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RUNX1 overexpression in precursor B acute leukemia cells

ABSTRACT: RUNX1 overexpression in precursor B acute leukemia cells

PROVIDER: PRJNA623411 | ENA |

REPOSITORIES: ENA

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			Action	DRS
		Other
	SRR11492141.fastq.gz	Fastqsanger.gz
	SRR11492142.fastq.gz	Fastqsanger.gz
	SRR11492143.fastq.gz	Fastqsanger.gz
	SRR11492144.fastq.gz	Fastqsanger.gz

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RUNX1 overexpression in precursor B acute leukemia cells

Project description:Overexpression of the transcription factor RUNX1 was studied in Nalm-6 precursor B acute lymphoblastic leukemia cells. The active enhancer histone marker H3K27ac and RUNX1 were measured using ChIP-seq. The effect on gene expression was analyzed using single cell RNA-sequencing.

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Lnc-RNA expression pattern in ETV6/RUNX1-driven b-cell precursor acute lymphoblastic leukemia (BCP-ALL)

Project description:Overwhelming evidence indicates that long non-coding RNAs have essential roles in tumorigenesis. Nevertheless, their expression and role in pediatric B-cell precursor acute lymphoblastic leukemia has not been extensively explored. Here, we conducted a comprehensive analysis of the long non-coding RNA transcriptome in ETV6/RUNX1 positive BCP-ALL, one of the most frequent subtypes of pediatric leukemia. An ETV6/RUNX1 expression signature was established, consisting of 596 lncRNAs (434 up and 162 down) using expression analysis of a series of primary patient samples. Subsequently, RNA sequencing from BCP-ALL cell lines and shRNA-mediated silencing of ETV6/RUNX1, illustrated that lnc-NKX2-3-1, lnc-TIMM21-5, lnc-ASTN1-1 and lnc-RTN4R-1 are bona fide ETV6/RUNX1 targets and could serve as novel biomarkers of this prevalent subtype of human leukemia.

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A T-cell receptor targeting RUNX1 frameshift mutations in acute myeloid leukemia

Project description:Runt-related transcription factor 1 (RUNX1) is a key regulator of hematopoietic differentiation. Disruption of RUNX1 in acute myeloid leukemia (AML) induces a maturation arrest and early myeloid progenitor phenotype. RUNX1 mutations occur in 10-15% of AML and are associated with poor prognosis. One-third are frameshift mutations encoding an oncogenic protein with an elongated C-terminus translated in an alternative reading frame. Here, we investigated whether the alternative reading frame of oncogenic RUNX1 can be targeted by immunotherapy. We introduced a construct with a RUNX1 frameshift mutation into EBV-B cells with common HLA class I alleles and identified 13 neopeptides by HLA-immunopeptidomics. To investigate whether these peptides are neoantigens that can be recognized by T cells, peptide-MHC tetramers were used to screen 42 healthy individuals for specific CD8 T cells. T-cell clones were isolated for 6 neopeptides in 5 HLA alleles. Three T-cell clones recognized two HLA-B*07:02 neoantigens on AML cell line SIG-M5 C9, which was edited by CRISPR/Cas9 to express a RUNX1 frameshift mutation. The T-cell receptors (TCRs) of these clones were sequenced, and analyzed after transfer to CD8 T cells. One TCR showed effective killing of SIG-M5 C9 in vitro and in immunodeficient mice. The TCR-engineered T cells also killed patient-derived AML cells with early progenitor phenotypes, including leukemic stem cells. In conclusion, we showed that the alternative reading frame created by RUNX1 frameshift mutations can be effectively targeted, demonstrating the potential relevance of TCR-based immunotherapy to treat and improve the prognosis of patients with RUNX1-mutated AML.

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Project description:Unique long non-coding RNA expression signature in ETV6/RUNX1-driven B-cell precursor acute lymphoblastic leukemia

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RUNX1 colludes with NOTCH1 to reprogram chromatin in T cell acute lymphoblastic leukemia

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Transcriptome Profiling of Leukemia Initiating Cells in Acute Precursor B Lymphoblastic Leukemia

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