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Kmt2c-mutations superimpose properties of activated and quiescent HSCs to convey a selective advantage after chemotherapy [ChIP-seq]

ABSTRACT: Kmt2c-mutations superimpose properties of activated and quiescent HSCs to convey a selective advantage after chemotherapy [ChIP-seq]

PROVIDER: PRJNA664185 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12662027_1.fastq.gz	Fastqsanger.gz
	SRR12662027_2.fastq.gz	Fastqsanger.gz
	SRR12662028_1.fastq.gz	Fastqsanger.gz
	SRR12662028_2.fastq.gz	Fastqsanger.gz
	SRR12662029.fastq.gz	Fastqsanger.gz

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Kmt2c-mutations superimpose properties of activated and quiescent HSCs to convey a selective advantage after chemotherapy

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Project description:Kmt2c-mutations superimpose properties of activated and quiescent HSCs to convey a selective advantage after chemotherapy [ATAC-seq]

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Kmt2c-mutations superimpose properties of activated and quiescent HSCs to convey a selective advantage after chemotherapy [RNA-seq]

Project description:Rna-seq analysis of wild type and Kmt2c mutant hematopoietic progenitors

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Kmt2c-mutations superimpose properties of activated and quiescent HSCs to convey a selective advantage after chemotherapy [ChIP-seq]

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Kmt2c-mutations superimpose properties of activated and quiescent HSCs to convey a selective advantage after chemotherapy

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

2021-02-18 | GSE158162 | GEO

Kmt2c mutations enhance HSC self-renewal capacity and convey a selective advantage after chemotherapy.

Project description:The myeloid tumor suppressor KMT2C is recurrently deleted in myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML), particularly therapy-related MDS/AML (t-MDS/t-AML), as part of larger chromosome 7 deletions. Here, we show that KMT2C deletions convey a selective advantage to hematopoietic stem cells (HSCs) after chemotherapy treatment that may precipitate t-MDS/t-AML. Kmt2c deletions markedly enhance murine HSC self-renewal capacity without altering proliferation rates. Haploid Kmt2c deletions convey a selective advantage only when HSCs are driven into cycle by a strong proliferative stimulus, such as chemotherapy. Cycling Kmt2c-deficient HSCs fail to differentiate appropriately, particularly in response to interleukin-1. Kmt2c deletions mitigate histone methylation/acetylation changes that accrue as HSCs cycle after chemotherapy, and they impair enhancer recruitment during HSC differentiation. These findings help explain why Kmt2c deletions are more common in t-MDS/t-AML than in de novo AML or clonal hematopoiesis: they selectively protect cycling HSCs from differentiation without inducing HSC proliferation themselves.

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KMT2C methyltransferase domain regulated INK4A expression suppresses prostate cancer metastasis

Project description:Frequent truncating mutations of the histone lysine N‑methyltransferase KMT2C have been detected by whole exome sequencing studies in various cancers, including malignancies of the prostate. However, the biological consequences of these alterations in prostate cancer have not yet been elucidated. To investigate the functional impact of these mutations we deleted the C-terminal catalytic core motif of KMT2C specifically in the prostate epithelium of mice. We show here that impaired KMT2C methyltransferase activity drives proliferation and, when combined with loss of the tumour suppressor PTEN, triggers metastatic dissemination and reduces life expectancy. In our model system and human prostate cancer samples we show that KMT2C-mutated tumours activate the proliferative MYC signalling axis and fail to express the oncogene-induced cell cycle repressor p16INK4A. In addition, we observe a striking reduction in disease-free survival of patients with KMT2C-mutated prostate cancer. Thus, we identify truncated KMT2C as a driver of aggressive prostate cancer.

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Epigenetic and transcriptional alterations with Kmt2c and Kmt2d knockout

Project description:KMT2C and KMT2D are two of the most frequently mutated genes in bladder cancer and in histologically normal urothelium. In this study, we developed mouse models to investigate the molecular mechanism of Kmt2c/d loss in urothelial tumorigenesis.

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