Project description:Choroid plexus carcinomas (CPC) are poorly understood and frequently lethal brain tumors with minimal treatment options. Using a new mouse model of the disease and a large cohort of human CPCs [GSE60892; GSE60899], we performed a cross-species, genome-wide search for novel oncogenes within syntenic regions of chromosome gain. TAF12, NFYC and RAD54L, co-located on human chromosome 1p32-35.3 and mouse chromosome 4qD1-D3, were identified as oncogenes that are gained in tumors in both species and required to initiate and progress the disease in mice. TAF12 and NFYC are transcription factors that regulate the epigenome, while RAD54L plays a central role in DNA repair. Our data identify a group of concurrently gained, novel oncogenes that cooperate in the formation of CPC and unmask potential new avenues for therapy. CPC mouse model samples of tumors derived from choroid plexus epithelium (CPE) cells that are Tp53/RB/Pten null in FVB mice. Female CD1 nude (host) mice were transfected with postanatal CPE and compared with a medulloblastoma normal mouse embryonic, postnatal and adult controls (loxP TP53/RB/PTEN (no Cre)) Implanted and reimplanted are from the orthotropic transplants of the primary tumor or later tumors
Project description:We investigated the gene expression of the human CPE in Braak stadia 0, 3 and 6.We isolated CPE cells with laser dissection microscopy from healthy human donor choroid plexus tissues and from human choroid plexus tissue from brains that were post-mortem staged in Braak 3 and Braak 6 Alzheimer disease stages . Next, we performed RNA isolation, amplification, labeling and hybridization against 44k Agilent microarrays.
Project description:We investigated the gene expression of the human CPE.We isolated CPE cells from healthy human donor choroid plexus tissues with laser dissection microscopy. Next, we performed RNA isolation, amplification, labeling and hybridization against 44k Agilent microarrays. We performed the microarrays against a common reference sample, namely human RPE/choroid RNA. We performed 7 replicates of human CPE samples from 7 different donors.
Project description:Atoh1-Cre; Myc/Myc mice developed choroid plexus papilloma and Atoh1-Cre; Myc/Myc; p53fl/fl mice developed choroid plexus carcinoma. By studying the gene expression profiles of normal choroid plexus, choroid plexus papilloma and choroid plexus carcinoma in mice, we aim to gain a better understanding of the biology of choroid plexus tumors
Project description:Choroid plexus carcinomas (CPC) are poorly understood and frequently lethal brain tumors with minimal treatment options. Using a new mouse model of the disease and a large cohort of human CPCs [GSE60892; GSE60899], we performed a cross-species, genome-wide search for novel oncogenes within syntenic regions of chromosome gain. TAF12, NFYC and RAD54L, co-located on human chromosome 1p32-35.3 and mouse chromosome 4qD1-D3, were identified as oncogenes that are gained in tumors in both species and required to initiate and progress the disease in mice. TAF12 and NFYC are transcription factors that regulate the epigenome, while RAD54L plays a central role in DNA repair. Our data identify a group of concurrently gained, novel oncogenes that cooperate in the formation of CPC and unmask potential new avenues for therapy.
Project description:We investigated the gene expression of the human CPE.We isolated CPE cells from healthy human donor choroid plexus tissues with laser dissection microscopy. Next, we performed RNA isolation, amplification, labeling and hybridization against 44k Agilent microarrays.
Project description:Choroid plexus carcinomas (CPC) are poorly understood and frequently lethal brain tumors with minimal treatment options. Using a new mouse model of the disease and a large cohort of human CPCs, we performed a cross-species, genome-wide search for novel oncogenes within syntenic regions of chromosome gain. TAF12, NFYC and RAD54L, co-located on human chromosome 1p32-35.3 and mouse chromosome 4qD1-D3, were identified as oncogenes that are gained in tumors in both species and required to initiate and progress the disease in mice. TAF12 and NFYC are transcription factors that regulate the epigenome, while RAD54L plays a central role in DNA repair. Our data identify a group of concurrently gained, novel oncogenes that cooperate in the formation of CPC and unmask potential new avenues for therapy.
Project description:Aggresome is a para nuclear inclusion body that functions as a storage compartment for misfolded proteins. Our previous work revealed the presence of aggresomes in pediatric choroid plexus tumors (CPT). CPTs are rare neoplasms comprised of three pathological subgroups; choroid plexus carcinoma (CPC), a grade III tumor, atypical choroid plexus papilloma (ACPP), a grade II tumor, and choroid plexus papilloma (CPP), a grade I tumor. In the current study, we aimed to investigate the prognostic value of aggresomes-positivity and its correlation to the pathological and molecular subtypes. The proteomics profiling of 21 CPT pediatric samples was investigated using ABSciex Triple TOF 5600+ mass spectrometer.
2021-02-11 | PXD021076 | Pride
Project description:Gene expression of the choroid plexus epithelium (CPE)
Project description:Gene expression profiles generated from human tumor cells laser-microdissected from surgical samples of seven choroid plexus papillomas (Grade I WHO) as eight samples of epithelial cells lasermicrodissected from normal choroid plexus obtained at autopsy. Choroid plexus tumors are rare pediatric brain tumors derrived from the choroid plexus epithelium. Gene expression profiles of lasermicrodissected tumor cells from 7 individual choroid plexus tumor samples obtained at surgery were compared to gene expression profiles from non-neoplastic choroid plexus epithelial cells lasermicrodissected from normal non-neoplastic choroid plexus obtained at autopsy (Am J Surg Pathol. 2006 Jan;30(1):66-74.) in order to identfy genes differentially expressed in choroid plexus tumor cells.