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UBTF tandem duplication AMLs are sensitive to menin inhibition

ABSTRACT: UBTF tandem duplication AMLs are sensitive to menin inhibition

PROVIDER: PRJNA978037 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24781059_1.fastq.gz	Fastqsanger.gz
	SRR24781059_2.fastq.gz	Fastqsanger.gz
	SRR24781060_1.fastq.gz	Fastqsanger.gz
	SRR24781060_2.fastq.gz	Fastqsanger.gz
	SRR24781061_1.fastq.gz	Fastqsanger.gz

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UBTF tandem duplication AMLs are sensitive to menin inhibition

Project description:To investigate the effect of Menin inhibitor on UBTF-TD harboring AML. We characterized UBTF-TD interaction with KMT2A and Menin in different leukemia models including KMT2A-r, transduced and normal cbCD34+ cells as well as in primary AML cells with UBTF-TD mutation. We also analized gene expression pattern upon treatment with Menin inhibitor.

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UBTF tandem duplication acute myeloid leukemias are sensitive to menin inhibition [Cut&Run]

Project description:UBTF tandem duplications (TD) have recently emerged as a subtype-defining alteration in pediatric acute myeloid leukemia (pAML), which is characterized by HOXB gene dysregulation and a poor response to conventional chemotherapy. Here, we use protein-protein interaction studies to show that UBTF-TD maintains interactions with components of the RNA pol I complex, while also engaging with a network of unique protein interactors specific to UBTF-TD, like KMT2A. These data suggest that UBTF- TD both preserves canonical UBTF functions and demonstrates gain of function activities. Furthermore, we show that UBTF-TD and KMT2A co-localize to key genomic targets dysregulated in UBTF-TD myeloid malignancies, like HOXB gene clusters and MEIS1. Using a protein degradation system, we show that stemness, proliferation, and the HOXB molecular signature are dependent on sustained UBTF-TD localization to chromatin. Finally, we show UBTF-TD leukemias are sensitive to menin inhibition—providing a viable therapeutic strategy for children with this high-risk AML subtype.

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UBTF tandem duplication acute myeloid leukemias are sensitive to menin inhibition [RNA-seq]

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UBTF tandem duplication acute myeloid leukemias are sensitive to menin inhibition

Project description:UBTF tandem duplication acute myeloid leukemias are sensitive to menin inhibition

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UBTF tandem duplication acute myeloid leukemias are sensitive to menin inhibition [RNA-seq]

Project description:UBTF tandem duplication acute myeloid leukemias are sensitive to menin inhibition [RNA-seq]

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UBTF tandem duplication acute myeloid leukemias are sensitive to menin inhibition [Cut&Run]

Project description:UBTF tandem duplication acute myeloid leukemias are sensitive to menin inhibition [Cut&Run]

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UBTF tandem duplication defines High-risk Pediatric Acute Myeloid Leukemia

Project description:Genomic profiling of relapsed pediatric AML demonstrated an increase in KMT2A and NUP98 rearrangements when compared to de novo pediatric AML, as well as an increase in WT1 mutations. Notably, we identified recurrent (9% of relapse cohort) exon 13 duplications in UBTF in pediatric AML cases that previously lacked known driver alterations. These UBTF-tandem duplication (TD) pediatric AMLs occur in approximately 4% of all pediatric AMLs and are less common in adult AMLs, are associated with normal karyotype or trisomy 8 cytogenetic abnormalities, co-occur with WT1 and FLT3-ITD, have an expression profile similar to NUP98-NSD1 and NPM1 mutant AMLs and are independently associated with poor outcome.

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Expression data from cord blood CD34+ cells transduced with UBTF wildtype expression vectors, UBTF-TD expression vectors, or empty control vector.

Project description:UBTF tandem duplications (UBTF-TD) were identified frequently in relapsed pediatric acute myeloid leukemia. The purpose of this study is to investigate the functional consequence of the overexpression of UBTF-TD in normal cord blood CD34+ cells.

2022-02-22 | GSE189901 | GEO

UBTF tandem duplication acute myeloid leukemias are sensitive to menin inhibition

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

2024-02-12 | GSE229666 | GEO

GATA2 deficiency phenotype associated with tandem duplication of the GATA2 locus linked to a common structural variant

Project description:Typical features of GATA2 deficiency were observed in a individual with wild-type GATA2 sequence. The patient had a de novo tandem duplication of 187Kb spanning GATA2 and RPN1 containing a deletion of 25Kb 5’ of RPN1, inherited from the mother. The deletion is a copy number variant present in about 4% of Europeans (GRCh37: esv2725896 and nsv513733; GRCh38: esv3597711) and removes an alternative 5’ start site of RPN1 at 128,400Kb, associated with CTCF and H3K27ac binding peaks. A second copy of GATA2 is translocated to this region by the tandem duplication. RNA-Seq was underatken in order to identify any gene fussion events resulting from the mutation and to inverstigate differences in gene expression between the patient and controls.

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