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Expression in mouse oviduct and Dicer1 tumors

ABSTRACT: Expression in mouse oviduct and Dicer1 tumors

PROVIDER: PRJNA976192 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24735479.fastq.gz	Fastqsanger.gz
	SRR24735380_1.fastq.gz	Fastqsanger.gz
	SRR24735380_2.fastq.gz	Fastqsanger.gz
	SRR24735480.fastq.gz	Fastqsanger.gz
	SRR24735381_1.fastq.gz	Fastqsanger.gz

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mRNA expression in mouse oviduct and Dicer1 tumors

Project description:mRNA expression in mouse oviduct and Dicer1 tumors

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microRNA expression in mouse oviduct and Dicer1 tumors

Project description:microRNA expression in mouse oviduct and Dicer1 tumors

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microRNA expression in mouse oviduct and Dicer1 tumors

Project description:We developed a genetically engineered conditional compound heterozygous Dicer1 mouse strain that fully recapitulates the bi-allelic mutations of DICER1 in DICER1 syndrome-associated cancers. Embryonic activation of bi-allelic Dicer1 mutations, driven by the anti-Müllerian hormone receptor 2 (Amhr2)-driven Cre strain (Amhr2+/cre), drove cancer development from oviduct. Small RNA sequencing was performed to compare the microRNA expression profiles between tumor and normal oviduct.

2023-07-18 | GSE233398 | GEO

mRNA expression in mouse oviduct and Dicer1 tumors

Project description:We developed a genetically engineered conditional compound heterozygous Dicer1 mouse strain that fully recapitulates the bi-allelic mutations of DICER1 in DICER1 syndrome-associated cancers. Embryonic activation of bi-allelic Dicer1 mutations, driven by the anti-Müllerian hormone receptor 2 (Amhr2)-driven Cre strain (Amhr2+/cre), drove cancer development from oviduct. mRNA sequencing was performed to compare the mRNA expression profiles between tumor and normal oviduct.

2023-07-18 | GSE233397 | GEO

Liver-specific DICER1 syndrome model mice develop cystic liver tumors with defective primary cilia

Project description:DICER1 syndrome is a tumor predisposition syndrome caused by familial genetic mutations in DICER1. Pathogenic variants of DICER1 have been discovered in many rare cancers, including cystic liver tumors. However, the molecular mechanisms underlying liver lesions induced by these variants remain unclear. In the present study, we sought to gain a better understanding of the pathogenesis of these variants by generating a mouse model of liver-specific DICER1 syndrome. The mouse model developed bile duct hyperplasia with fibrosis, similar to congenital hepatic fibrosis, as well as cystic liver tumors resembling those in Caroli's syndrome, intrahepatic cholangiocarcinoma, and hepatocellular carcinoma. Interestingly, the mouse model of DICER1 syndrome showed abnormal formation of primary cilia in the bile duct epithelium, which is a known cause of bile duct hyperplasia and cyst formation. These results indicated that DICER1 mutations contribute to cystic liver tumors by inducing defective primary cilia. The mouse model generated in this study will be useful for elucidating the potential mechanisms of tumorigenesis induced by DICER1 variants and for obtaining a comprehensive understanding of DICER1 syndrome.

2024-05-02 | GSE231487 | GEO

Somatic mutations in DROSHA and DICER1 impair microRNA biogenesis in Wilms tumors

Project description:Through whole-exome sequencing we identified somatic missense mutations in DICER1 and DROSHA in Wilms tumor, a childhood kidney cancer. DICER1 and DROSHA are key enzymes in the microRNA biogenesis pathway. To determine the effect of these mutations on microRNA expression, we prepared small RNAs from Wilms tumors and used next-generation sequencing to determine the expression levels of microRNAs in the tumors. Comparison of miRNA expression in tumors with and without mutations in DICER1 or DROSHA.

2015-04-21 | E-GEOD-56955 | biostudies-arrayexpress

Expression in mouse oviduct and Dicer1 tumors

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

2023-07-18 | GSE233399 | GEO

Somatic mutations in DROSHA and DICER1 impair microRNA biogenesis in Wilms tumors

2015-04-21 | GSE56955 | GEO

ETMR-like infantile cerebellar embryonal tumors in the extended morphologic spectrum of DICER1-related tumors

Project description:Description of two cases of ETMR-like cerebellar tumors with DICER1 mutations

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Drosha loss drives pineoblastoma by upregulating Ccnd2 [RNA-seq of Dicer1 tumors]

Project description:Mutations in the microRNA processing genes DICER1 and DROSHA drive childhood cancers such as pineoblastoma, a brain tumor that resembles undifferentiated precursors of the pineal gland. To understand how microRNAs regulate proliferation of these progenitors, we developed a mouse model of pineoblastoma by ablating Drosha or Dicer1 in the developing pineal gland. The tumors that arise in these models resemble proliferative, undifferentiated embryonic progenitors. They are marked by loss of microRNAs, including the let-7 family, and de-repression of let-7 target genes. One upregulated let-7 target gene is the oncofetal transcription factor Plagl2, which activates expression of key pro-growth genes Igf2 and Ccnd2, and we show that small molecules targeting these two drivers block tumor growth. Thus, our results demonstrate that tumors driven by loss of microRNA processing may be therapeutically targeted by inhibiting downstream drivers of proliferation.

2024-10-03 | GSE278579 | GEO

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