Ontology highlight
ABSTRACT:
PROVIDER: PRJNA988250 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Human epithelial cancers are defined by a recurrent distribution of specific chromosomal aneuploidies. In our model system, mouse bladder and kidney epithelial cells spontaneously immortalize, transform and become tumorigenic after prolonged culture. We assessed genome and transcriptome alterations and found wide-spread aneuploidy, early transcriptional deregulation, and massive genomic dereguation of the cellular transcriptome. The results reveal a remarkable similarity with genome and transcriptome aberrations detected in human tumorigenesis, hence validating our newly derived cancer models. Epithelial cells were isolated from the C57BL/6 mouse bladder and kidney. These cells underwent spontaneous transformation in culture. We sought to identify the molecuar genomic alterations that occur during the transformation process and to compare these with the changes observed in human bladder and kidney cancers.
2013-03-14 | E-GEOD-45127 | biostudies-arrayexpress
Project description:Human epithelial cancers are defined by a recurrent distribution of specific chromosomal aneuploidies. In our model system, mouse bladder and kidney epithelial cells spontaneously immortalize, transform and become tumorigenic after prolonged culture. We assessed genome and transcriptome alterations and found wide-spread aneuploidy, early transcriptional deregulation, and massive genomic dereguation of the cellular transcriptome. The results reveal a remarkable similarity with genome and transcriptome aberrations detected in human tumorigenesis, hence validating our newly derived cancer models. Epithelial cells were isolated from the C57BL/6 mouse bladder and kidney. These cells underwent spontaneous transformation in culture. We sought to identify the molecuar genomic alterations that occur during the transformation process and to compare these with the changes observed in human bladder and kidney cancers.
2013-03-14 | E-GEOD-45128 | biostudies-arrayexpress
Project description:Urinary microbiota and bladder cancer
| PRJEB39977 | ENA
Project description:This SuperSeries is composed of the following subset Series: GSE14740: FFPE study using MIP copy number platform - kidney GSE14741: FFPE study using MIP copy number platform - bladder/colorectal/kidney/liver GSE14742: FFPE study using MIP copy number platform - colorectal GSE14743: FFPE study using MIP copy number platform - breast cancer I GSE14744: FFPE study using MIP copy number platform - breast cancer II GSE14745: FFPE study using MIP copy number platform - liver Refer to individual Series, GSE14856_quartets.txt contains list of matched samples
2010-05-06 | E-GEOD-14856 | biostudies-arrayexpress
Project description:Role of microbiota in bladder cancer development
| PRJEB75372 | ENA
Project description:Bladder cancer characterized by RNA methylation abnormalities and NOTCH pathway dysregulation exhibits high recurrence that remains the major obstacle for bladder cancer treatment. Targeting methyltransferase-like 3 (METTL3) and NOTCH signal is a potential strategy to block bladder cancer progression. However, the underlying mechanisms by which METTL3-manipulated NOTCH signal and its effect on bladder cancer tumorigenesis remain to be clarified. Here we showed that METTL3-guided m6A modification methylated pri-miR-146 at the flaking sequence, which was responsible for the pri-miR-146 maturation. Furthermore, NUMB/NOTCH2 axis was identified as the functional downstream target signal that mediated the pro-survival role of miR-146a-5p in bladder cancer cells. Therapeutically, the polypeptide melittin was demonstrated to induce apoptosis of bladder cancer cells in a METTL3-dependent manner. Importantly, METTL3 and miR-146a-5p were positively correlated with recurrence and poor prognosis of bladder cancer patient. Our studies indicate that METTL3/miR-146a-5p/NUMB/NOTCH2 axis could be a potential therapeutic target for recurrent bladder cancer treatment and METTL3 acts as a fate determinant that controls sensitivity of bladder cancer cells to melittin treatment.
2024-10-01 | GSE185272 | GEO
Project description:Human epithelial cancers are defined by a recurrent distribution of specific chromosomal aneuploidies. In our model system, mouse bladder and kidney epithelial cells spontaneously immortalize, transform and become tumorigenic after prolonged culture. We assessed genome and transcriptome alterations and found wide-spread aneuploidy, early transcriptional deregulation, and massive genomic dereguation of the cellular transcriptome. The results reveal a remarkable similarity with genome and transcriptome aberrations detected in human tumorigenesis, hence validating our newly derived cancer models.
2013-03-14 | GSE45128 | GEO