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accession-icon GSE37182
Time course analysis of colon cancer samples
  • organism-icon Homo sapiens
  • sample-icon 144 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V3.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Effects of warm ischemic time on gene expression profiling in colorectal cancer tissues and normal mucosa.

Sample Metadata Fields

Specimen part, Disease, Disease stage, Subject, Time

View Samples
accession-icon GSE37175
Time course analysis of colon cancer samples (part 1)
  • organism-icon Homo sapiens
  • sample-icon 60 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V3.0 expression beadchip

Description

The study outcome was to evaluate the effect of the time on normal colon mucosa samples and possibly select specific genes whose expression is time-related, that could be used as detectors of tissue degradation.

Publication Title

Effects of warm ischemic time on gene expression profiling in colorectal cancer tissues and normal mucosa.

Sample Metadata Fields

Specimen part, Disease, Disease stage, Subject, Time

View Samples
accession-icon GSE37178
Time course analysis of colon cancer samples (part 2)
  • organism-icon Homo sapiens
  • sample-icon 49 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V3.0 expression beadchip

Description

The study outcome was to evaluate the effect of the time on tumor samples and possibly select specific genes whose expression is time-related, that could be used as detectors of tissue degradation.

Publication Title

Effects of warm ischemic time on gene expression profiling in colorectal cancer tissues and normal mucosa.

Sample Metadata Fields

Specimen part, Disease, Disease stage, Subject, Time

View Samples
accession-icon GSE38554
Gene expression profiling of FFPE breast cancer samples
  • organism-icon Homo sapiens
  • sample-icon 44 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

We implemented an optimized processing, using alternative Chip Description Files (CDFs) and fRMA normalization, which improve the quality of downstream analysis.

Publication Title

Accurate data processing improves the reliability of Affymetrix gene expression profiles from FFPE samples.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE51452
Gene expression profiling of FFPE breast cancer samples [Affymetrix vs. Illumina]
  • organism-icon Homo sapiens
  • sample-icon 12 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

Use of formalin-fixed paraffin-embedded samples for gene expression studies in breast cancer patients.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE68166
Integrated miRNA and gene expression analysis of prostate cancer associated fibroblasts supports a prominent role for interleukin-6 in fibroblast activation
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Integrated gene and miRNA expression analysis of prostate cancer associated fibroblasts supports a prominent role for interleukin-6 in fibroblast activation.

Sample Metadata Fields

Specimen part, Treatment

View Samples
accession-icon GSE11559
Identification of transcriptional changes induced by FHIT in lung cancer cells NCI-H460
  • organism-icon Homo sapiens
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U95 Version 2 Array (hgu95av2)

Description

The FHIT gene, at 3p14.2, encompasses the common fragile site FRA3B and is frequently inactivated in primary tumors and cell lines of lung, head and neck, stomach, esophagus, cervix and breast cancer. In particular, loss of the FHIT protein is one of the most frequent alteration in lung tumors and pre-invasive lung lesions, suggesting a role for this gene in the early stages of lung carcinogenesis. Adenoviral-mediated restoration of FHIT expression in FHIT-negative cell lines results in cell cycle alteration, induction of apoptosis (through activation of the cytoplasmic apoptotic pathway) and regression of the tumorigenic phenotype. Taken together these observations support the hypothesis of a role for FHIT in human carcinogenesis, but little is known about its mechanism of action. Identification of transcriptional targets of FHIT is therefore critical to understand the pathways by which FHIT promotes growth arrest and apoptosis.

Publication Title

No associated publication

Sample Metadata Fields

Specimen part, Disease, Cell line

View Samples
accession-icon GSE51450
Gene expression profiling of FFPE breast cancer samples [Affymetrix platform]
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

The use of Affymetrix U133 2.0 Plus chips on FFPE samples when coupled with a qPCR-based sample pre-assessment step, yielded satisfactory results from the point of view of biological reliability. When compared with the Illumina DASL WG platform, specifically designed for degraded RNA, the data generated with the Affymetrix platform showed a wider interquartile range (IQR 1.32 vs 0.57, p<2.2x10-16) suggesting a superior discriminatory power within samples as indicated by the good agreement with the immunohistiochemically derived ER status.

Publication Title

Use of formalin-fixed paraffin-embedded samples for gene expression studies in breast cancer patients.

Sample Metadata Fields

Specimen part

View Samples
accession-icon GSE68164
Integrated miRNA and gene expression analysis of prostate cancer associated fibroblasts supports a prominent role for interleukin-6 in fibroblast activation [gene]
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V4.0 expression beadchip

