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accession-icon GSE36665
Gene expression profiling of Wwox targeted ablation in mouse mammary epithelial cells
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

The WWOX gene has been implicated in human cancers, including breast cancer.The development and tumorigenesis between human and mouse mammary glands (MGs) share similar molecular details and signal transduction pathways. We established mouse line that specifically knockout the expression of WWOX gene in the MG epithelial cells (MECs) by crossing BK5-cre mice with our WWOX flox stain. In order to study the gene expression profile in the subpopulation MECs, we isolated the organoids from the 4th MGs of both BK5-cre +; WWOX flox/flox (KO) mice and their WT counterparts (BK5-cre -; WWOX flox/flox), 3 mice each genotype. The total RNA from the mouse MG organoids was extracted and purified by TRIzol/RNeasy Kit and their integrity was checked on Agilent RNA 6000 Nanochip.

Publication Title

Conditional Wwox deletion in mouse mammary gland by means of two Cre recombinase approaches.

Sample Metadata Fields

Age, Specimen part

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accession-icon GSE36372
Wnt Pathway Contributes to the Protection of Acute Lymphoblastic Leukemia Cells by Bone Marrow Stromal Cells and May Be a Therapeutic Target
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconIllumina HumanHT-12 V3.0 expression beadchip

Description

Acute lymphoblastic leukemia (ALL) is the most common cancer in children and one of the most common cancers in adults. Although most children with ALL can be cured, approximately 60% of adults with ALL develop drug resistance or experience relapse and cannot be cured with traditional chemotherapy. One possible reason that treatment fails to eradicate ALL cells is that residual leukemia cells are protected by various components of the bone marrow microenvironment, such as marrow stromal cells (MSCs). To evaluate the effects of MSCs on ALL cell survival and response to chemotherapy, we co-cultured ALL cells with human or murine MSCs. We found that both human and murine MSCs protected human ALL cell lines and primary ALL cells from spontaneous and Ara-C-induced apoptosis. MSCs also modulated the cell cycle and increased ALL cell proliferation. Specifically, we found that Wnt signaling activation contributed to MSC-mediated drug resistance. In contrast, blocking the Wnt pathway led to decreased ALL cell viability. Chemotherapy plus the -catenin inhibitor XAV939 resulted in a decreased tumor burden and improved overall survival in an ALL mouse model compared with chemotherapy alone. Our data demonstrate that targeting the Wnt pathway may represent an innovative approach to the treatment of ALL.

Publication Title

No associated publication

Sample Metadata Fields

Treatment

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accession-icon GSE30687
Genes that mediate colorectal cancer liver metastasis
  • organism-icon Homo sapiens
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A 2.0 Array (hgu133a2)

Description

The study identifies a set of genes through functional selection in an orthotopic colorectal cancer mouse model that play an important role in mediating colorectal cancer liver metastasis. We look at the gene profiling of metastatic colorectal cancer cells (L1 and L2) and non-mestastatic colorectal cancer cells (sw620 and sw480) using Affymetrix U133A oligonucleotide arrays.

Publication Title

APOBEC3G promotes liver metastasis in an orthotopic mouse model of colorectal cancer and predicts human hepatic metastasis.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE33072
An epithelial-mesenchymal transition (EMT) gene signature predicts resistance to erlotinib and PI3K pathway inhibitors and identifies Axl as a novel EMT marker in non-small cell lung cancer.
  • organism-icon Homo sapiens
  • sample-icon 130 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Epithelial/mesenchymal transition (EMT) is associated with loss of cell adhesion molecules, such as E-cadherin, and increased invasion, migration, and proliferation in epithelial cancers. In non-small cell lung cancer (NSCLC), EMT is associated with greater resistance to EGFR inhibitors. However, its potential to predict response to other targeted drugs or chemotherapy has not been well characterized. The goal of this study was to develop a robust, platform-independent EMT gene expression signature and to investigate the association of EMT and drug response in NSCLC.

Publication Title

An epithelial-mesenchymal transition gene signature predicts resistance to EGFR and PI3K inhibitors and identifies Axl as a therapeutic target for overcoming EGFR inhibitor resistance.

