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Gene expression analysis of dendritic cells from normal or tumor bearing prostates

ABSTRACT: Tumors cause the induction or repression of many genes associated with inflammation. To investigate the up and down regulation of genes associated with immune stimulation or immune tolerance RNA was isolated from dendritic cells from normal or tumor bearing prostate for microarray analysis. Using the TRansgenic Adenocarcinoma of the Mouse Prostate (TRAMP) model and a fold change comparison system we identified genes that are associated with immune tolerance to be up-regulated and genes associated with immunity to be down regulated in tumor associated dendritic cells. Keywords: Comparative gene expression, prostate cancer, dendritic cells

ORGANISM(S): Mus musculus

PROVIDER: GSE26719 | GEO | 2011/01/20

SECONDARY ACCESSION(S): PRJNA136127

REPOSITORIES: GEO

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Gene expression analysis of dendritic cells from normal or tumor bearing prostates

Project description:Tumors cause the induction or repression of many genes associated with inflammation. To investigate the up and down regulation of genes associated with immune stimulation or immune tolerance RNA was isolated from dendritic cells from normal or tumor bearing prostate for microarray analysis. Using the TRansgenic Adenocarcinoma of the Mouse Prostate (TRAMP) model and a fold change comparison system we identified genes that are associated with immune tolerance to be up-regulated and genes associated with immunity to be down regulated in tumor associated dendritic cells. Keywords: Comparative gene expression, prostate cancer, dendritic cells Prostatic dendritic cells were isolated from 4 normal and 6 tumor bearing mice for comparison of gene expression.

2011-01-20 | E-GEOD-26719 | biostudies-arrayexpress

Gene expression analysis of dendritic cells from normal or tumor sections of human prostates

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2011-01-21 | E-GEOD-26747 | biostudies-arrayexpress

Gene expression analysis of dendritic cells from normal or tumor sections of human prostates

2011-01-21 | GSE26747 | GEO

Genetic deletion of osteopontin in TRAMP mice enhances the growth of aggressive prostate cancer with feature of human neuroendocrine tumors

Project description:Osteopontin (OPN) is a secreted glycoprotein, belonging to the non-structural extracellular matrix (ECM), and its over expression in human prostate cancer cells has been associated with disease progression, androgen independence and metastases. Nevertheless the pathophysiology of OPN in prostate tumorigenesis has never been studied. We crossed TRansgenic Adenocarcinoma of the Mouse Prostate (TRAMP) mice with OPN deficient (OPN-/-) mice and followed tumor onset and progression in these double mutants. Ultrasound examination detected the early onset of a spherical homogeneous tumor in about 60% of OPN-/- TRAMP mice that seldom occurs in parental TRAMP mice. Histology and immunohistochemistry characterized these tumors for being Tag positive but negative for AR, highly proliferative and endowed of neuroendocrine (NE) features. Gene expression profiling showed up-regulation of genes involved in tumor progression, cell cycle and neuronal differentiation in OPN-deficient versus -sufficient TRAMP tumors. Down-regulated genes included key genes of TGFï?¢ pathway, and a role for TGFï?¢ in NE differentiation of prostate cancer was also confirmed at the protein level. Furthermore, NE genes and particularly those characterizing early prostatic lesions of OPN-deficient mice were found to correlate with those of human NE tumours. These data underscore a novel role of OPN at early stages of prostate cancer growth, protecting against the development of aggressive NE tumors. Total RNA obtained from prostate tumors from 18 and 30 weeks old TRAMP mice, compared to RNA extracted from prostate tumors and prostate tissue from Osteopontin-deleted TRAMP mice

2016-01-20 | E-GEOD-69903 | biostudies-arrayexpress

Genetic deletion of osteopontin in TRAMP mice enhances the growth of aggressive prostate cancer with feature of human neuroendocrine tumors

Project description:Osteopontin (OPN) is a secreted glycoprotein, belonging to the non-structural extracellular matrix (ECM), and its over expression in human prostate cancer cells has been associated with disease progression, androgen independence and metastases. Nevertheless the pathophysiology of OPN in prostate tumorigenesis has never been studied. We crossed TRansgenic Adenocarcinoma of the Mouse Prostate (TRAMP) mice with OPN deficient (OPN-/-) mice and followed tumor onset and progression in these double mutants. Ultrasound examination detected the early onset of a spherical homogeneous tumor in about 60% of OPN-/- TRAMP mice that seldom occurs in parental TRAMP mice. Histology and immunohistochemistry characterized these tumors for being Tag positive but negative for AR, highly proliferative and endowed of neuroendocrine (NE) features. Gene expression profiling showed up-regulation of genes involved in tumor progression, cell cycle and neuronal differentiation in OPN-deficient versus -sufficient TRAMP tumors. Down-regulated genes included key genes of TGF pathway, and a role for TGF in NE differentiation of prostate cancer was also confirmed at the protein level. Furthermore, NE genes and particularly those characterizing early prostatic lesions of OPN-deficient mice were found to correlate with those of human NE tumours. These data underscore a novel role of OPN at early stages of prostate cancer growth, protecting against the development of aggressive NE tumors.

