This SuperSeries is composed of the SubSeries listed below.
Evidence that bovine forebrain embryonic zinc finger-like gene influences immune response associated with mastitis resistance.
No sample metadata fields
View SamplesTo investigate genes that might influence resistance to infection through IGF1R, we screened human breast cancer-derived OCUB-M cells transfected with expression vector encoding IGF1R using microarray analysis.
Evidence that bovine forebrain embryonic zinc finger-like gene influences immune response associated with mastitis resistance.
No sample metadata fields
View SamplesTo identify genes that influence resistance to mastitis, we scanned
Evidence that bovine forebrain embryonic zinc finger-like gene influences immune response associated with mastitis resistance.
No sample metadata fields
View SamplesIn this study we demonstrate that Tgif1 has a role in HSCs maintenance, self-renewal and quiescence. RNA sequencing data of LSK cells (HSCs enriched cell population) from Tgif1-/- and wild type mice implicates that multiple pathways involved in HSC quiescence and self-renewal are disturbed in Tgif1 deficient mice. Overall design: RNA expression profiles of wild type (WT) and Tgif1-/- LSK cells were generated by RNA sequencing, in triplicate, using Illumina HiSeq 2000.
Tgif1 regulates quiescence and self-renewal of hematopoietic stem cells.
Specimen part, Cell line, Subject
View SamplesSelective RAF inhibitors including vemurafenib (PLX4032) have demonstrated clinical efficacy in mutant BRAF driven metastatic melanoma. The clinical effectiveness of RAF inhibitors depends on near complete abolition of the MAPK pathway output in tumors harboring BRAF mutations. However these compounds paradoxically activate the MAPK pathway in cells bearing oncogenic RAS or elevated upstream receptor signaling. This paradox can promote cellular proliferation and can manifest clinically with progression of secondary malignancies such as cutaneous squamous cell carcinomas (cuSCC). We have identified next generation RAF inhibitors (paradox breakers, e.g. PLX7904) that inhibit mutant BRAF cells without activating the MAPK pathway in cells bearing upstream activation.
RAF inhibitors that evade paradoxical MAPK pathway activation.
Specimen part, Treatment
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Gene Expression Profiling of Ewing Sarcoma Tumors Reveals the Prognostic Importance of Tumor-Stromal Interactions: A Report from the Children's Oncology Group.
Sex, Age, Disease
View SamplesFor the current study we performed whole genome expression profiling on two independent cohorts of clinically annotated, localized Ewing sarcoma (ES) tumors in an effort to identify and validate prognostic gene signatures. ES specimens were obtained from the Childrens Oncology Group (COG) and whole genome expression profiling performed using Affymetrix Human Exon 1.0 ST arrays. Lists of differentially expressed genes between survivors and non-survivors were used to identify prognostic gene signatures
Gene Expression Profiling of Ewing Sarcoma Tumors Reveals the Prognostic Importance of Tumor-Stromal Interactions: A Report from the Children's Oncology Group.
Sex, Disease
View SamplesFor the current study we performed whole genome expression profiling on two independent cohorts of clinically annotated, localized Ewing sarcoma (ES) tumors in an effort to identify and validate prognostic gene signatures. ES specimens were obtained from the Childrens Oncology Group (COG) and whole genome expression profiling performed using Affymetrix Human Exon 1.0 ST arrays. Lists of differentially expressed genes between survivors and non-survivors were used to identify prognostic gene signatures
Gene Expression Profiling of Ewing Sarcoma Tumors Reveals the Prognostic Importance of Tumor-Stromal Interactions: A Report from the Children's Oncology Group.
Sex, Age, Disease
View SamplesEwing sarcoma family tumors (ESFTs) are aggressive tumors of putative stem cell origin for which prognostic biomarkers and novel treatments are needed. We have previously shown that the polycomb gene BMI-1 functions as an oncogene in ESFT. In several human cancers, high expression of BMI-1 is associated with poor outcome. For the current study, we evaluated the significance of variable BMI-1 expression levels in a large cohort of primary ESFT. Immunohistochemical staining of 130 tumors revealed that BMI-1 is over-expressed by the vast majority of ESFT. However, in 20% of cases, BMI-1 levels are low to undetectable. Significantly, although clinical presentation and outcome were found to be similar between BMI-1-high and BMI-1-low tumors, gene expression profiling studies showed marked differences in their respective gene expression profiles. Gene specific enrichment analysis identified that several cancer-associated canonical biologic pathways, including IGF1, mTOR and WNT, are significantly down-regulated in BMI-1-low compared to BMI-1-high tumors. Consistent with these in vivo data, in vitro studies of IGF1-R inhibition showed that the growth inhibitory effects of IGF1-R blockade are diminished in BMI-1-low ESFT cells. ESFT that do not over-express BMI-1 represent a novel subclass with a distinct molecular profile and altered activation of cancer-associated pathways.
Ewing tumors that do not overexpress BMI-1 are a distinct molecular subclass with variant biology: a report from the Children's Oncology Group.
Specimen part
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