Objective: To study if diabetic and insulin-resistant states lead to mitochondrial dysfunction in the liver, or alternatively, if there is adaption of mitochondrial function to these states in the long-term range.
Liver adapts mitochondrial function to insulin resistant and diabetic states in mice.
Sex, Specimen part, Treatment
View SamplesWe performed a single-cell transcriptome analysis of double-negative developing thymocytes from the DN2, DN3 and DN4 populations Overall design: Double-negative developing thymocytes from the DN2, DN3 and DN4 populations were sorted from six WT mice and used for single cell RNA Seq (10x genomics platform)
The transcription factor Duxbl mediates elimination of pre-T cells that fail β-selection.
Sex, Specimen part, Cell line, Subject
View SamplesWe performed a transcriptome comparison of double-negative developing thymocytes from the DN3-4 population, from mice overexpressing the transcription factor Duxbl and wild type mice Overall design: Double-negative developing thymocytes from both WT and Duxbl[ind]xpTa[Cre] mice were gated for CD4-, CD8-, CD3-, B220-, CD25int, CD44low and CD117low expression, which define the DN3-4 stage of thymocyte development. The experiment was performed in four replicates, giving a total of 8 samples.
The transcription factor Duxbl mediates elimination of pre-T cells that fail β-selection.
Sex, Cell line, Subject
View SamplesMice used were B6/129 F2's, 3-5 weeks of age, either wild type or with both copies of the autoimmune regulator gene (aire, GenBank #AF079536) disrupted. Thymi from five of these mice of both sexes were removed and pooled. After collagenase/dispase digestion, density gradient fractionation, and fluorescent antibody staining, cells with the phenotype CD45-, G8.8+, CDR1int and B7.1hi were FACS-sorted and total RNA was made from them. RNA was twice-amplified using a T7 polymerase-based method.
Projection of an immunological self shadow within the thymus by the aire protein.
No sample metadata fields
View SamplesThe Philadelphia chromosome (Ph) encoding the oncogenic BCR-ABL1 kinase defines a subset of ALL with a particularly unfavorable prognosis. Acute lymphoblastic leukemia (ALL) cells are derived from B cell precursors in most cases and typically carry rearranged immunglobulin heavy chain (IGH) variable (V) region genes devoid of somatic mutations. Somatic hypermutation is restricted to mature germinal center B cells and depends on activation-induced cytidine deaminase (AID). Studying AID expression in 108 cases of ALL, we detected AID mRNA in 24 of 28 Ph-positive ALLs as compared to 6 of 80 Ph-negative ALLs. Forced expression of BCR-ABL1 in Ph-negative ALL cells and inhibition of the BCR-ABL1-kinase showed that aberrant expression of AID depends on BCR-ABL1 kinase activity. Consistent with aberrant AID expression in Ph-positive ALL, IGH V region genes and BCL6 were mutated in many Ph-positive but unmutated in most Ph-negative cases. In addition, AID introduced DNA-single-strand breaks within the tumor suppressor gene CDKN2B in Ph-positive ALL cells, which was sensitive to BCR-ABL1 kinase inhibition and silencing of AID expression by RNA interference. These findings identify AID as a BCR-ABL1-induced mutator in Ph-positive ALL cells, which may be relevant with respect to the particularly unfavorable prognosis of this leukemia subset.
Activation-induced cytidine deaminase acts as a mutator in BCR-ABL1-transformed acute lymphoblastic leukemia cells.
No sample metadata fields
View SamplesGene expression patterns of testicular seminoma were analysed applying oligonucleotide microarrays in 40 specimens of different tumour stages (pT1, pT2, pT3) and in 3 normal testes.
Gene signatures of testicular seminoma with emphasis on expression of ets variant gene 4.
No sample metadata fields
View SamplesLoss of p120ctn results in dysplasia and invasive cancer in the mouse esophagus and squamous forestomach.
Deletion of p120-catenin results in a tumor microenvironment with inflammation and cancer that establishes it as a tumor suppressor gene.
Specimen part
View SamplesAffymetrix gene expression AID-GFP-positive vs AID-GFP-negative
The B cell mutator AID promotes B lymphoid blast crisis and drug resistance in chronic myeloid leukemia.
No sample metadata fields
View SamplesPrecursor B-lineage acute lymphoblastic leukemia (pre-B ALL) can be subdivided into different categories based on genetic abnormalities.
Pre-B cell receptor-mediated cell cycle arrest in Philadelphia chromosome-positive acute lymphoblastic leukemia requires IKAROS function.
Specimen part
View SamplesMutations in the enzymes IDH1 and IDH2 have been identified in a wide variety of tumors like glioma, chondrosarcoma, thyroid cancer, lymphoma, melanoma, and in acute myeloid leukemia. Mutated IDH1/2 produces the metabolite 2-hydroxyglutarate (2HG), which interferes with epigenetic regulation of gene expression, and thus may promote tumorigenesis.
Pan-mutant-IDH1 inhibitor BAY1436032 is highly effective against human IDH1 mutant acute myeloid leukemia in vivo.
Specimen part, Treatment
View Samples