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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.

Project description:Colon tumours are hierarchically organized and contain multipotent self-renewing cells, called Cancer Stem Cells (CSCs). We have previously shown that the Notch1 receptor is expressed in Intestinal Stem Cells (ISCs); given the critical role played by Notch signalling in promoting intestinal tumourigenesis, we explored Notch1 expression in tumours. Combining lineage tracing in two tumour models with transcriptomic analyses, we found that Notch1+ tumour cells are undifferentiated, proliferative and capable of indefinite self-renewal and of generating a heterogeneous clonal progeny. Molecularly, the transcriptional signature of Notch1+ tumour cells highly correlates with ISCs, suggestive of their origin from normal crypt cells. Surprisingly, Notch1+ expression labels a subset of CSCs that shows reduced levels of Lgr5, a reported CSCs marker. The existence of distinct stem cell populations within intestinal tumours highlights the necessity of better understanding their hierarchy and behaviour, to identify the correct cellular targets for therapy.

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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:Rare protein-truncating variants (PTVs) in PALB2 confer increased risk to breast cancer, but relatively few studies have reported the characteristics of tumours with PALB2 PTVs. In this study, we describe molecular characteristics of tumours with either germline or somatic alterations in PALB2. DNA from fresh frozen tumour tissues and matched peripheral blood lymphocytes for 560 breast cancer patients was subjected for whole-exome sequencing (WES), and RNA from tumour tissues was subjected to RNA sequencing (RNA-seq). We found six cases with germline and three with somatic protein-truncating variants in PALB2. The characteristics of tumours in patients with PALB2 PTVs were similar to those with BRCA1 and BRCA2 PTVs, having significantly more somatic alterations, and a high proportion of the mutational signature and genomic scar scores characteristic of deficiencies in homologous recombination (HR), compared to tumours arising in non-carriers. Unlike tumours arising in patients with BRCA1 and BRCA2 PTVs, PALB2 tumours did not have high prevalence of TP53 somatic alterations or an enriched immune microenvironment. In summary, PALB2 tumours show the homologous recombination deficiencies characteristic of BRCA1 and BRCA2 tumours, and highlight the potential clinical relevance of PALB2 mutational status in guiding therapeutic choices.

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

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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.

2017-03-24 | GSE92701 | GEO

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