzed by RNA-seq. OTX2 was depleted by infection with lentiviral shRNAs (sh OTX2 and sh GFP control). Raw data not provided for primary Medulloblastoma samples due to patient privacy concerns. Submitter states that the raw data for these samples will be submitted to dbGaP.

Publication Title

OTX2 Activity at Distal Regulatory Elements Shapes the Chromatin Landscape of Group 3 Medulloblastoma.

Sample Metadata Fields

Cell line, Subject

View Samples
accession-icon GSE86477
Small and big Hodgkin-Reed-Sternberg cells of Hodgkin lymphoma cell lines L-428 and L-1236 lack consistent differences in gene expression profiles and are capable to reconstitute each other
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Gene expression analysis was performed from microdissected small and big HRS cells, which were taken from smears of the Hodgkin cell lines

Publication Title

Small and big Hodgkin-Reed-Sternberg cells of Hodgkin lymphoma cell lines L-428 and L-1236 lack consistent differences in gene expression profiles and are capable to reconstitute each other.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE84464
Genexpression Profiling of DLBCL derived from NLPHL
  • organism-icon Homo sapiens
  • sample-icon 29 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Nodular lymphocyte predominant Hodgkin lymphoma (NLPHL) is an indolent lymphoma, but can transform into diffuse large B cell lymphoma (DLBCL), showing a more aggressive clinical behavior. Little is known about these cases on the molecular level. Therefore, the aim of the present study was to characterize DLBCL transformed from NLPHL (LP-DLBCL) by gene expression profiling (GEP). GEP revealed an inflammatory signature pinpointing to a specific host response. In a coculture model resembling this host response, DEV tumor cells showed an impaired growth behavior. Mechanisms involved in the reduced tumor cell proliferation included a downregulation of MYC and its target genes. Lack of MYC expression was also confirmed in 12/16 LP-DLBCL by immunohistochemistry. Furthermore, CD274/PD-L1 was upregulated in tumor cells after coculture with T cells or monocytes and its expression was validated in 12/19 cases of LP-DLBCL. Thereby, our data provide new insights into the pathogenesis of LP-DLBCL and a concrete explanation of the relatively low tumor cell content. Moreover, our results suggest that treatment of these patients with checkpoint inhibitors may enhance an already ongoing host response in these patients.

Publication Title

A strong host response and lack of MYC expression are characteristic for diffuse large B cell lymphoma transformed from nodular lymphocyte predominant Hodgkin lymphoma.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE84688
Gene expression profiling of the NLPHL cell line DEV after coculture with T cells and monocytes
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Nodular lymphocyte predominant Hodgkin lymphoma (NLPHL) is an indolent lymphoma, but can transform into diffuse large B cell lymphoma (DLBCL), showing a more aggressive clinical behavior. Little is known about these cases on the molecular level. Therefore, the aim of the present study was to characterize DLBCL transformed from NLPHL

Publication Title

A strong host response and lack of MYC expression are characteristic for diffuse large B cell lymphoma transformed from nodular lymphocyte predominant Hodgkin lymphoma.

Sample Metadata Fields

Specimen part, Cell line

View Samples
accession-icon SRP101969
COX-2 mediates tumor-stromal Prolactin signaling to initiate tumorigenesis [single cells]
  • organism-icon Mus musculus
  • sample-icon 254 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Tumor-stromal communication within the microenvironment contributes to initiation of metastasis and may present a therapeutic opportunity. Using serial single cell RNA-sequencing in an orthotopic mouse prostate cancer model, we find upregulation of Prolactin receptor as cancer cells that have disseminated to the lung expand into micrometastases. Secretion of the ligand Prolactin by adjacent lung stromal cells is induced by tumor cell production of the COX-2 synthetic product prostaglandin E-2 (PGE-2). PGE-2 treatment of fibroblasts activates the nuclear orphan receptor NR4A (Nur77), with Prolactin as a major transcriptional target for the NR4A-Retinoid X receptor (RXR) heterodimer. Ectopic expression of Prolactin receptor in mouse cancer cells enhances micrometastasis, while treatment with the COX-2 inhibitor Celecoxib abrogates Prolactin secretion by fibroblasts and reduces tumor initiation. Across multiple human cancers, COX-2, Prolactin, and Prolactin receptor show consistent differential expression in tumor and stromal compartments. Such paracrine crosstalk may thus contribute to the documented efficacy of COX-2 inhibitors in cancer suppression. Overall design: Primary tumors were established by direct prostate inoculation into immunosuppressed NSG mice of CE1-4 prostate cancer cells, derived from tissue-specific inactivation of PTEN [Pubmed ID: 20631921]. These cells, which were GFP-luciferase tagged, are noteworthy in that they have preserved expression of the androgen receptor and epithelial markers and recapitulate biological features of human prostate cancer. Six weeks following intra-prostate inoculation, multiple single DTCs were identified microscopically within the lungs (394 cells/hpf), with a smaller number in liver (54 cells/hpf), brain (9 cells/hpf) and bone marrow (1 cell/hpf). To undertake RNA sequencing of single cells during progression from quiescent DTCs to proliferative lesions, we identified GFP-tagged single tumor cells from lung harvested at various intervals, analyzing these separately from microdissected multicellular lesions. Individual DTCs collected at 6-7 weeks (DTC-I; N=20) and at 9-11 weeks (DTC-II; N=55) were compared with single cells derived from the primary tumor (N=29), lung micro-metastases (N=33), and CTCs isolated by microfluidic capture from blood specimens (N=12) [Pubmed ID: 28181495].

Publication Title

COX-2 mediates tumor-stromal prolactin signaling to initiate tumorigenesis.

Sample Metadata Fields

Disease, Subject

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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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