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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE207264 | GEO | 2022/07/05

REPOSITORIES: GEO

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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

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

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

| PRJNA854593 | ENA

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.

| S-EPMC9825320 | biostudies-literature

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.

2014-06-02 | GSE55061 | GEO

Effect of ATRX deficiency on gene expression of RCAS-nTva derived murine gliomas [RNA-seq: ATRX_Immuno_Tumor]

Project description:To investigate the impact of ATRX loss on tumor microenvironment we generated ATRX-intact and -deficient tumors in immune competent mice with the RCA-nTva system. Mice were injected with a tumorigenic RCAS construct (PDGFa and shTP53) and an RCAS bearing CRE recombinase. This was performed in mice that were ATRX wt and ATRX floxed.

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Effect of ATRX deficiency on gene expression of RCAS-nTva derived murine gliomas [RNA-seq: ATRX_Immuno_cell_line]

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Transcription profiling of human 293 cells infected with either RCAS-beta-catenin S37A or RCAS-GFP

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2007-08-04 | E-GEOD-1473 | biostudies-arrayexpress

Gene expression profiling of mouse tumors arising from Keratin 6-positive mammary cells

Project description:Conventional transgenic and knockout models do not allow selective introduction of oncogenic alterations into the progenitor population of mammary cells; thus, the role of progenitor cells in mammary tumorigenesis is yet unknown. By generating transgenic mice expressing tva – encoding the receptor for avian leukosis virus subgroup A (ALV/A) – from the Keratin 6a (K6) gene promoter, we found that K6+ mammary cells are bipotential progenitor cells, but not stem cells. These K6+ cells were readily induced to form tumors by intraductal injection of RCAS (an ALV/A-derived vector) carrying the gene encoding polyoma middle T antigen. Compared with tumors induced by the same oncogene-expressing virus in transgenic mice expressing tva from the commonly used MMTV LTR or other murine models of breast cancer, tumors in this K6-tva line were unique in that they resemble the normal breast-like subtype of human breast cancer. Consequently, these observations suggest that the cell of origin affects mammary tumor phenotypes. This K6-tva model may be useful for preclinical testing of targeted therapy for normal-like breast cancers in patients. Keywords: Three group comparison We carried out Affymetrix array analysis of five RCAS-PyMT-induced tumors each from K6-tva mice and MMTV-tva mice, as well as five mammary tumors from MMTV-PyMT transgenic mice.

2011-05-09 | E-GEOD-20614 | biostudies-arrayexpress

RNA-seq data from NSCs and tumorspheres generated using the RCAS/TVA-CRISPR/Cas9 system

Project description:It has been gradually established that the vast majority of human tumors are extraordinarily heterogeneous at a genetic level. To accurately recapitulate this complexity, it is now evident that in vivo animal models of cancers will require to recreate not just a handful of simple genetic alterations, but possibly dozens and increasingly intricate. Here, we have combined the RCAS/TVA system with the CRISPR/Cas9 genome editing tools for precise modelling of human tumors. We show that somatic deletion in neural stem cells (NSCs) of a variety of known tumor suppressor genes (Trp53, Cdkn2a and Pten), in combination with the expression of an oncogene driver, leads to high-grade glioma formation. Moreover, by simultaneous delivery of pairs of guide RNAs (gRNAs) we generated different gene fusions, either by chromosomal deletion (Bcan-Ntrk1) or by chromosomal translocation (Myb-Qk), and we show that they have transforming potential in vivo and in vitro.

2018-03-02 | GSE110700 | GEO

Genome-wide maps in PDGFB-induced glioma

Project description:We performed genome-wide profiling of oligodendrocyte lineage transcription factor 2 (Olig2) and other histone markers in platelet-derived growth factor subunit B (PDGFB)-induced glioma and genome-occupancy analyses coupled with transcriptome profiling to reveal gene regulatory network. Examination of Olig2, H327Ac, and H3K4me3 genome-wide occupancy in PDGFB-induced Ctrl-T and Olig2cKO brain tumors (gliomas).

2016-05-17 | E-GEOD-80088 | biostudies-arrayexpress

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