Sample Metadata Fields

Sex, Disease, Treatment, Race

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accession-icon GSE31852
An EGFR-mutation signature reveals features of the EGFR-dependent phenotype and identifies MACC1 as an EGFR-associated regulator of MET.
  • organism-icon Homo sapiens
  • sample-icon 123 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

EGFR-mutated non-small cell lung cancers bear hallmarks including sensitivity to EGFR inhibitors, and low proliferation, and increased MET. However, the biology of EGFR dependence is still poorly understood. Using a training cohort of chemo-naive lung adenocarcinomas, we have developed a 72-gene signature that predicts (i) EGFR mutation status in four independent datasets; (ii) sensitivity to erlotinib in vitro; and (iii) improved survival, even in the wild-type EGFR subgroup. The signature includes differences associated with enhanced receptor tyrosine kinase (RTK) signaling, such as increased expression of endocytosis-related genes, decreased phosphatase levels, decreased expression of proliferation-related genes, increased folate receptor-1 (FOLR1) (a determinant of pemetrexed response), and higher levels of MACC1 (which we identify as a regulator of MET in EGFR-mutant NSCLC). Those observations provide evidence that the EGFR-mutant phenotype is associated with alterations in the cellular machinery that links the EGFR and MET pathways and create a permissive environment for RTK signaling.

Publication Title

No associated publication

Sample Metadata Fields

Sex, Disease, Treatment, Race

View Samples
accession-icon GSE26549
Gene Expression Profiling Predicts the Development of Oral Cancer
  • organism-icon Homo sapiens
  • sample-icon 86 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Patients with oral preneoplastic lesion (OPL) have high risk of developing oral cancer. Although certain risk factors such as smoking status and histology are known, our ability to predict oral cancer risk remains poor. The study objective was to determine the value of gene expression profiling in predicting oral cancer development. Gene expression profile was measured in 86 of 162 OPL patients who were enrolled in a clinical chemoprevention trial that used the incidence of oral cancer development as a prespecified endpoint. The median follow-up time was 6.08 years and 35 of the 86 patients developed oral cancer over the course. Gene expression profiles were associated with oral cancer-free survival and used to develope multivariate predictive models for oral cancer prediction.

Publication Title

Gene expression profiling predicts the development of oral cancer.

Sample Metadata Fields

Sex, Age, Race

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accession-icon GSE31428
Final efficacy and biomarker analysis of the sorafenib arm of the BATTLE (Biomarker-Integrated Approaches of Targeted Therapy for Lung Cancer Elimination) trial
  • organism-icon Homo sapiens
  • sample-icon 37 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Purpose: To determine the 8-week disease control rate (DCR) of sorafenib monotherapy in patients with advanced non-small-cell lung cancer (NSCLC) in the BATTLE trial.

Publication Title

No associated publication

Sample Metadata Fields

Sex, Treatment, Race

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accession-icon GSE27389
Substitutions in the KRas oncogene determine protein behavior: Implications for signaling and clinical outcome.
  • organism-icon Homo sapiens
  • sample-icon 22 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Mutant KRAS (mut-KRAS) is present in 30% of all human cancers and plays a critical role in cancer cell growth and resistance to therapy. There is evidence from colon cancer that mut-KRAS is a poor prognostic factor and negative predictor of patient response to molecularly targeted therapy. However, evidence for such a relationship in non small cell lung cancer (NSCLC) is conflicting. KRAS mutations are primarily found at codons 12 and 13, where different base changes lead to alternate amino acid substitutions that lock the protein in an active state. The patterns of mut-KRas amino acid substitutions in colon cancer and NSCLC are quite different, with aspartate (D) predominating in colon cancer (50%) and cysteine (C) in NSCLC (47%).

Publication Title

Effect of KRAS oncogene substitutions on protein behavior: implications for signaling and clinical outcome.

Sample Metadata Fields

Sex, Disease, Treatment, Race

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accession-icon GSE27523
Identification of hypoxia regulated HIF-1A and HIF-2A specific target genes in Glioblastoma
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Exon 1.0 ST Array [transcript (gene) version (huex10st)

Description

HIF-1A and HIF-2A regulate both overlapping and unique target genes in response to hypoxia.

Publication Title

The hypoxia-associated factor switches cells from HIF-1α- to HIF-2α-dependent signaling promoting stem cell characteristics, aggressive tumor growth and invasion.

Sample Metadata Fields

Specimen part, Cell line

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accession-icon GSE52032
14-3-3 overexpression-induced gene signature in MCF-10A cells
  • organism-icon Homo sapiens
  • sample-icon 3 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)

Description

To study the function of 14-3-3, we established MCF-10A human mammary epithelial cells transduced with 14-3-3 (10A.) and vector (10A.Vec)

Publication Title

14-3-3ζ turns TGF-β's function from tumor suppressor to metastasis promoter in breast cancer by contextual changes of Smad partners from p53 to Gli2.

Sample Metadata Fields

Specimen part, Cell line

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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)

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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