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Novel cancer gene discovery using a forward genetic screen in RCAS-PDGFB driven gliomas

ABSTRACT: Novel cancer gene discovery using a forward genetic screen in RCAS-PDGFB driven gliomas

PROVIDER: PRJNA854593 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19908000.fastq.gz	Fastqsanger.gz
	SRR19908001.fastq.gz	Fastqsanger.gz
	SRR19908002.fastq.gz	Fastqsanger.gz
	SRR19908003.fastq.gz	Fastqsanger.gz
	SRR19908004.fastq.gz	Fastqsanger.gz

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Novel cancer gene discovery using a forward genetic screen in RCAS-PDGFB driven gliomas

Project description:Here we describe the use of a high-throughput pipeline coupled to the commonly used tissue-specific retroviral RCAS-TVA mouse tumor model system. Utilizing next generation sequencing, we show that retroviral integration sites can be reproducibly detected in malignant stem cell lines generated from RCAS-PDGFB-driven glioma biopsies.

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Novel cancer gene discovery using a forward genetic screen in RCAS-PDGFB-driven gliomas.

Project description:BackgroundMalignant gliomas, the most common malignant brain tumors in adults, represent a heterogeneous group of diseases with poor prognosis. Retroviruses can cause permanent genetic alterations that modify genes close to the viral integration site.MethodsHere we describe the use of a high-throughput pipeline coupled to the commonly used tissue-specific retroviral RCAS-TVA mouse tumor model system. Utilizing next-generation sequencing, we show that retroviral integration sites can be reproducibly detected in malignant stem cell lines generated from RCAS-PDGFB-driven glioma biopsies.ResultsA large fraction of common integration sites contained genes that have been dysregulated or misexpressed in glioma. Others overlapped with loci identified in previous glioma-related forward genetic screens, but several novel putative cancer-causing genes were also found. Integrating retroviral tagging and clinical data, Ppfibp1 was highlighted as a frequently tagged novel glioma-causing gene. Retroviral integrations into the locus resulted in Ppfibp1 upregulation, and Ppfibp1-tagged cells generated tumors with shorter latency on orthotopic transplantation. In human gliomas, increased PPFIBP1 expression was significantly linked to poor prognosis and PDGF treatment resistance.ConclusionsAltogether, the current study has demonstrated a novel approach to tagging glioma genes via forward genetics, validating previous results, and identifying PPFIBP1 as a putative oncogene in gliomagenesis.

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Expression data from RCAS PDGFB/Nestin tv-A glioma cells within Ptprd+/+p16-/- (n=2), Ptprd+/-p16-/- (n=2), and Ptrpd-/-p16-/- (n=3) mice.

Project description:PTPRD is a tumor suppressor of glioma that is frequently co-deleted with CDKN2A/p16. We show that Ptprd and p16 cooperate to promote gliomagenesis in the RCAS PDGFB / Nestin tv-A glioma mouse model. We found unique gene expression changes within tumor cells of Ptprd+/-p16-/- vs. Ptprd+/+p16-/- and Ptprd-/-p16-/- tumor cells. Neonatal mice were injected with RCAS PDGFB GFP. At symptoms, or at 12 weeks post injection, GFP+DAPI- tumor cells were sorted for RNA extraction and hybridization on Affymetrix microarrays. The mouse strain used was a mixed background of C57/BL6 and FVB/N. Ptprd mice were from Uetani et al. 2000 and p16/Nestin-tvA mice were from Tchouganouva et al. 2007.

2014-06-02 | E-GEOD-55061 | biostudies-arrayexpress

Expression data from RCAS PDGFB/Nestin tv-A glioma cells within Ptprd+/+p16-/- (n=2), Ptprd+/-p16-/- (n=2), and Ptrpd-/-p16-/- (n=3) mice.

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