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Whole-genome transcriptomic analysis of Notch1-expressing cells in mouse intestinal tumours

ABSTRACT: Whole-genome transcriptomic analysis of Notch1-expressing cells in mouse intestinal tumours

PROVIDER: PRJNA437483 | ENA |

REPOSITORIES: ENA

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Whole-genome transcriptomic analysis of Notch1-expressing cells in mouse intestinal tumours

Project description:To define and compare the genome-wide transcriptional signatures of Notch1+ cells in intestinal tumors and in normal ISCs we performed Affymetrix analyses of these two populations.

2019-02-06 | GSE111594 | GEO

Transcriptional Profiling of Mouse Tumours

Project description:Murine small intestinal and colonic tumours with mutations in combinations of Kras, P53, Notch1, Apc and Braf.

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Lineage tracing of Notch1-expressing cells in intestinal tumours reveals a distinct population of cancer stem cells.

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Transcriptional profiling of intestinal changes in Apc Kras tumours with MYC activation and/or drug combination treatment

Project description:Transcriptional profiling of intestinal changes in Apc Kras tumours with MYC activation and/or drug combination treatment

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RNA-seq of irradiated intestinal organoid-derived subcutaneous heterotopic tumours and non-irradiated controls

Project description:In this project, we aimed to examine the transcriptional changes that occur after irradiation of intestinal organoid-derived subcutaneous heterotopic tumors over a 7 day period post-radiation treatment. AKPT (villinCreER;Apcfl/fl;KrasG12D/+;Trp53fl/fl;TgfbrIfl/fl) intestinal organoids were cultured, then suspended in a 50:50 phosphate buffered-saline and Matrigel mixture and subcutaneously implanted into male C57BL/6 mice. Two weeks after implantation, mice were given either a single dose of 15 Gy radiation or 3 doses of 7 Gy radiation. Tumours were harvested 4 hours, 24 hours, 3 days, and 7 days after receiving the single dose of 15 Gy or the final dose of 7 Gy radiation, as well as from corresponding non-irradiated controls. RNA was extracted from the collected tumours and processed for RNA sequencing.

2023-01-25 | E-MTAB-12538 | biostudies-arrayexpress

RNA-seq transcriptomic comparison between PyVmT-driven mammary tumours either expressing or lacking epithelial beta 1 integrin (Itgb1)

Project description:Using inducible oncogene (PyVmT) and conditional knockout transgenic systems, we generated mammary tumours lacking expression of beta 1 integrin specifically in epithelial cells. By RNA-sequencing profiling of the tumours, we identified transcripts and gene fusions that were differential between beta 1 integrin-proficient and -deficient tumours.

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Characterisation of PALB2 tumours through whole-exome and whole-transcriptomic analyses.

Project description: Not available

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Gene expression profile of primary CLL cells transduced with a retrovirus expressing mutated NOTCH1

Project description:In CLL, NOTCH1 is the most commonly mutated gene at diagnosis and it is associated with a poor outcome. The mechanisms underlying how NOTCH1 contributes to disease progression, resistance to treatment and Richter’s transformation remain largely unknown. The main goal of this study is to compare the gene expression profile of primary CLL cells transduced with the intracellular part of NOTCH1 lacking of the PEST domain vs cells transduced with an empty vector. Additionally, patients with the Trisomy 12 abnormality are included in this study to clarify the role of the mutations in this specific sub-group of CLL patients that are strongly associated with NOTCH1 mutations.

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Identification of NOTCH1 bound genes in chronic lymphocytic leukaemia (CLL) cells

Project description:NOTCH1 is mutationally activated in ~15% of cases of chronic lymphocytic leukaemia (CLL), but its role in B-cell development and leukemogenesis is not known. Here, we report that the active intracellular portion of NOTCH1 (ICN1) is detectable in ~50% of peripheral blood CLL cases lacking gene mutations. We identify a ‘NOTCH1 CLL gene expression signature’ in CLL cells, and show that this signature is significantly enriched in primary CLL cases expressing ICN1, independent of NOTCH1 mutation. NOTCH1 target genes include key regulators of B-cell proliferation, survival and signal transduction physiology. In particular, we show that MYC is a direct target of NOTCH1 via B-cell specific distal regulatory elements, thus implicating this oncogene in the pathogenesis of the disease.

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NOTCH1 mediates a reciprocal switch between two distinct secretomes during senescence

Project description:Senescence, a persistent form of cell cycle arrest, is often associated with a diverse secretome, which provides complex downstream functionality for senescent cells within the tissue microenvironment. We show that oncogene-induced senescence (OIS) is accompanied by a dynamic fluctuation of NOTCH1 activity, which drives a TGF-β-rich secretome, whilst suppressing the senescence-associated pro-inflammatory secretome through inhibition of C/EBPβ. NOTCH1 and NOTCH1-driven TGF-β contribute to ‘lateral induction of senescence’ through a juxtacrine NOTCH-JAG1 pathway. In addition, NOTCH1 inhibition during senescence facilitates upregulation of pro-inflammatory cytokines, promoting lymphocyte recruitment and senescence surveillance in vivo. Because enforced activation of NOTCH1 signalling confers a near mutually exclusive secretory profile compared to typical senescence, our data collectively indicate that the dynamic alteration of NOTCH1 activity during senescence dictates a functional balance between these two distinct secretomes: one representing TGF-β and the other pro-inflammatory cytokines, highlighting that NOTCH1 is a temporospatial controller of secretome composition.

2016-08-03 | PXD004168 | Pride

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