The immortalized human urothelial cell line, UROtsa, was transformed in six parallel cultures with continual passaging in1 M Cd+2 until the cells were able to attain the ability to form colonies in soft agar and subcutaneous tumors in nude mice. The gene expression profiles between cadmium-transformed and control samples were compared and the differentially expressed genes were identified.
Variation of keratin 7 expression and other phenotypic characteristics of independent isolates of cadmium transformed human urothelial cells (UROtsa).
Cell line
View SamplesWe have isolated cells from the B16F10 melanoma cell line which express the vascular-selective marker PECAM1
Vascular channels formed by subpopulations of PECAM1+ melanoma cells.
Cell line
View SamplesWe provide direct in vivo evidence for activation of the BCR and canonical NF-KB pathways in MCL that, in the absence of activating mutations, is dependent on the lymph node microenvironment.
Pathogenic role of B-cell receptor signaling and canonical NF-κB activation in mantle cell lymphoma.
Specimen part
View SamplesWe provide direct in vivo evidence for activation of the BCR and canonical NF-KB pathways in MCL that, in the absence of activating mutations, is dependent on the lymph node microenvironment. This finding provides a mechanistic explanation for the surprising efficacy of ibrutinib for the treatment of this type of lymphoma. Mutations in components of the BCR and NF-KB pathways are associated with cell-autonomous signaling and resistance to ibrutinib. Overall design: Lymph node biopsies and peripheral blood samples were obtained from patients with previously untreated MCL.
Pathogenic role of B-cell receptor signaling and canonical NF-κB activation in mantle cell lymphoma.
No sample metadata fields
View SamplesBortezomib-induced resistant MCL cell lines (HBL2 BR and JEKO BR) were generated by continuous cultured of corresponding parental cell lines (HBL2 PT and JEKO PT) with increasing bortezomib concentrations
Bortezomib resistance in mantle cell lymphoma is associated with plasmacytic differentiation.
Specimen part, Cell line
View SamplesCanonical Hedgehog (Hh) signaling regulates the expression of genes that are critical to the patterning and development of a variety of organ systems. In adult, both ligand-dependent and ligand-independent Hh pathway activation are known to promote tumorigenesis. Recent studies have shown that in tumors promoted by Hh ligand, activation occurs within the stromal microenvironment (Yauch et al., 2009). In situ hybridization of the pathway target gene, Ptch1, shows that signaling is located at stromal perivascular fibroblast-like cells in xenograft tumor sections derived from Hh-expressing colorectal cancer cell lines.
Canonical hedgehog signaling augments tumor angiogenesis by induction of VEGF-A in stromal perivascular cells.
Specimen part, Cell line, Treatment
View SamplesMutation or deletion of Neurofibromin (NF1), an inhibitor of RAS signaling, frequently occurs in epithelial ovarian cancer (EOC), supporting therapies that target downstream RAS effectors, such as the RAF-MEK-ERK pathway. However, no comprehensive studies have been carried out testing the efficacy of MEK inhibition in NF1-deficient EOC. Here, we performed a detailed characterization of MEK inhibition in NF1-deficient EOC cell lines using kinome profiling and RNA sequencing. Our studies showed MEK inhibitors were ineffective at providing durable growth inhibition in NF1-deficient cells due to kinome reprogramming. MEKi-mediated destabilization of FOSL1 resulted in induced expression of RTKs and their downstream RAF and PI3K signaling overcoming MEKi therapy. MEKi synthetic enhancement screens identified BRD2 and BRD4 as integral mediators of the MEKi-induced RTK signatures. Inhibition of BET proteins using BET bromodomain inhibitors (BETi) blocked MEKi-induced RTK reprogramming, indicating BRD2 and BRD4 represent promising therapeutic targets in combination with MEKi to block resistance due to kinome reprogramming in NF1-deficient EOC. Overall design: Examination of the global effects on transcription in response to trametinib (GSK212) in A1847 cells.
Intrinsic Resistance to MEK Inhibition through BET Protein-Mediated Kinome Reprogramming in NF1-Deficient Ovarian Cancer.
Specimen part, Cell line, Treatment, Subject
View SamplesGene expression profiles of a single Arabidopsis genotype (Col-0) in response to isogenic Pseudomonas syringae strains expressing one of four different cloned avr genes was studied (avrRpt2, avrRpm1, avrPphB, avrRps4; responses mediated by the R genes RPS2, RPM1, RPS5 and RPS4 ).
Discovery of ADP-ribosylation and other plant defense pathway elements through expression profiling of four different Arabidopsis-Pseudomonas R-avr interactions.
Age, Specimen part, Disease, Disease stage
View SamplesTo investigate the systemic molecular changes occurring as a result of Dhr96 knockdown or over-expression, a comparison between knockdown or overexpression lines and their genetic controls were performed. 0-3 day old adult males or females were reared on 3 separate batches of diet (this was the standard diet we used for culturing Drosophila melanogaster and was made up of 10L water, 100g agar (USP #7060 Bio-serve), 350g Brewers dried yeast (Sunshine Health), 300g black treacle (Lyles), 150g sucrose (Tate & Lyle), 300g Difco dextrose (Becton Dickinson), 150g cornmeal (#1151, Bioserve), 100g wheatgerm (#1659, Bioserve), 200g soya bean flour (#S9633 Sigma Aldrich), 10g methyl-4-hydroxybenzoate (#H3647 Sigma Aldrich) in 10ml ethanol, 50ml proprionic acid (#P5561 Sigma Aldrich)). Each of these 3 batches was considered to represent independent biological replication. The RNA samples were hybridized to the Affymetrix Drosophila GeneChip 2.
Insecticide detoxification indicator strains as tools for enhancing chemical discovery screens.
Sex, Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Insecticide detoxification indicator strains as tools for enhancing chemical discovery screens.
No sample metadata fields
View Samples