2016-01-20 | GSE69903 | GEO

Gene expression profile of Transgenic Adenocarcinoma of the Mouse Prostate (TRAMP)

Project description:Gene expression profile of Transgenic Adenocarcinoma of the Mouse Prostate (TRAMP) reveals murine targets for preclinical development of human prostate cancer therapy In this study, we have generated an open source TRAMP microarray dataset to identify differentially expressed genes from human prostate cancer that have concordant expression in TRAMP tumors, and thereby represent lead targets for preclinical therapy development. Affymetrix Mouse 430 2.0 chips were used for microarrays of total RNA from 9 TRAMP tumors and 9 normal prostates (ventral and dorsolateral lobes). Keywords: prostate cancer, TRAMP

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2014-09-16 | E-GEOD-61416 | biostudies-arrayexpress

The Aged Microenvironment Enhances the Tumorigenic Potential of Malignant Prostate Epithelial Cells

Project description:The incidence of prostate cancer is directly linked to age, but we still lack an adequate understanding of the prostatic aging-associated changes that facilitate carcinogenesis. In this study, we investigated possible associated factors in the aged prostate microenvironment, using an orthotopic mouse model of prostate cancer. We found that aged mice showed accelerated growth of TRAMP-C2 cells, compared with young mice. Metastatic lesions following intravenous injection were also more numerous in aged mice. TRAMP-C2 tumors from young and aged mice showed no significant differences concerning their proliferation index, apoptosis or angiogenesis. However, analysis of tumor-infiltrating immune cells by immunohistochemistry and RNA-seq gene expression revealed that aged mice present higher numbers of macrophages in normal prostatic tissue and that these are quickly polarized towards an M2 phenotype upon TRAMP-C2 cells engraftment.

2019-04-23 | GSE110643 | GEO

An Immune and Inflammation Signature in Prostate Tumors of Smokers (part 3)

Project description:Current smokers develop metastatic prostate cancer more frequently than nonsmokers, suggesting that a tobacco-derived factor induces metastasis. To identify smoking-induced alterations in human prostate tumors, we analyzed gene and protein expression of tumors from current, past, and never smokers and observed distinct molecular alterations in current smokers. Specifically, an immune and inflammation signature was identified in prostate tumors of current smokers that was either attenuated or absent in past and never smokers. Key characteristics of this signature included augmented immunoglobulin expression by tumor-infiltrating B cells, NF-kB activation, and increased interleukin-8 in tumor and blood. In an alternate approach to characterize smoking-induced oncogenic alterations, we explored the effects of nicotine in prostate cancer cells and prostate cancer-prone TRAMP mice. These experiments showed that nicotine increases both invasiveness of human prostate cancer cells and metastasis in tumor-bearing TRAMP mice, indicating that nicotine can induce a phenotype that resembles the epidemiology of smoking-associated prostate cancer progression. In summary, we describe distinct oncogenic alterations in prostate tumors from current smokers and show that nicotine can enhance prostate cancer metastasis. TRAMP mice in five replicates received either tap water or a solution of 250 µg/ml of nicotine [nicotine tartrate salt (Sigma-Aldrich, St. Louis, MO)] in tap water

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Transcription profiling of mouse transgenic adenocarcinoma of the prostate (TRAMP)

Project description:Gene expression profile of Transgenic Adenocarcinoma of the Mouse Prostate (TRAMP) reveals murine targets for preclinical development of human prostate cancer therapy; In this study, we have generated an open source TRAMP microarray dataset to identify differentially expressed genes from human prostate cancer that have concordant expression in TRAMP tumors, and thereby represent lead targets for preclinical therapy development. Affymetrix Mouse 430 2.0 chips were used for microarrays of total RNA from 9 TRAMP tumors and 9 normal prostates (ventral and dorsolateral lobes). Experiment Overall Design: normal prostate vs. TRAMP

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