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RNA-seq on NUT Carcinoma (NC) cell lines treated with DMSO, Panobinostat or IRBM6

ABSTRACT: HDAC inhibitor induce transcriptional program driving cellular differentiation and growth arrest in NUT Carcinoma (NC) cell lines TC-797 and 10-15.

ORGANISM(S): Homo sapiens

PROVIDER: GSE179693 | GEO | 2021/07/14

REPOSITORIES: GEO

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ChIP-seq analysis of BRD4-NUT and H3K27ac distribution in NUT Carcinoma cell line TC-797 treated with DMSO or Panobinostat

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ChIP-seq analysis of BRD4-NUT and H3K27ac distribution in NUT Carcinoma cell line TC-797 treated with DMSO or Panobinostat

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RNA-seq on NUT Carcinoma (NC) cell lines treated with DMSO, Panobinostat or IRBM6

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H3K9/14Ac in TC-797 genome

Project description:The goal is to localize "active" histone marks known to bind BRD4-NUT in the NMC genome. Characterization of the reference epigenome in humans by use of ChIP-Seq in the TC-797 human NMC cell line. ChIP-seq of untreated TC-797 cells using H3K9/14Ac antibodies versus IgG control.

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Brd4::Nutm1 fusion gene initiates NUT carcinoma in vivo [WGS]

Project description:NUT carcinoma (NC) is an aggressive cancer with no effective treatment. About 70% of NUT carcinoma is associated with chromosome translocation events that lead to the formation of a BRD4::NUTM1 fusion gene. Because the BRD4::NUTM1 gene is unequivocally cytotoxic when ectopically expressed in cell lines, questions remain on whether the fusion gene can initiate NC. Here, we report the first genetically engineered mouse model (GEMM) for NUT carcinoma that recapitulates the t(15;19) chromosome translocation in mice. We demonstrated that the mouse t(2;17) syntenic chromosome translocation, forming the Brd4::Nutm1 fusion gene, could induce aggressive carcinomas in mice. The tumors present histopathological and molecular features similar to human NC, with an enrichment of undifferentiated cells. Similar to the reports of human NC incidence, Brd4::Nutm1 can induce NC from a broad range of tissues with a strong phenotypical variability. The consistent induction of poorly differentiated carcinoma demonstrated a strong reprogramming activity of BRD4::NUTM1. The new mouse model provided a critical preclinical model for NC that will lead to better understanding and therapy development for NC.

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A genetically engineered mouse model (GEMM) of NUT carcinoma (RNA-Seq)

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