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accession-icon GSE42743
Oral Cavity Cancer Compared to Adjacent "Normal" Tissue [Validation Set]
  • organism-icon Homo sapiens
  • sample-icon 99 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Oral Cavity Cancer

Publication Title

A 13-gene signature prognostic of HPV-negative OSCC: discovery and external validation.

Sample Metadata Fields

Sex

View Samples
accession-icon GSE41613
A 13-gene signature prognostic of HPV-negative OSCC: discovery and external validation
  • organism-icon Homo sapiens
  • sample-icon 94 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

OSCC is associated with substantial mortality and morbidity. In this study, we built on our previous molecular work to identify and validate a prognostic 13-gene signature that showed a higher ability than tumor stage in predicting survival for patients with

Publication Title

A 13-gene signature prognostic of HPV-negative OSCC: discovery and external validation.

Sample Metadata Fields

Sex, Specimen part, Treatment

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accession-icon GSE30784
Gene expression profiling of oral squamous cell carcinoma (OSCC)
  • organism-icon Homo sapiens
  • sample-icon 221 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

OSCC is associated with substantial mortality and morbidity. To identify potential biomarkers for the early detection of invasive OSCC, we compared the gene expressions of OSCC, oral dysplasia, and normal

Publication Title

Gene expression profiling identifies genes predictive of oral squamous cell carcinoma.

Sample Metadata Fields

Sex

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accession-icon GSE72353
A lincRNA connected to cell mortality and epigenetically-silenced in most common human cancers
  • organism-icon Homo sapiens
  • sample-icon 16 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

- Gene expression changes linked to two step immortalization of human mammary epithelial cells (HMEC).

Publication Title

A lincRNA connected to cell mortality and epigenetically-silenced in most common human cancers.

Sample Metadata Fields

Specimen part

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accession-icon GSE85898
Gene expression data before and after interferon-gamma stimulatinon
  • organism-icon Homo sapiens
  • sample-icon 11 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

Three of the melanoma cell lines show higher expression fold change after stimulation than the other 3.

Publication Title

Loss of IFN-γ Pathway Genes in Tumor Cells as a Mechanism of Resistance to Anti-CTLA-4 Therapy.

Sample Metadata Fields

Specimen part

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accession-icon GSE47047
Gene expression data from immortal and arsenite-transformed malignant prostate epithelial cells
  • organism-icon Homo sapiens
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

The aim of this study was to determine how gene expression is changed after arsenite-induced malignant transformation of prostate epithelial cells.

Publication Title

Coordinate H3K9 and DNA methylation silencing of ZNFs in toxicant-induced malignant transformation.

Sample Metadata Fields

Specimen part, Cell line, Treatment

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accession-icon GSE22325
Expression data from interleukin-stimulated HUVEC
  • organism-icon Homo sapiens
  • sample-icon 18 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

In the hematopoietic microenvironment, endothelial cells (ECs) play an important role in the regulation of hematopoietic cell proliferation and trafficking. We previously demonstrated that EC stimulated with tumor necrosis factor alpha (TNF-) induce the generation of dendritic cells from CD34(+) stem cells, whereas in contrast, interleukins were capable of inducing the proliferation of hematopoietic and myeloid progenitors.

Publication Title

Transcriptional profiling of the hematopoietic support of interleukin-stimulated human umbilical vein endothelial cells (HUVECs).

Sample Metadata Fields

Specimen part, Treatment

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accession-icon SRP115226
Transcriptome sequencing of 15 normal lung parenchyma (NL), 17 atypical adenomatous hyperplasia (AAH) and 16 lung adenocarcinoma (LUAD) samples from 17 patients
  • organism-icon Homo sapiens
  • sample-icon 40 Downloadable Samples
  • Technology Badge IconIon Torrent Proton

Description

We sought to characterize expression profiles signifying the development of atypical adenomatous hyperplasia (AAH) from normal lung parenchyma (NL), and its progression to lung adenocarcinomas (LUAD). Overall design: We performed transcriptome sequencing of 48 samples, comprising NLs, AAHs and LUADs, from 17 patients. Sequencing was performed using the Ion Torrent platform afterwhich gene profiles differentially expressed among the three groups were determined.

Publication Title

Genomic Landscape of Atypical Adenomatous Hyperplasia Reveals Divergent Modes to Lung Adenocarcinoma.

Sample Metadata Fields

Specimen part, Subject

View Samples
accession-icon GSE9200
Feedback Circuit among INK4 Tumor Suppressors Constrains Human Glioblastoma Development
  • organism-icon Homo sapiens
  • sample-icon 28 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

We have developed a nonheuristic genome topography scan (GTS) algorithm to characterize the patterns of genomic alterations in human glioblastoma (GBM), identifying frequent p18INK4C and p16INK4A codeletion. Functional reconstitution of p18INK4C in GBM cells null for both p16INK4A and p18INK4C resulted in impaired cell-cycle progression and tumorigenic potential. Conversely, RNAi-mediated depletion of p18INK4C in p16INK4A-deficient primary astrocytes or established GBM cells enhanced tumorigenicity in vitro and in vivo. Furthermore, acute suppression of p16INK4A in primary astrocytes induced a concomitant increase in p18INK4C. Together, these findings uncover a feedback regulatory circuit in the astrocytic lineage and demonstrate a bona fide tumor suppressor role for p18INK4C in human GBM wherein it functions cooperatively with other INK4 family members to constrain inappropriate proliferation.

Publication Title

Feedback circuit among INK4 tumor suppressors constrains human glioblastoma development.

Sample Metadata Fields

No sample metadata fields

View Samples
accession-icon GSE9171
Expression profiles of human glioblastoma frozen tumors and cell lines
  • organism-icon Homo sapiens
  • sample-icon 28 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

We have developed a nonheuristic genome topography scan (GTS) algorithm to characterize the patterns of genomic alterations in human glioblastoma (GBM), identifying frequent p18INK4C and p16INK4A codeletion. Functional reconstitution of p18INK4C in GBM cells null for both p16INK4A and p18INK4C resulted in impaired cell-cycle progression and tumorigenic potential. Conversely, RNAi-mediated depletion of p18INK4C in p16INK4A-deficient primary astrocytes or established GBM cells enhanced tumorigenicity in vitro and in vivo. Furthermore, acute suppression of p16INK4A in primary astrocytes induced a concomitant increase in p18INK4C. Together, these findings uncover a feedback regulatory circuit in the astrocytic lineage and demonstrate a bona fide tumor suppressor role for p18INK4C in human GBM wherein it functions cooperatively with other INK4 family members to constrain inappropriate proliferation.

Publication Title

Feedback circuit among INK4 tumor suppressors constrains human glioblastoma development.

Sample Metadata Fields

No sample metadata fields

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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