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Identifying STRN3-RARA as a new fusion gene for acute promyelocytic leukemia [RNA-seq]

ABSTRACT: Identifying STRN3-RARA as a new fusion gene for acute promyelocytic leukemia [RNA-seq]

PROVIDER: PRJNA934520 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23372054_1.fastq.gz	Fastqsanger.gz
	SRR23372054_2.fastq.gz	Fastqsanger.gz
	SRR23372055_1.fastq.gz	Fastqsanger.gz
	SRR23372055_2.fastq.gz	Fastqsanger.gz
	SRR23372056_1.fastq.gz	Fastqsanger.gz

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Identifying STRN3-RARA as a new fusion gene for acute promyelocytic leukemia

Project description:Here we report a new fusion gene, STRN3-RARA, in acute promyelocytic leukemia (APL). It cooperates with UTX deficiency to drive full-blown APL in mice. Although STRN3-RARA leukemia quickly relapses after all-trans retinoic acid treatment, it can be restrained by cepharanthine.

2024-04-23 | GSE224816 | GEO

Identifying of a novel RUNX1-RARA fusion in variant acute promyelocytic leukemia

Project description:Here we report a novel fusion gene, RUNX1-RARA, in acute promyelocytic leukemia (APL). RUNX1-RARA triggers APL genesis by mediating transcriptional repression of target genes, and it can be potently restrained by all-trans retinoic acid treatment.

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Identifying STRN3-RARA as a new fusion gene for acute promyelocytic leukemia

Project description:Identifying STRN3-RARA as a new fusion gene for acute promyelocytic leukemia

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Identifying STRN3-RARA as a new fusion gene for acute promyelocytic leukemia [RNA-seq]

Project description:Acute promyelocytic leukemia (APL) is a distinct subtype of acute myeloid leukemia, that is generally driven by PML-RARA, resulting from a balanced chromosomal translocation t(15;17) (q24.1;q21.2). However, approximately 2% of APL patients carry other variants of RARA-fusions, which pose challenges for diagnosis and treatment. Here, we report a novel t(14;17) translocation in an APL patient that gave rise to a new fusion gene, STRN3-RARA. STRN3 forms a complex called the striatin-interacting phosphatase and kinase (STRIPAK), which couples kinases to protein phosphatase 2A and regulates their activities. Like other APL patients with RARA-variants, this patient quickly relapsed after the initial response to all-trans retinoic acid (ATRA) treatment. Mechanistically, we demonstrated that STRN3-RARA, in cooperating with UTX deficiency, which was mutated in the patient, drove APL formation in mice. Additionally, we found that STRN3-RARA cells were specifically susceptible to the TNFα pathway. Inhibition of this pathway by cepharanthine, an FDA-approved drug, effectively suppressed the growth of U937 cells with STRN3-RARA expression, as well as relapsed APL cells from the patient. Taken together, our study identified a new APL fusion gene, STRN3-RARA, and validated it as a functional APL driver, providing insight into the diagnosis and treatment of non-classic APL patients.

2024-04-23 | GSE224815 | GEO

Identifying STRN3-RARA as a new fusion gene for acute promyelocytic leukemia [CUT&TAG]

2024-04-23 | GSE224813 | GEO

Identifying STRN3-RARA as a new fusion gene for acute promyelocytic leukemia [RNA-seq 2]

2024-04-23 | GSE239350 | GEO

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Project description:Identifying of a novel RUNX1-RARA fusion in variant acute promyelocytic leukemia

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Identifying STRN3-RARA as a new fusion gene for acute promyelocytic leukemia [CUT&TAG]

Project description:Identifying STRN3-RARA as a new fusion gene for acute promyelocytic leukemia [CUT&TAG]

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Project description:Identifying STRN3-RARA as a new fusion gene for acute promyelocytic leukemia [RNA-seq 2]

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Torque Teno Mini Virus as a cause of childhood acute promyelocytic leukemia lacking PML/RARA fusion

Project description:We describe a case of a child affected by a relapsed PML/RARA-negative acute promyelocytic leukemia (APL) rescued by a combination of all-trans retinoic acid (ATRA) and arsenic trioxide (ATO) and subsequent HSCT. We provide evidence of the presence of a chimeric viral transcript generated through genomic integration of a Torque Teno Mini Virus sequence into RARA intron 2, the recurrent breakpoint of all chimeric RARA fusions found in APL. This generates an in-frame TTMV/RARA chimeric fusion that is highly expressed at disease diagnosis and relapse and fully cleared at remission achievement.

2021-12-01 | GSE169521 | GEO

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