Expression analysis of KHR and KHR-NICD oral tumors
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
SUBMITTER: Michael Spiotto
PROVIDER: E-GEOD-59950 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:KHR and KR tumors grow faster when deficient for Notch1. The hypothesis was to test for differences in gene expression between KHR and KHR oral tumors with intact or deficient Notch1 haplotypes. Total RNA was isolated for KHR (n=5), KHR-N+/- (n=4), KHR-N-/- (n=5), KR-N+/- (n=5), KR-N-/- (n=4) oral tumors. Expression profiling was performed using the Illumina MouseRef-8 v2 (GPL6885) array. Studies were conducted using tumors from C57BL/6 mice.
2015-09-09 | E-GEOD-59951 | biostudies-arrayexpress
Project description:Characterization of gene expression profile of normal human and Kindler Syndrome (KS) patients skin biopsies samples, to extend the knowledge of transcriptional changes in the Kindler syndrome disease. For this micro array three age-, site - and sex-matched biopsies form control and Kindler Syndrome patients were analyzed.
2013-12-01 | E-GEOD-47642 | biostudies-arrayexpress
Project description:We hypothesized that sexual dimorphism in experimental autoimmune enecphalomyelitis arises from sexually dimorphic and CNS-region specific expression of genes that regulate BBB permeability and leukocyte entry. To test this hypothesis, we profiled total RNA from the cerebella and frontal cortices of naïve female versus male SJL mice 100 ng of total RNA was extracted from cerebella and frontal cortices of naïve SJL female and male littermates to identify differential expression of gene transcripts unique to female cerebellum.
2014-04-15 | E-GEOD-55718 | biostudies-arrayexpress
Project description:The SNAI1 and SNAI2 embryonic genes are reactivated in numerous cancer types, including carcinomas. They promote cancer cell dissemination by inducing an epithelial-to-mesenchymal transition (EMT) and by protecting cells from anoikis. We now have demonstrated that the sequentially related SNAI3 gene is aberrantly reactivated in human breast carcinomas. To compare the functional properties of the three SNAIL family members, the transcription factors were ectopically expressed in immortalized mammary epithelial cells. Immortalized human mammary epithelial cells (HMEC-hTERT cells) or MCF10A cells were infected with SNAIL retroviral expression constructs. The gene expression profiles of the resulting cell lines, cultured in standard conditions or after plating them 24h in low-adherent (LA) conditions, were performed.
2013-09-30 | E-GEOD-40690 | biostudies-arrayexpress
Project description:Nemaline myopathy (NM) is a congenital myopathy that can result in lethal muscle dysfunction and is thought to be a disease of the sarcomere thin filament. Recently, several proteins of unknown function have been implicated in NM, and their role in the disease remains unresolved. Here, we demonstrate that loss of a muscle-specific protein, Klhl40, results in a nemaline-like myopathy in mice that closely phenocopies the muscle abnormalities observed KLHL40 deficient patients. We show that Klhl40 dynamically localizes to the sarcomere I-band and A-band and binds to Nebulin (Neb), a protein frequently implicated in NM, as well as a putative thin filament protein, Lmod3. Klhl40 belongs to the BTB-BACK-Kelch (BBK) family of proteins, some of which have been previously shown to promote degradation of their substrates. In contrast, we find that Klhl40 promotes stability of Neb and Lmod3 and blocks Lmod3 ubiquitination. Accordingly, loss of Klhl40 reduces Neb and Lmod3 protein in skeletal muscle of mice and KLHL40 deficient patients. Because loss of sarcomere thin filament proteins is a frequent cause of NM, our data establishes a possible molecular basis for NM in KLHL40 deficient patients by establishing a novel pro-stability function of Klhl40 for Neb and Lmod3. Total RNA was harvested from quadriceps muscle of three Klhl40 WT (control) and three Klhl40 KO mice. Each KO mouse was sacrificed with a corresponding WT littermate. Tissues were also taken at 0 days of age to minimize confounding gene changes occurring due to malnourishment as the phenotype worsens.
2014-04-08 | E-GEOD-56570 | biostudies-arrayexpress
Project description:CD133+ and CD133 negative cells from pancreatic cancer cell line KPC001 were sorted using MACS technique. RNA was isolated using trizol (Invitrogen) and cleaned up using Qiagen RNAeasy columns. The RNA passed QC by the Biomedical Genomic Center (BMGC) of University of Minnesota. cDNA was prepared and hybridized by BMGC according to standard protocol. The goal of the experiment was to see changes in the expression of genes in the CD133+ vs CD133- population in the pancreatic cancer cell line derived from KPC mouse model.
