Prostate cancer fiber model
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE9666 | GEO | 2008/07/01
SECONDARY ACCESSION(S): PRJNA103545
REPOSITORIES: GEO
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Project description:hormonal progression in prostate cancer fiber model Experiment Overall Design: The LNCaP Hollow Fiber model of prostate cancer was appied. A total of 24 fibers were implanted in each animal, in bundles of eight fibers at three different regions in the animal. Castration of mice was performed At each time point, eight fibers from the same mouse were harvested and total RNA was isolated from LNCaP cells grown inside the fibers using Trizol
2008-10-20 | E-GEOD-9666 | biostudies-arrayexpress
Project description:Prostate cancer is the most frequently diagnosed malignancy in adult males. Though multiple factors have been implicated in prostate cancer progression, the trigger for initiation of malignancy is still a topic of debate. Advanced age is the single most significant risk factor for prostate cancer. Epidemiological and clinical studies indicate oxidative stress as one of the major aging-associated influences on prostate carcinogenesis. In this study, for the first time, we demonstrated the intrinsic association of ROS and IL6/STAT3 in prostate carcinogenesis. The high levels of ROS/IL6/STAT3 activation in this carcinogenesis model will benefit understanding of the mechanism of prostate cancer initiation and progression, as well as therapeutic development of anti-cancer drug targeting of the IL6/STAT3 pathway.
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Project description:Samples of benign prostate tissue, localized prostate cancer tissue, and metastatic prostate cancer tissue are profiled to study expression changes in diagnosis and progression of prostate cancer. Each tissue sample is also profiled for metabolomics data Keywords: Cancer Progression 41 samples were analyzed (16 benign prostate tissue, 12 local prostate cancer tissue, 13 metastatic prostate cancer tissue)
2011-03-30 | E-GEOD-8511 | biostudies-arrayexpress
Project description:Samples of benign prostate tissue, localized prostate cancer tissue, and metastatic prostate cancer tissue are profiled to study expression changes in diagnosis and progression of prostate cancer. Each tissue sample is also profiled for metabolomics data Keywords: Cancer Progression
2011-03-30 | GSE8511 | GEO
Project description:Introduction: Neuroendocrine prostate cancer (NEPC) is an aggressive subtype of prostate cancer, exhibiting rapid progression and is unresponsive to hormone therapy. Reliable prognostic assays and more effective treatments are critically required. However, the research of NEPC has been hampered by a lack of clinically relevant in vivo models. Recently, we successfully developed a first-in-field patient tissue-derived xenograft model of complete neuroendocrine transdifferentiation from prostate adenocarcinoma. By comparing gene expression profiles of the parental adenocarcinoma line (LTL331) and the NEPC subline (LTL331R), we identified DEK, a gene not previously reported in prostate cancer, as a potential biomarker and target for NEPC. Methods: DEK protein expression in patient tissue-derived xenograft models and clinical samples was assessed by immunohistochemistry. The function of DEK was determined by siRNA-induced reduction of DEK expression in PC-3 cells, a cell line with NEPC characteristics, followed by functional assays and gene expression profiling analysis. Results: Elevated DEK protein expression was observed in all clinical NEPC cases, which is distinct from their benign counterparts (0%), hormonal naïve prostate cancer (2.45%) and castration resistant prostate cancer (29.55%). Increased DEK expression is an independent clinical risk factor and is associated with shorter disease free survival in hormonal naïve prostate cancer patients. Reduction of DEK expression in PC-3 cells led to a marked reduction in cell proliferation, cell migration and invasion. Conclusions: The results suggest that DEK may play an important role in the progression of prostate cancer, especially NEPC and provide a potential biomarker to aid risk stratification of prostate cancer and a novel therapeutic target for treating NEPC. The function of DEK was determined by siRNA-induced reduction of DEK expression in PC-3 cells, a cell line with NEPC characteristics, followed by functional assays and gene expression profiling analysis.
2015-01-15 | E-GEOD-61214 | biostudies-arrayexpress
Project description:LNCAP xenograft prostate cancer progression model in NOD-SCID mice
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2006-12-17 | GSE6099 | GEO
Project description:Introduction: Neuroendocrine prostate cancer (NEPC) is an aggressive subtype of prostate cancer, exhibiting rapid progression and is unresponsive to hormone therapy. Reliable prognostic assays and more effective treatments are critically required. However, the research of NEPC has been hampered by a lack of clinically relevant in vivo models. Recently, we successfully developed a first-in-field patient tissue-derived xenograft model of complete neuroendocrine transdifferentiation from prostate adenocarcinoma. By comparing gene expression profiles of the parental adenocarcinoma line (LTL331) and the NEPC subline (LTL331R), we identified DEK, a gene not previously reported in prostate cancer, as a potential biomarker and target for NEPC. Methods: DEK protein expression in patient tissue-derived xenograft models and clinical samples was assessed by immunohistochemistry. The function of DEK was determined by siRNA-induced reduction of DEK expression in PC-3 cells, a cell line with NEPC characteristics, followed by functional assays and gene expression profiling analysis. Results: Elevated DEK protein expression was observed in all clinical NEPC cases, which is distinct from their benign counterparts (0%), hormonal naïve prostate cancer (2.45%) and castration resistant prostate cancer (29.55%). Increased DEK expression is an independent clinical risk factor and is associated with shorter disease free survival in hormonal naïve prostate cancer patients. Reduction of DEK expression in PC-3 cells led to a marked reduction in cell proliferation, cell migration and invasion. Conclusions: The results suggest that DEK may play an important role in the progression of prostate cancer, especially NEPC and provide a potential biomarker to aid risk stratification of prostate cancer and a novel therapeutic target for treating NEPC.
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