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accession-icon SRP074349
Next Generation Sequencing (RNAseq) of non-small cell lung cancer
  • organism-icon Homo sapiens
  • sample-icon 171 Downloadable Samples
  • Technology Badge Icon

Description

Cancer testis antigens (CTAs) are of clinical interest as biomarkers and present valuable targets for immunotherapy. To comprehensively characterize the CTA landscape of non-small cell lung cancer (NSCLC), we compared RNAseq data of 199 NSCLC tissues to the normal transcriptome of 142 samples from 32 different normal organs. Of 232 CTAs currently annotated in the CTdatabase, 96 were confirmed in NSCLC. To obtain an unbiased CTA profile of NSCLC, we applied stringent criteria on our RNAseq data set and defined 90 genes as CTAs, of which 55 genes were not annotated in the CTdatabase. Cluster  analysis revealed that CTA expression is histology-dependent and concurrent expression is common. Immunohistochemistry confirmed tissue specific protein expression of selected genes. Furthermore, methylation was identified as a regulatory mechanism of CTA expression based on independent data from the Cancer Genome Atlas. The proposed prognostic impact of CTAs in lung cancer, was not confirmed, neither in our RNAseq-cohort nor in an independent meta-analysis of 1117 NSCLC cases. Overall design: Fresh frozen tumor tissue from 199 patients diagnosed with NSCLC and surgically treated 2006-2010 at the Uppsala University Hospital, Uppsala, Sweden and 19 paired normal lung tissues. Clinical data were retrieved from the regional lung cancer registry. Several of the new CTAs are poorly characterized Sample characteristics values represent; pTNM: decided by Hans Brunnström, pathologist in Lund Spring 2013 Stage according to pTNM: 1=1a 2=1b 3=2a 4=2b 5=3a 6=3b 7=IV Histology diagnosis spring 2013 HB: 1=squamous cell cancer 2=AC unspecified 3=Large cell/ NOS Surgery date: the date when sample arrived at Patologen UAS Age: age when surgery was performed Vital date: day of death or latest contact Dead: 0=no 1= yes Smoking history : 1=current 2=ex >1year 3=never WHO performance status: Performance status 0-4 Please note that the L608T_2122, L771T_1 data columns (in the processed data files) are associated with L608T and L771T samples, respectively.

Publication Title

Multispectral imaging for quantitative and compartment-specific immune infiltrates reveals distinct immune profiles that classify lung cancer patients.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE86309
VLX60 characterization II
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Microarray based mRNA profiling was used to identify the mechanism of action for the small molecule VLX60.

Publication Title

Mechanistic characterization of a copper containing thiosemicarbazone with potent antitumor activity.

Sample Metadata Fields

Cell line

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accession-icon SRP067175
Transposon mutagenesis reveals fludarabine-resistance mechanisms in chronic lymphocytic leukemia
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIon Torrent Proton

Description

Purpose:To identify resistance mechanisms for the chemotherapeutic drug fludarabine in chronic lymphocytic leukemia (CLL), as innate and acquired resistance to fludarabine-based chemotherapy represents a major challenge for long-term disease control. Methods: We employed piggyBac transposon-mediated mutagenesis, combined with next-generation sequencing, to identify genes that confer resistance to fludarabine in a human CLL cell line. Results: RNA-seq profiling of fludarabine-resistant cells suggested deregulated MAPK signaling as involved in mediating drug resistance in CLL. Overall design: To address if the fludarabine-resistant HG3 cells were transcriptionally different at a global level compared to their parental cells, we performed RNA-sequencing of three pairs of HG3 pools

Publication Title

Transposon Mutagenesis Reveals Fludarabine Resistance Mechanisms in Chronic Lymphocytic Leukemia.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE73989
Chromatin relaxation is a feature of advanced prostate cancer
  • organism-icon Homo sapiens
  • sample-icon 5 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Androgen Receptor Deregulation Drives Bromodomain-Mediated Chromatin Alterations in Prostate Cancer.

