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Homo sapiens
115 Downloadable Samples
Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Background: The prognostic value of histologic grade (HG) in invasive lobular carcinoma (ILC) remains uncertain, and most ILC tumors are graded as HG2. Genomic grade (GG) is a 97-gene signature that improves the prognostic value of HG. This study evaluates whether GG may overcome the limitations of HG in ILC.
Publication Title
Genomic grade adds prognostic value in invasive lobular carcinoma.
Sample Metadata Fields
Sex, Specimen part, Disease, Disease stage
View Samples- Homo sapiens
- 120 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
PURPOSE: Validated biomarkers predictive of response/resistance to anthracyclines in breast cancer are currently lacking. The neoadjuvant TOP trial, in which patients with estrogen receptor (ER)-negative tumors were treated with anthracycline (epirubicin) monotherapy, was specifically designed to evaluate the predictive value of topoisomerase II (TOP2A) and to develop a gene expression signature to identify those patients who do not benefit from anthracyclines.
Publication Title
Multifactorial approach to predicting resistance to anthracyclines.
Sample Metadata Fields
Disease stage
View Samples- Mus musculus
- 4 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Interferon is effective at inducing complete remissions in patients with Chronic Myelogenous Leukemia (CML), and evidence supports an immune mechanism. Here we show that the Type I Interferons (alpha and beta) regulate expression of the Interferon consensus sequence binding protein (ICSBP) in bcr-abl transformed cells and as shown previously for ICSBP, induce a vaccine-like immunoprotective effect in a murine model of bcr-abl induced leukemia. We identify the chemokines CCL6 and CCL9 as genes prominently induced by the Type I Interferons and ICSBP, and demonstrate that these immunomodulators are required for the immunoprotective effect of ICSBP expression. Insights into the role of these chemokines in the anti-leukemic response of interferons suggest new strategies for immunotherapy of CML.
Publication Title
ICSBP-mediated immune protection against BCR-ABL-induced leukemia requires the CCL6 and CCL9 chemokines.
Sample Metadata Fields
No sample metadata fields
View Samples
GSE75058- Mus musculus, Homo sapiens
- 8 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Targeting c-FOS and DUSP1 abrogates intrinsic resistance to tyrosine-kinase inhibitor therapy in BCR-ABL-induced leukemia.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Mus musculus
- 11 Downloadable Samples
Illumina HiSeq 2500
Description
We performed whole genome expression analysis using BCR/ABL expressing Kit+ cells derived from wild type and ROSACreERT2c-Fosfl/flDusp1-/- bone marrow cells. Wild type kit+ cells were treated with DFC+BCI and DFC+BC+Im to mimic the genetic loss of c-Fos and Dusp1. Overall design: The experiment was designed to test whether chemical inhibition by FOS and Dusp1 Inhibitor mimics the genetic deletion of cFOS and Dusp1 in mouse primary cells transduced with BCR-ABL. This data is part of the super series Mechanism of Oncogene addiction GSE75058.
Publication Title
Targeting c-FOS and DUSP1 abrogates intrinsic resistance to tyrosine-kinase inhibitor therapy in BCR-ABL-induced leukemia.
Sample Metadata Fields
Specimen part, Cell line, Subject
View Samples- Mus musculus
- 4 Downloadable Samples
Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
The Baf3 are dependent on IL-3 for grwoth however transformation by BCR -ABL oncogene causes BAf3 cells independent of IL-3. The BAf3 cells expressing BCR-ABL are dependent on continuous expression of BCR_ABL for growth. Inhibitionof BCR-ABL by its inhibitor Imatinib cause these cells to undergo apoptosis. When these cells are grown with IL-3 these cells do not respond to Imatinib mediated grwoth arrest.
Publication Title
Targeting c-FOS and DUSP1 abrogates intrinsic resistance to tyrosine-kinase inhibitor therapy in BCR-ABL-induced leukemia.
Sample Metadata Fields
Cell line
View Samples- Homo sapiens
- 2 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
K562 cells when grown with erythropeitin do not respond to Imatinib. Here we are comparing the gene expression profile from imatinib resistant and sensitive cells.
Publication Title
Targeting c-FOS and DUSP1 abrogates intrinsic resistance to tyrosine-kinase inhibitor therapy in BCR-ABL-induced leukemia.
Sample Metadata Fields
Cell line
View Samples- Mus musculus
- 2 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
BAF3 cells harboring constitutively expressing BCR-ABL were grown with or without IL-3 supplement and treated with Imatinib and live cells from the IL-3 and without IL-3 were sorted by FACS.
Publication Title
Targeting c-FOS and DUSP1 abrogates intrinsic resistance to tyrosine-kinase inhibitor therapy in BCR-ABL-induced leukemia.
Sample Metadata Fields
Cell line
View Samples- Mus musculus
- 9 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Klf5 has essential functions during early embryogenesis and in the derivation of ES cells from inner-cell mass of blastocyst. Among Kruppel-like factor (Klf) family members, only Klf5 shows peri-implantation lethal phenotype, but the precise mechanisms still remain unknown. To understand and identify molecular mechanisms, we performed microarray analysis by using E3.0 WT and Klf5 KO embryos when first phenotype of Klf5 deficiency appears.
Publication Title
<i>Klf5</i> maintains the balance of primitive endoderm versus epiblast specification during mouse embryonic development by suppression of <i>Fgf4</i>.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 6 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
Cancer incidence increases in the elderly, although the underlying reasons for this association are unknown. We show that B-progenitors in old mice exhibit profound signaling and metabolic defects, and that expression of BCR-ABL, NRASV12 and MYC reverses these fitness defects, leading to selection of oncogenically-initiated cells and leukemogenesis in old hematopoietic backgrounds. Aging is associated with increased inflammation in the BM microenvironment, and inducing inflammation in young mice phenocopies aging B-lymphopoiesis. Importantly, reducing inflammation in aged mice preserves the function of B-progenitors and prevents NRasV12-mediated oncogenesis. We conclude that chronic microenvironments in old age lead to reductions in the fitness of hematopoietic stem and progenitor cell populations. This reduced progenitor pool fitness leads to selection for cells harboring oncogenic mutations in part due to their ability to correct aging-associated functional defects.
Publication Title
Aging-associated inflammation promotes selection for adaptive oncogenic events in B cell progenitors.
Sample Metadata Fields
Age, Specimen part
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