Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: phs000310.v1.p1GSE21032
PROVIDER: PRJNA126455 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Prostate cancer is readily curable if detected early. The overall goal of this study is to conduct integrative profiling of tumor and blood genomics and transcriptomics.
2021-09-30 | GSE162868 | GEO
Project description:Advanced prostate cancer is often associated with the emergence of more aggressive disease phenotypes, including neuroendocrine prostate cancer (NEPC), which are currently incurable. To identify drivers of aggressive prostate cancer, we conducted a Sleeping Beauty (SB) transposon mutagenesis screen based on a mouse model having conditional loss of function of Pten and Tp53 prostate (NPp53). Compared with the control mice (NPp53-SB(—)), the experimental mice (NPp53-SB(+)) develop aggressive prostate cancer phenotypes that are highly heterogeneous and highly metastasis. Most notably, a high percentage of NPp53-SB(+) prostate tumors have features of NEPC, which are conserved with human prostate cancer. To identify and prioritize drivers of NEPC in these NPp53-SB(+) tumors, we used a novel integrative approach that combines (i) genomic analyses of common insert sites (CIS) for the SB transposon, (ii) VIPER analyses of control NPp53-SB(+) prostate tumors to identify master regulators (MRs) enriched in NEPC, and (iii) comparative transcriptomic analyses with data from human prostate cancer patients followed by integrative analyses using of these data using a CINDy algorithm to identify CIS-associated genes that modulate the NEPC phenotypes. Among these the nicotinamide adenosine dinucleotide (NAD)-dependent deacetylase, sirtuin 1 (Sirt1). Loss- and gain-of-function studies in human prostate cancer cell lines showed that SIRT1 promotes NEPC, while its depletion or inhibition reduces NEPC. Overall, this integrative phenotypic and systems analyses have identified of candidate drivers of NEPC and may be generalizable to analyzing and interpreting data from analogous in vivo mutagenesis screens.
2026-04-13 | GSE271054 | GEO
Project description:Advanced prostate cancer is often associated with the emergence of more aggressive disease phenotypes, including neuroendocrine prostate cancer (NEPC), which are currently incurable. To identify drivers of aggressive prostate cancer, we conducted a Sleeping Beauty (SB) transposon mutagenesis screen based on a mouse model having conditional loss of function of Pten and Tp53 prostate (NPp53). Compared with the control mice (NPp53-SB(—)), the experimental mice (NPp53-SB(+)) develop aggressive prostate cancer phenotypes that are highly heterogeneous and highly metastasis. Most notably, a high percentage of NPp53-SB(+) prostate tumors have features of NEPC, which are conserved with human prostate cancer. To identify and prioritize drivers of NEPC in these NPp53-SB(+) tumors, we used a novel integrative approach that combines (i) genomic analyses of common insert sites (CIS) for the SB transposon, (ii) VIPER analyses of control NPp53-SB(+) prostate tumors to identify master regulators (MRs) enriched in NEPC, and (iii) comparative transcriptomic analyses with data from human prostate cancer patients followed by integrative analyses using of these data using a CINDy algorithm to identify CIS-associated genes that modulate the NEPC phenotypes. Among these the nicotinamide adenosine dinucleotide (NAD)-dependent deacetylase, sirtuin 1 (Sirt1). Loss- and gain-of-function studies in human prostate cancer cell lines showed that SIRT1 promotes NEPC, while its depletion or inhibition reduces NEPC. Overall, this integrative phenotypic and systems analyses have identified of candidate drivers of NEPC and may be generalizable to analyzing and interpreting data from analogous in vivo mutagenesis screens.
2026-04-13 | GSE271053 | GEO
Project description:To identify genomic regions which display concordant epigenetics alterations in prostate cancer, we performed MeDIP and ChIP-on-chip profiling of normal prostate epithelial cells (PrEC) and the prostate cancer cell line LNCaP. These promoter arrays were integrated with expression arrays of the same cells to discover and characterise regions of Long Range Epigenetic Silencing (LRES) in prostate cancer.
2010-01-04 | GSE19600 | GEO
Project description:Prostate cancer is readily curable if detected early. The overall goal of this study is to conduct integrative profiling of tumor and blood genomics and transcriptomics.
2021-09-30 | GSE183019 | GEO
Project description:Prostate cancer is readily curable if detected early. The overall goal of this study is to conduct integrative profiling of tumor and blood genomics and transcriptomics.
2021-09-30 | GSE183015 | GEO
Project description:Prostate cancer is readily curable if detected early. The overall goal of this study is to conduct integrative profiling of tumor and blood genomics and transcriptomics.
2022-04-27 | GSE201284 | GEO
Project description:This SuperSeries is composed of the following subset Series: GSE32676: Integrative Survival-Based Molecular Profiling of Human Pancreatic Cancer [mRNA] GSE32678: Integrative Survival-Based Molecular Profiling of Human Pancreatic Cancer [miRNA] GSE32682: Integrative Survival-Based Molecular Profiling of Human Pancreatic Cancer [SNP] Refer to individual Series
2011-10-07 | E-GEOD-32688 | biostudies-arrayexpress
Project description:Aggressive variant prostate cancer is characterized by poor clinical outcomes and profound molecular heterogeneity. In this study, we performed integrative genomic analyses of AVPC to identify potential drug sensitivities and molecular features associated with platinum response.
2026-01-31 | GSE309839 | GEO
Project description:Tumour cells sustain their high proliferation rate through metabolic reprogramming, whereby cellular metabolism shifts from oxidative phosphorylation to aerobic glycolysis, even under normal oxygen levels. HIF1A is a major regulator of this process but activation of HIF1A under normoxic conditions, termed pseudohypoxia, is not well documented. Here, using an integrative approach combining the first genome-wide mapping of chromatin binding for an endocytic adaptor, ARRB1, both in vitro and in vivo with gene expression profiling, we demonstrate that nuclear ARRB1 contributes to this metabolic shift in prostate cancer cells via regulation of Hypoxia Inducible Factor 1A (HIF1A) transcriptional activity under normoxic conditions through regulation of succinate dehydrogenase A (SDHA) and fumarate hydratase (FH) expression. ARRB1-induced pseudohypoxia may facilitate adaptation of cancer cells to growth in the harsh conditions that are frequently encountered within solid tumours. Our study is the first example of an endocytic adaptor protein regulating metabolic pathways. It implicates ARRB1 as a potential tumour promoter in prostate cancer and highlights the importance of metabolic alterations in prostate cancer. In an attempt to identify the ARRB1 cistrome in prostate cancer cells, C4-2 prostate cancer cells expressing endogenous levels of ARRB1 were used to ChIP for ARRB1, p300 (previously shown to interact with ARRB1within transcriptional complexes), RNA PolII and histone markers H3K4me1 and H4K4me3 (markers for enhancer and promoter regions, respectively). Cells were untreated and cultured in FBS supplemented with 10%FBS. In parallel, C4-2 cells stably expressing a nuclear form of ARRB1 (nucARRB1) were also used to ChIP the same complexes under the same conditions. Finally, human prostate tissue was used to ChIP for ARRB1 and histone markers.
2014-11-26 | E-GEOD-55615 | biostudies-arrayexpress