Description

Tumor microenvironment coevolves with and simultaneously sustains cancer progression. Reactive fibroblasts found in prostate cancer (PCa), known as cancer associated fibroblasts (CAF), have been indeed shown to fuel tumor development and metastasis by mutually interacting with PCa cells. Little is known about the molecular mechanisms that lead to activation of CAFs from tissue-resident fibroblasts, circulating marrow-derived fibroblast progenitors or mesenchymal stem cells. Through integrated gene and microRNA expression profiling, here we showed that transcriptome of CAFs isolated from prostate tumors strictly resembles that of normal fibroblasts stimulated in vitro with interleukin-6 (IL6), thus confirming the capability of the cytokine to promote acquisition of an activated and cancer-promoting phenotype, and, for the first time, proving that IL6 is able per se to induce all the complex transcriptional changes characteristic of patient-derived CAFs. Comparison with publicly available datasets, however, suggested that prostate CAFs may be alternatively characterized by IL6 and TGF-related signatures, indicating that either signal, depending on the context, tumor stage and etiology, may concur to fibroblast activation. Our analyses also highlighted pathways relevant for induction of reactive stroma, including genes the role of which in fibroblast activation is still to be explored. In addition, we revealed a role for muscle-specific miR-133b as a soluble factor secreted by activated fibroblasts to support paracrine activation of non-activated fibroblasts or promote tumor progression. Overall, in this study we provided insights on the molecular mechanisms driving fibroblast activation in prostate cancer, thus contributing to identify novel hits for the development of therapeutic strategies targeting the crucial interplay between tumor cells and their microenvironment. Tumor microenvironment coevolves with and simultaneously sustains cancer progression. Reactive fibroblasts found in prostate cancer (PCa), known as cancer associated fibroblasts (CAF), have been indeed shown to fuel tumor development and metastasis by mutually interacting with PCa cells. Little is known about the molecular mechanisms that lead to activation of CAFs from tissue-resident fibroblasts, circulating marrow-derived fibroblast progenitors or mesenchymal stem cells. Through integrated gene and microRNA expression profiling, here we showed that transcriptome of CAFs isolated from prostate tumors strictly resembles that of normal fibroblasts stimulated in vitro with interleukin-6 (IL6), thus confirming the capability of the cytokine to promote acquisition of an activated and cancer-promoting phenotype, and, for the first time, proving that IL6 is able per se to induce all the complex transcriptional changes characteristic of patient-derived CAFs. Comparison with publicly available datasets, however, suggested that prostate CAFs may be alternatively characterized by IL6 and TGF-related signatures, indicating that either signal, depending on the context, tumor stage and etiology, may concur to fibroblast activation. Our analyses also highlighted pathways relevant for induction of reactive stroma, including genes the role of which in fibroblast activation is still to be explored. In addition, we revealed a role for muscle-specific miR-133b as a soluble factor secreted by activated fibroblasts to support paracrine activation of non-activated fibroblasts or promote tumor progression. Overall, in this study we provided insights on the molecular mechanisms driving fibroblast activation in prostate cancer, thus contributing to identify novel hits for the development of therapeutic strategies targeting the crucial interplay between tumor cells and their microenvironment. Tumor microenvironment coevolves with and simultaneously sustains cancer progression. Reactive fibroblasts found in prostate cancer (PCa), known as cancer associated fibroblasts (CAF), have been indeed shown to fuel tumor development and metastasis by mutually interacting with PCa cells. Little is known about the molecular mechanisms that lead to activation of CAFs from tissue-resident fibroblasts, circulating marrow-derived fibroblast progenitors or mesenchymal stem cells. Through integrated gene and microRNA expression profiling, here we showed that transcriptome of CAFs isolated from prostate tumors strictly resembles that of normal fibroblasts stimulated in vitro with interleukin-6 (IL6), thus confirming the capability of the cytokine to promote acquisition of an activated and cancer-promoting phenotype, and, for the first time, proving that IL6 is able per se to induce all the complex transcriptional changes characteristic of patient-derived CAFs. Comparison with publicly available datasets, however, suggested that prostate CAFs may be alternatively characterized by IL6 and TGF-related signatures, indicating that either signal, depending on the context, tumor stage and etiology, may concur to fibroblast activation. Our analyses also highlighted pathways relevant for induction of reactive stroma, including genes the role of which in fibroblast activation is still to be explored. In addition, we revealed a role for muscle-specific miR-133b as a soluble factor secreted by activated fibroblasts to support paracrine activation of non-activated fibroblasts or promote tumor progression. Overall, in this study we provided insights on the molecular mechanisms driving fibroblast activation in prostate cancer, thus contributing to identify novel hits for the development of therapeutic strategies targeting the crucial interplay between tumor cells and their microenvironment.

Publication Title

Integrated gene and miRNA expression analysis of prostate cancer associated fibroblasts supports a prominent role for interleukin-6 in fibroblast activation.

Sample Metadata Fields

Specimen part, Treatment

View Samples
accession-icon GSE52246
Mesenchymal to amoeboid transition is associated with stem-like features of melanoma cells
  • organism-icon Homo sapiens
  • sample-icon 8 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Cellular plasticity confers cancer cells the ability to adapt to micro-environmental changes, a fundamental requirement for tumour progression and metastasis. The epithelial to mesenchymal transition (EMT) is a transcriptional programme associated with increased cell motility and stemness. Beside EMT, the mesenchymal to amoeboid transition (MAT) has been described during tumour progression but, to date, little is known about its transcriptional control and involvement in stemness. The aim of this study is to investigate (i) the transcriptional profile associated with the MAT programme and (ii) to study whether MAT acquisition in melanoma cancer cells correlate with clonogenic potential to promote tumor growth. Our results demonstrate that MAT programme in melanoma is characterised by increased stemness and clonogenic features of cancer cells, thus sustaining tumour progression. Furthermore, these data suggest that stemness is not an exclusive feature of cells undergoing EMT, but more generally is associated with an increase in cellular plasticity of cancer cells.

Publication Title

Mesenchymal to amoeboid transition is associated with stem-like features of melanoma cells.

Sample Metadata Fields

Cell line, Treatment

View Samples
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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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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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