Sample Metadata Fields

Specimen part, Cell line, Time

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accession-icon GSE73930
Chromatin relaxation is a feature of advanced prostate cancer [expression]
  • organism-icon Homo sapiens
  • sample-icon 5 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

Altered patterns of transcription factor (TF) binding are now accepted as a hallmark of many aggressive cancers including prostate and breast cancers1,2. This implies that underlying global changes in chromatin accessibility may drive cancer progression, as previously hypothesized3-5. In addition there are epigenetic readers such as bromodomain containing protein 4 (BRD4), which have been shown to associate with these TFs6-8 and also to contribute to aggressive cancers of many types8,9 including prostate cancer (PC)6,10. Here we show for the first time that formaldehyde-assisted isolation of regulatory elements followed by sequencing (FAIRE-seq) applied to human prostate tumors tissue can define castrate-resistant prostate cancer (CRPC) and can be used to inform the discovery of gene-level classifiers for therapy. In addition, we show that the androgen receptor (AR) overexpression alone is a primary driver for chromatin relaxation and that this effect can be reversed using bromodomain inhibitors. We also report that bromodomain-containing proteins (BRDs) are overexpressed in advanced CRPCs and that ATAD2 and BRD2 have prognostic value. In conclusion, this is the first study demonstrating a major impact of BRDs on chromatin accessibility in CRPC in patient samples. Consequently, targeting bromodomains provides a compelling rational for combination therapy in which BRD-mediated TF binding is enhanced or modified as cancer progresses.

Publication Title

Androgen Receptor Deregulation Drives Bromodomain-Mediated Chromatin Alterations in Prostate Cancer.

Sample Metadata Fields

Time

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accession-icon GSE106260
Immunopathology of childhood celiac disease-Key role of intestinal epithelial cells
  • organism-icon Homo sapiens
  • sample-icon 52 Downloadable Samples
  • Technology Badge IconIllumina HumanRef-8 v3.0 expression beadchip, Illumina HumanHT-12 V4.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Immunopathology of childhood celiac disease-Key role of intestinal epithelial cells.

Sample Metadata Fields

Specimen part, Cell line, Treatment

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accession-icon GSE103374
Gene expression assessed by genome wide hybridization bead array in T84 polarized tight monolayers after challenge with celiac disease-associated bacteria and gluten [CTR glut bmix, bmix and gluten]
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

Analysis of the influence of celiac disease-associated bacteria and gluten on intestinal epithelial cells

Publication Title

Immunopathology of childhood celiac disease-Key role of intestinal epithelial cells.

Sample Metadata Fields

Cell line, Treatment

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accession-icon GSE103100
Gene expression assessed by genome wide hybridization bead array in T84 polarized tight monolayers after challenge with celiac disease-associated bacteria and gluten [A grav, Bmix Bmix glut]
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

Analysis of the influence of celiac disease-associated bacteria and gluten on intestinal epithelial cells

Publication Title

Immunopathology of childhood celiac disease-Key role of intestinal epithelial cells.

Sample Metadata Fields

Cell line, Treatment

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accession-icon GSE103107
Gene expression assessed by genome wide hybridization bead array in T84 polarized tight monolayers after challenge with celiac disease-associated bacteria [CTR 22 28 27]
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

Analysis of the influence of celiac disease-associated bacteria on intestinal epithelial cells

Publication Title

Immunopathology of childhood celiac disease-Key role of intestinal epithelial cells.

Sample Metadata Fields

Cell line, Treatment

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accession-icon GSE102993
Gene expression assessed by genome wide hybridization bead array in intraepithelial lymphocytes (IELs) isolated from small intestinal biopsies of celiac disease patients with active disease and clinical controls
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge IconIllumina HumanRef-8 v3.0 expression beadchip

Description

Analysis of role of small intestinal intraepithelial lymphocytes (IELs) in the immunopathology of celiac disease

Publication Title

Immunopathology of childhood celiac disease-Key role of intestinal epithelial 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)

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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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