2014-05-01 | E-GEOD-46571 | biostudies-arrayexpress
Project description:Differential gene expression study comparing choriogonadotropin alpha (Cga) gene deficient and wild type adult mouse pituitary. Thyrotrope hyperplasia and hypertrophy are common responses to primary hypothyroidism. To understand the genetic regulation of these processes, we studied gene expression changes in the pituitaries of Cga-/- mice, which are deficient in the common alpha subunit of TSH, LH and FSH. These mice have thyrotrope hypertrophy and hyperplasia and develop thyrotrope adenoma. We report that cell proliferation is increased, but the expression of most stem cell markers is unchanged. The alpha subunit is required for secretion of the glycoprotein hormone beta subunits, and mutants exhibit elevated expression of many genes involved in the unfolded protein response, consistent with dilation and stress of the endoplasmic reticulum. Mutants have elevated expression of transcription factors that are important in thyrotrope function, such as Gata2 and Isl1, and those that stimulate proliferation, including Nupr1, E2f1 and Etv5. We characterized the expression and function of a novel, over-expressed gene, transcription elongation factor A (SII)-like 5 (Tceal5). Stable expression of Tceal5 in a pituitary progenitor cell line is sufficient to increase cell proliferation. Thus, Tceal5 may act as a proto-oncogene. This study provides a rich resource for comparing pituitary transcriptomes and an analysis of gene expression networks. Total RNA was obtained from 8 week old Cga-deficient and littermate wild type mouse pituitary tissue. Total sample number was 24 as follows: 6 male and 6 female wild types, 6 male and 6 female mutants. Each sample was applied to an individual microarray.
2016-08-05 | E-GEOD-79451 | biostudies-arrayexpress
Project description:Pancreatic ductal adenocarcinoma (PDAC) is a lethal malignancy that resists current treatments. To test epigenetic therapy against this cancer we used the DNA demethylating drug 5-aza-2’-deoxycytidine (DAC) in a KrasLSL-G12D; p53LSL-R270H/+; Pdx1-cre; Brca1flex2/flex2 (KPC-Brca1) mouse model of aggressive stroma-rich PDAC. In untreated tumors, we found globally decreased 5-methyl-cytosine (5mC) in malignant epithelial cells and in cancer-associated myofibroblasts (CAFs), and increased amounts of 5-hydroxymethyl-cytosine (5HmC) in CAFs, in progression from pancreatic intraepithelial neoplasia (PanIN) to PDAC. DAC further reduced DNA methylation and slowed PDAC progression, markedly extending survival in an early treatment protocol and significantly though transiently inhibiting tumor growth when initiated later, without adverse side effects. Escaping tumors contained areas of sarcomatoid transformation with disappearance of CAFs. Mixing-allografting experiments and proliferation indices showed that DAC efficacy was due to inhibition of both the malignant epithelial cells and the stromal CAFs. Expression profiling and immunohistochemistry highlighted DAC-induction of STAT1 in the tumors, and DAC plus gamma-interferon produced an additive anti-proliferative effect on PDAC cells. DAC induced strong expression of the testis antigen DAZL in CAFs. These data show that DAC is effective against PDAC in vivo and provide a rationale for future studies combining hypomethylating agents with cytokines and immunotherapy. Treatment of a short-term explant culture of cancer-associated fibroblasts (CAFs) from a KPC-Brca1 mouse pancreatic carcinoma, with 2 micromolar 5-aza-dC (decitabine; DAC) for 48 hours. The experiment includes 3 replicate plates untreated and 3 replicates treated.
2013-01-01 | E-GEOD-42364 | biostudies-arrayexpress
Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series
2013-01-01 | E-GEOD-42366 | biostudies-arrayexpress
Project description:Pancreatic ductal adenocarcinoma (PDAC) is a lethal malignancy that resists current treatments. To test epigenetic therapy against this cancer we used the DNA demethylating drug 5-aza-2’-deoxycytidine (DAC) in a KrasLSL-G12D; p53LSL-R270H/+; Pdx1-cre; Brca1flex2/flex2 (KPC-Brca1) mouse model of aggressive stroma-rich PDAC. In untreated tumors, we found globally decreased 5-methyl-cytosine (5mC) in malignant epithelial cells and in cancer-associated myofibroblasts (CAFs), and increased amounts of 5-hydroxymethyl-cytosine (5HmC) in CAFs, in progression from pancreatic intraepithelial neoplasia (PanIN) to PDAC. DAC further reduced DNA methylation and slowed PDAC progression, markedly extending survival in an early treatment protocol and significantly though transiently inhibiting tumor growth when initiated later, without adverse side effects. Escaping tumors contained areas of sarcomatoid transformation with disappearance of CAFs. Mixing-allografting experiments and proliferation indices showed that DAC efficacy was due to inhibition of both the malignant epithelial cells and the stromal CAFs. Expression profiling and immunohistochemistry highlighted DAC-induction of STAT1 in the tumors, and DAC plus gamma-interferon produced an additive anti-proliferative effect on PDAC cells. DAC induced strong expression of the testis antigen DAZL in CAFs. These data show that DAC is effective against PDAC in vivo and provide a rationale for future studies combining hypomethylating agents with cytokines and immunotherapy. Treatment of a short-term explant culture of malignant epithelial cells from a KPC-Brca1 mouse pancreatic carcinoma, with 0.5 micromolar 5-aza-dC (decitabine; DAC) for 48 hours. The experiment includes 3 replicate plates untreated and 3 replicates treated.
2013-01-01 | E-GEOD-42365 | biostudies-arrayexpress