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N-Myc overexpression leads to multiple types of acute leukemia in mice [WGS]

ABSTRACT: N-Myc overexpression leads to multiple types of acute leukemia in mice [WGS]

PROVIDER: PRJNA610170 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11234884_1.fastq.gz	Fastqsanger.gz
	SRR11234884_2.fastq.gz	Fastqsanger.gz
	SRR11234885_1.fastq.gz	Fastqsanger.gz
	SRR11234885_2.fastq.gz	Fastqsanger.gz
	SRR11234886_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

N-Myc overexpression leads to multiple types of acute leukemia in mice [WGS]

Project description:The expression of the oncogene MYCN is upregulated in acute leukemia. However, the role of MYCN in leukemogenesis is poorly understood. We established multiple types of leukemia by retroviral overexpression of N-Myc in mice and studied the mechanism of leukemogenesis. Two types of hematopoietic stem cells and three types of hematopoietic progenitor cells highly purified from the bone marrow of adult C57BL/6 mice were transduced with N-Myc and transplanted into lethally irradiated mice. Acute leukemia developed from all these populations. Notably, not only B cell acute lymphoid leukemia, but also T cell acute lymphoid leukemia, acute myeloid leukemia, acute undifferentiated leukemia, and mixed phenotype acute leukemia developed, suggesting the multiple cells of origin, regardless types of leukemia. Moreover, leukemic stem cells were identified in Kit+Sca-1+Lin- bone marrow cells. RNA-seq data revealed the leukemia type-specific transcription profiles. Interestingly, acute undifferentiated leukemia appeared to be transcriptionally close to T cell acute lymphoid leukemia. Whole genome sequencing suggested that different types of leukemia arose associated with a large number of gene mutations induced by N-Myc overexpression but independent of retroviral integration sites. This study provides a new mouse model in which varying types of leukemia develop by only one oncogene.

2023-03-01 | GSE146331 | GEO

N-Myc overexpression leads to multiple types of acute leukemia in mice

Project description:N-Myc overexpression leads to multiple types of acute leukemia in mice

| PRJNA610169 | ENA

N-Myc overexpression leads to multiple types of acute leukemia in mice [RNA-Seq]

Project description:N-Myc overexpression leads to multiple types of acute leukemia in mice [RNA-Seq]

| PRJNA610171 | ENA

N-Myc overexpression leads to multiple types of acute leukemia in mice [RNA-Seq]

2023-03-01 | GSE146330 | GEO

MYC overexpression leads to increased chromatin interactions at superenhancers and MYC binding sites

Project description:The MYC oncogene encodes for the MYC protein and is frequently dysregulated across multiple cancer cell types, making it an attractive target for cancer therapy. MYC overexpression leads to MYC binding at active enhancers, resulting in a global transcriptional amplification of active genes. Since superenhancers are frequently dysregulated in cancer, we hypothesized that MYC preferentially invades into superenhancers and alters the cancer genome organization. To that end, we performed ChIP-seq, RNA-seq, 4C-seq and SIQHiC (Spike-in Quantitative Hi-C) on the U2OS osteosarcoma cell line with tetracycline-inducible MYC. MYC overexpression in U2OS cells modulated histone acetylation and increased MYC binding at superenhancers. SIQHiC analysis revealed increased global chromatin contact frequency, particularly at chromatin interactions connecting MYC binding sites at promoters and enhancers. Immunofluorescence staining showed that MYC molecules formed punctate foci at these transcriptionally active domains after MYC overexpression. These results demonstrate the accumulation of overexpressed MYC at promoter-enhancer hubs and suggest that MYC invades into enhancers through spatial proximity. At the same time, the increased protein-protein interactions may strengthen these chromatin interactions to increase chromatin contact frequency. CTCF siRNA knockdown in MYC overexpressed U2OS cells demonstrated that removal of architectural proteins can disperse MYC and abrogate the increase in chromatin contacts. By elucidating the chromatin landscape of MYC driven cancers, we can potentially target MYC associated chromatin interactions for cancer therapy.

2022-01-17 | GSE164777 | GEO

MYC overexpression leads to increased chromatin interactions at superenhancers and MYC binding sites

Project description:MYC overexpression leads to increased chromatin interactions at superenhancers and MYC binding sites

| PRJNA691927 | ENA

N-Myc overexpression leads to multiple types of acute leukemia in mice

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-03-01 | GSE146333 | GEO

TCGA WGS Variants Across 18 Cancer Types

Project description:TCGA WGS Variants Across 18 Cancer Types

| PRJNA912837 | ENA

TCGA WGS Variants Across 18 Cancer Types

Project description:TCGA WGS Variants Across 18 Cancer Types

| PRJNA912838 | ENA

MYC drives temporal evolution of small cell lung cancer subtypes by reprogramming neuroendocrine fate [WGS data]

Project description:Distinct SCLC molecular subtypes have been defined based on expression of lineage-related transcription factors: ASCL1, NEUROD1, POU2F3 or YAP1, but their origins remain unknown. To study transcriptional dynamics of MYC-driven tumor evolution and compare transcriptional states to human SCLC tumors, we performed bulk and single-cell RNA-sequencing on various timepoints of Rb1/Trp53/MycT58A (RPM) tumor cells (from Ad-Cgrp-Cre infected mice) as they progress in culture, and on RPM bulk tumors. Here, to complement these analyses we performed ~30X whole-genome sequencing (WGS) of early (day 4) and late (day 23) time-point RPM tumor cells from culture, along with a matching normal blood control to confirm complete loss of expected regions of Rb1 and Trp53. WGS analyses revealed no detectable copy number variations (CNVs), and SNV analysis suggests that minimal clonal and subclonal evolution occurs in vitro. Together, these data ultimately reveal that MYC drives the dynamic evolution of SCLC subtypes. We find that MYC promotes a temporal shift from an ASCL1-to-NEUROD1-to-YAP1+ state from a neuroendocrine cell of origin. MYC activates Notch signaling to dedifferentiate tumor cells to non-neuroendocrine fates. These findings support our overall conclusions that genetics, cell of origin, and tumor cell plasticity determine SCLC subtype.

2020-05-28 | GSE149444 | GEO

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