Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Heritable states influence stem cell fates upon acquisition of cancer mutations

ABSTRACT: Heritable states influence stem cell fates upon acquisition of cancer mutations

PROVIDER: PRJNA1106425 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR28845400_1.fastq.gz	Fastqsanger.gz
	SRR28845400_2.fastq.gz	Fastqsanger.gz
	SRR28845401_1.fastq.gz	Fastqsanger.gz
	SRR28845401_2.fastq.gz	Fastqsanger.gz
	SRR28845402_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 44

Similar Datasets

Heritable states influence stem cell fates upon acquisition of cancer mutations [Third]

Project description:Heritable states influence stem cell fates upon acquisition of cancer mutations [Third]

| PRJNA1190366 | ENA

Heritable states influence stem cell fates upon acquisition of cancer mutations [Second]

Project description:Heritable states influence stem cell fates upon acquisition of cancer mutations [Second]

| PRJNA1190370 | ENA

Heritable states influence stem cell fates upon acquisition of cancer mutations

Project description:Tumors with the same driver mutations can display a striking variation in their progression and treatment response, but the origins of this variation are still unclear. In this study, we use state-fate analysis to unveil that heritable stem cell states can influence how individual cells respond to the acquisition of the same cancer mutation. We develop a new methodological pipeline, single-cell Tracking of Recombinase Activation And Clonal Kinetics, and apply it to hematopoietic stem cells carrying Cre/Flp-conditional leukemia alleles. Tracking the gene expression changes and expansion kinetics of a common set of stem cell clones, with and without the same myeloid leukemia mutations, we unveil a striking heterogeneity in the malignant fates of diverse stem cells. First, we define that heritable clonal states persist in expansion cultures and cause the selection of a small group of clones with a specific fitness signature. Then, using mouse models of the most frequent initiating mutations, we define that these pre-existent stem cell states influence the mutation-induced changes in expansion, fate, and malignant gene expression programs. Initiating driver mutations increase the survival probability of clones with low fitness through enhancing their stemness programs. Surprisingly, the fate of high-fitness stem-cell clones is sometimes reversed, producing more mature leukemias, yet still carrying markers of their cell of origin. We further validate these HSC-of-origin signatures in bulk and single-cell RNAseq datasets from cancer patients. Our findings suggest that aggressive premalignant clonal expansions arise from low-fitness stem cells more frequently than previously expected.

2024-09-17 | GSE266232 | GEO

Heritable states influence stem cell fates upon acquisition of cancer mutations [Third]

2025-04-30 | GSE282756 | GEO

Heritable states influence stem cell fates upon acquisition of cancer mutations [Second]

2025-04-30 | GSE282755 | GEO

Tissue-specific non-heritable influence drive uterine immune system variation

Project description:Tissue-specific non-heritable influence drive uterine immune system variation

| PRJNA933605 | ENA

Tissue-specific non-heritable influence drive uterine immune system variation (RNA-seq)

Project description:Tissue-specific non-heritable influence drive uterine immune system variation (RNA-seq)

| PRJNA934581 | ENA

Tissue-specific non-heritable influence drive uterine immune system variation (ATAC-seq)

Project description:Tissue-specific non-heritable influence drive uterine immune system variation (ATAC-seq)

| PRJNA934582 | ENA

Tissue-specific non-heritable influence drive uterine immune system variation (RNA-seq)

Project description:Human twin studies have revealed the combined contribution of heritable and non-heritable (environmental) factors in shaping peripheral blood immune system variability. However, the heterogeneity within tissue immune compartments and the contribution of tissue-specific external factors remain unexplored. The human uterus is a tissue under constant regeneration exposed to distinct environmental factors. To assess uterine immune system variation, we have performed a transcriptomic and epigenetic analysis of uterine and peripheral blood immune cells in monozygotic twins and longitudinal samples in relation to heritable versus non-heritable factors.

2024-04-12 | GSE225041 | GEO

Tissue-specific non-heritable influence drive uterine immune system variation (ATAC-seq)

2024-04-12 | GSE225040 | GEO