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ABSTRACT: Raw sequences for MHC typing of Tasmanian devils

PROVIDER: PRJNA1101685 | ENA |

REPOSITORIES: ENA

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Dataset's files

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			Action	DRS
	SRR28728400_subreads.fastq.gz	Fastqsanger.gz
	SRR28728500_subreads.fastq.gz	Fastqsanger.gz
	SRR28728401_subreads.fastq.gz	Fastqsanger.gz
	SRR28728501_subreads.fastq.gz	Fastqsanger.gz
	SRR28728402_subreads.fastq.gz	Fastqsanger.gz

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Project description:Tasmanian devil MHC typing

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The Tasmanian devil transcriptome reveals Schwann cell origins of a clonally transmissible cancer (small RNA sequencing)

Project description:The Tasmanian devil, a marsupial carnivore, is endangered due to the emergence of a clonally transmissible cancer known as Devil Facial Tumor Disease (DFTD). This fatal cancer is clonally derived and is an allograft transmitted between devils by biting. We performed a large-scale genetic analysis of DFTD with microsatellite genotyping, mitochondrial genome analysis, as well as deep sequencing of the DFTD transcriptome and miRNAs. These studies confirm that DFTD is a monophyletic clonally transmissible tumor, and suggest that the disease is of Schwann cell origin. On the basis of these results we have generated a diagnostic marker for DFTD, and identify a suite of genes of relevance to DFTD pathology and transmission. We provide a genomic dataset for the Tasmanian devil, which is applicable to cancer diagnosis, disease evolution and conservation biology. This submission contains only small RNA sequence data from this study. Small RNA (18 - 24 nt) sequences from 15 Tasmanian devil (Sarcophilus harrisii) tissue samples

2010-01-01 | E-GEOD-18352 | biostudies-arrayexpress

Biomarker discovery for Tasmanian Devil Facial Tumour Disease using serum-derived extracellular vesicles

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The ERBB-STAT3 Axis Drives Tasmanian Devil Facial Tumor Disease

Project description:The marsupial Tasmanian devil (Sarcophilus harrisii) faces extinction due to transmissible devil facial tumor disease (DFTD). To unveil the culprit molecular underpinnings, we designed an approach that combines sensitivity to drugs with an integrated systems-biology characterization. Sensitivity to inhibitors of the ERBB family of receptor tyrosine kinases correlated with their overexpression, suggesting a causative link. Proteomic and DNA methylation analyses revealed tumor-specific signatures linked to oncogenic signaling hubs including evolutionary conserved STAT3. Indeed, inhibition of ERBB blocked phosphorylation of STAT3 and arrested cancer cells. Blockade of ERBB signaling prevented tumor growth in a xenograft model and resulted in recovery of MHC-I gene expression. This link between the hyperactive ERBB-STAT3 axis and decreased MHC-I mediated tumor immunosurveillance provides mechanistic insights into horizontal transmissibility and lets us propose a dual chemo-immunotherapeutic strategy to save Tasmanian devils from DFTD.

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Project description:DArTseq raw sequence reads for Tasmanian devils

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The Tasmanian devil transcriptome reveals Schwann cell origins of a clonally transmissible cancer (small RNA sequencing)

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Project description:Whole genome resequencing of 25 Tasmanian devils.

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Project description:Characterising the pouch microbiome of Tasmanian devils

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An evolutionarily conserved function of polycomb silences the MHC class I antigen presentation pathway and enables immune evasion in cancer [ChIP-Seq]

Project description:Loss of MHC class I (MHC-I) antigen presentation in cancer cells can lead to immunotherapy resistance. Using a genome-wide CRISPR/Cas9 screen we identify a critical role for polycomb repressive complex 2 (PRC2) in the coordinated transcriptional silencing of the MHC-I antigen processing pathway (MHC-I APP). This evolutionarily conserved function of PRC2 promotes evasion of T-cell mediated immunity, enabling tumor transmission to non-histocompatible recipients in small cell lung cancer (SCLC) and Tasmanian Devil Facial Tumor. MHC-I APP gene promoters in MHC-I low cancers harbour bivalent activating H3K4me3 and repressive H3K27me3 histone modifications, silencing basal MHC-I expression and restricting cytokine induced MHC-I APP gene upregulation. Bivalent chromatin at MHC-I APP genes is a normal developmental process active in embryonic stem cells and maintained during neural progenitor differentiation. This physiological silencing of MHC-I expression highlights a conserved mechanism by which cancers arising from these primitive tissues coopt PRC2 activity to enable immune evasion.

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Project description:Tasmanian devils are threatened with extinction because of two genetically independent transmissible cancers which are termed as Devil Facial Tumour Disease one and two (DFTD-1 and DFTD-2). The cancers are indistinguishable by gross examination and require laboratory procedures such as immunohistochemistry and/or PCR for diagnosis. Here we used proteomics to analyse extracellular vesicles from DFTD cells to better understand the potentail role of EV's in DFTD cancer metastasis.

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