Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA150649 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:FOXO1 acts as a tumor suppressor in solid tumors. The oncogenic PI3K pathway suppresses FOXO1 transcriptional activity by enforcing its nuclear exclusion upon AKT-mediated phosphorylation. We show here abundant nuclear expression of FOXO1 in Burkitt lymphoma (BL), a germinal center (GC) B cell derived lymphoma whose pathogenesis is linked to PI3K activation. Recurrent FOXO1 mutations which prevent AKT targeting and lock the transcription factor in the nucleus are used by BL to circumvent mutual exclusivity between PI3K and FOXO1 activation. Using genome editing in human and mouse lymphomas in which MYC and PI3K cooperate synergistically in tumor development we demonstrate pro-proliferative and anti-apoptotic activity of FOXO1 in BL and identify its nuclear localization as an oncogenic event in GC B cell derived lymphomagenesis.
2018-12-21 | GSE119437 | GEO
Project description:Functional cooperativity between Myc and PI3K signaling for indefinite self-renewal property of embryonic stem cells
| PRJNA258069 | ENA
Project description:Gene Expression profiling of Myc-induced lymphomagenesis
| PRJNA147195 | ENA
Project description: Not available
| S-EPMC8784167 | biostudies-literature
Project description:IL-7 r and Stat5 signaling drives early B lymphopoiesis, but it remains poorly understood how Stat5-dependent and independent pathways contribute to this process. We report the discrete effects of PI3K and mTOR signaling on Stat5 signaling and B cell development. PI3K was not engaged by IL-7 in pro-B cells but was actively suppressed by PTEN to ensure proper IL-7 r expression, Stat5 signaling and pro-B cell survival. Further, IL-7-mediated mTORC1 activation, which was uncoupled from PI3K signaling, orchestrated a unique program in early B cell development in a Stat5-independent but Myc-dependent manner. mTORC1 was also required for immunoglobulin heavy chain rearrangement and Myc-driven lymphomagenesis. Finally, mTORC2 was not essential for early B cell development but contributed to peripheral B cell maturation. Altogether, genetic dissection of PI3K, mTORC1, and mTORC2 reveals the distinct effects of these seemingly related pathways on B cell development and the intricate interplay between PI3K, mTOR and IL-7 r-Stat5 signaling.
2018-02-14 | GSE81844 | GEO
Project description:We created mice, which are deficient for Myc specifically in cardiac myocytes by crossing crossed Myc-floxed mice (Mycfl/fl) and MLC-2VCre/+ mice. Serial analysis of earlier stages of gestation revealed that Myc-deficient mice died prematurely at E13.5-14.5. Morphological analyses of E13.5 Myc-null embryos showed normal ventricular size and structure; however, decreased cardiac myocyte proliferation and increased apoptosis was observed. BrdU incorporation rates were also decreased significantly in Myc-null myocardium. Myc-null mice displayed a 3.67-fold increase in apoptotic cardiomyocytes by TUNEL assay. We examined global gene expression using oligonucleotide microarrays. Numerous genes involved in mitochondrial death pathways were dysregulated including Bnip3L and Birc2. Keywords: wildtype vs Myc-null
2007-06-30 | GSE7162 | GEO
Project description:c-myc-3'RR mice developed Burkitt like lymphoma (IgM and IgD positive cells). We wished to study lymphomagenesis in mice carrying a modified B cell receptor with a higher level of tonic signal. The c-myc-3'RR transgene was introduced in a background with an IgH mutation that replaces IgM with IgA expression. Lymphoma arising in double mutant animals mostly carried the phenotype of activated cells, often expressing CD43, and in 10% of cases carrying a plasma cell phenotype. BCR tonic signal appears as a direct modulator of B cell malignancy phenotype. Burkitt lymphoma (BL) from 4 c-myc-3'RR mice, anaplastic (ANA) lymphoma from 4 c-myc-3'RR mice, CD43 negative lymphoma from 4 c-myc-IgA mice and CD43 positive lymphoma from 4 c-myc-IgA mice were investigated.
2012-02-01 | E-GEOD-32229 | biostudies-arrayexpress
Project description:Germinal centers (GCs) are the sites of secondary antibody diversification and underlie the mechanism of action of many vaccination strategies. Activation-induced deaminase (AID) triggers secondary antibody diversification through the introduction of somatic changes in immunoglobulin genes which lead to the generation of antibodies of higher affinity and more specialized effector functions. However, AID can also target other genomic regions, giving rise to mutations and chromosome translocations with oncogenic potential. Many human lymphomas originate from mature B cells that have undergone the GC reaction, such as the diffuse large B cell lymphoma, the follicular lymphoma and Burkitt lymphoma, and carry chromosome translocations. Mature B cell lymphomagenesis has been modeled in the mouse by the genetic introduction of chromosome translocations. Here, we present the first in-depth characterization of one such model, λ-MYC mice. We found that young pre-tumor stage mice had a prominent block in early B cell differentiation that resulted in the generation of very aggressive tumors lacking surface B cell receptor (BCR) expression, indicating that a large fraction of tumors in λ-MYC mice arise from B cell precursors rather than from mature B cells. Further, we assessed the contribution of AID to B cell lymphomagenesis in λ-MYC mice by using a genetic tracer of AID expression. Only a fraction of tumors contained GC-experienced cells defined by AID expression. AID-expressing tumors associated with longer survival and resembled mature Burkitt lymphomas. Thus, AID expression defines Burkitt lymphomagenesis in λ-MYC mice.
2023-09-06 | GSE239433 | GEO
Project description: Not available
| S-EPMC11335981 | biostudies-literature
Project description:Compare Epstein-Barr-positive and Epstein-Barr-negative Burkitt lymphoma cases forboth cellular and viral microRNA expression profile, and to assess the role of viralmicroRNAs in Burkitt lymphomagenesis
2015-11-30 | GSE52916 | GEO