Endometriosis is a complex pathological condition in which multiple components are involved in the disease development and clinical outcome. Endometriosis is mainly an inflammatory codition estrogen-dependent, with unknown pathogenesis, that is characterized by dissemination of edometrium tissue in ectopic position (ovary or pelvic peritoneum). Two main theories rise the pathologic onset: the presence of retrograde menstruation and celomic metaplasia in the pelvic peritoneum, that can occur for development defects. Endometriosis is related not only to genetic or immunological changes and to environmental pollution factors, as the endocrine interferents. The disease phenotype results from multiple events (genetics and enviromental), thus it is difficult to find a single gene as causative while is more probable that a gene network/s might involved in the onset and mantainement of the disease state. The peculiarity of endometriosis rely on the tissue speificity manteinance in the ectopic position, where it responds to the hormone stimuli as the tissue in the eutopic position.
Transcriptional profiling of endometriosis tissues identifies genes related to organogenesis defects.
Specimen part, Disease, Disease stage, Subject
View SamplesGene expression profiling was performed in ccRCC cells, which either express both HIF1alpha and HIF2alpha (either naturally or by virtue of induced expression of HIF1alpha) or express HIF2alpha alone (either naturally or by virtue of a HIF1alpha shRNA), to identify genes regulated by HIF1alpha in ccRCC cells.
Genetic and functional studies implicate HIF1α as a 14q kidney cancer suppressor gene.
Specimen part, Cell line
View SamplesThe global gene expression profiles of ventral prostates of wild type mice and p110 beta transgenic mice.
A constitutively activated form of the p110beta isoform of PI3-kinase induces prostatic intraepithelial neoplasia in mice.
Age, Specimen part, Disease, Disease stage
View SamplesThis SuperSeries is composed of the SubSeries listed below.
The requirement for cyclin D function in tumor maintenance.
Specimen part, Cell line
View SamplesD-cyclins represent components of cell cycle machinery. To test the efficacy of targeting D-cyclins in cancer treatment, we engineered mouse strains which allow acute and global ablation of individual D-cyclins in a living animal. Ubiquitous shutdown of cyclin D1 or inhibition of cyclin D associated kinase activity in mice bearing ErbB2-driven mammary carcinomas halted cancer progression and triggered tumor-specific senescence, without compromising the animals' health. Ablation of cyclin D3 in mice bearing T-cell acute lymphoblastic leukemias (T-ALL) triggered tumorspecific apoptosis. Such selective killing of leukemic cells can be also achieved by inhibiting cyclin D associated kinase activity in mouse and human T-ALL models. Hence, contrary to what one might expect from ablation of a cell cycle protein, acute shutdown of a D-cyclin leads not only to cell cycle arrest, but it also triggers tumor cell senescence or apoptosis, and it affects different tumor types through distinct cellular mechanisms. Inhibiting cyclin D-activity represents a highly-selective anticancer strategy which specifically targets cancer cells without significantly affecting normal tissues.
The requirement for cyclin D function in tumor maintenance.
Cell line
View SamplesD-cyclins represent components of cell cycle machinery. To test the efficacy of targeting D-cyclins in cancer treatment, we engineered mouse strains which allow acute and global ablation of individual D-cyclins in a living animal. Ubiquitous shutdown of cyclin D1 or inhibition of cyclin D associated kinase activity in mice bearing ErbB2-driven mammary carcinomas halted cancer progression and triggered tumor-specific senescence, without compromising the animals' health. Ablation of cyclin D3 in mice bearing T-cell acute lymphoblastic leukemias (T-ALL) triggered tumorspecific apoptosis. Such selective killing of leukemic cells can be also achieved by inhibiting cyclin D associated kinase activity in mouse and human T-ALL models. Hence, contrary to what one might expect from ablation of a cell cycle protein, acute shutdown of a D-cyclin leads not only to cell cycle arrest, but it also triggers tumor cell senescence or apoptosis, and it affects different tumor types through distinct cellular mechanisms. Inhibiting cyclin D-activity represents a highly-selective anticancer strategy which specifically targets cancer cells without significantly affecting normal tissues.
The requirement for cyclin D function in tumor maintenance.
Specimen part
View SamplesThis study was performed to understand the gene expression changes that accompany treatment of renal cell carcinoma (RCC) with vascular endothelial growth factor receptor (VEGFR) tyrosine kinase inhibitor (TKI) therapy. Human RCC cell lines were implanted into the flanks of nude beige mice, allowed to reach 12mm in long axis, and then treated with TKIs (sunitinib or sorafenib). Tumors were excised at 2 timepoints (prior to any therapy and at the 20mm endpoint of the study) and gene expression analysis was performed.
Anti-S1P Antibody as a Novel Therapeutic Strategy for VEGFR TKI-Resistant Renal Cancer.
Specimen part, Cell line, Treatment
View SamplesComparison of ccRCC cells with high HIF or low HIF activity Overall design: Cells expressing control (VEC) were compared to cells with ARNT1 loss using sh/sgRNA targeting ARNT1 The samples labeled 'con' are parental Vhl-null cells and represent the 'high HIF' state. The other 2 cell lines represent the 'low HIF' state. The cell line labeled shArnt have loss of a protein named ARNT by virtue of RNAi-mediated knockdown using a shRNA targeting ARNT. The sample labeled lcARNT has loss of ARNT protein using a lenti-crispr mediated sgRNA.
HIF activation causes synthetic lethality between the <i>VHL</i> tumor suppressor and the <i>EZH1</i> histone methyltransferase.
No sample metadata fields
View SamplesWe performed RNA-Seq analysis of wildtype and three EPAS1-/- 786-O single cell clones generated by CRISPR/Cas9 to identify the HIF-2a-responsive genes in this cell line. Samples from wildtype 786-O cells treated with DMSO or HIF-2a antagonist compound C2 were also included in this analysis. Overall design: In this experiment, we analyzed the transcriptomic profiles of 2 replicates of wildtype (WT) EPAS1+/+ 786-O cells, 1 replicate for each of the three independent EPAS1-/- 786-O single cell clones, 1 replicate of WT-786-O cells treated with DMSO and 1 replicate of WT-786-O cells treated with 10uM HIF-2a antagonist C2.
A GPX4-dependent cancer cell state underlies the clear-cell morphology and confers sensitivity to ferroptosis.
Subject
View SamplesWe used microarrays to analyze the global gene expression and to identify the differentially expressed genes among wild type, prostate-specific Pten knockout, and prostate-specific Pten and Pml double knockout prostates at 12 weeks of age.
An aberrant SREBP-dependent lipogenic program promotes metastatic prostate cancer.
Specimen part
View Samples