Gene expression analysis reveals a signature of estrogen receptor activation upon loss ofPten in a mouse model of endometrial cancer

2006 ◽  
Vol 208 (2) ◽  
pp. 255-266 ◽  
Author(s):  
Zenglin Lian ◽  
Pasquale De Luca ◽  
Antonio Di Cristofano
Keyword(s):  
Gene Expression ◽  
Estrogen Receptor ◽  
Endometrial Cancer ◽  
Mouse Model ◽  
Expression Analysis ◽  
Gene Expression Analysis ◽  
Receptor Activation

scholarly journals Gene Expression Analysis of the Activating Factor 3/Nuclear Protein 1 Axis in a Non-alcoholic Steatohepatitis Mouse Model

2019 ◽  
Vol 62 (1) ◽  
pp. 036-046 ◽  
Author(s):  
Ran Nagahara ◽  
Tomomitsu Matono ◽  
Takaaki Sugihara ◽  
Yukako Matsuki ◽  
Masafumi Yamane ◽  
...  
Keyword(s):  
Gene Expression ◽  
Mouse Model ◽  
Expression Analysis ◽  
Gene Expression Analysis ◽  
Nuclear Protein ◽  
Alcoholic Steatohepatitis

TAMI-06. TUMOR CELL-DERIVED CYTOKINE EXPRESSION CHANGES ASSOCIATED WITH BRAIN METASTASIS IN A SYNGENEIC MOUSE MODEL OF BREAST CANCER

2021 ◽  
Vol 23 (Supplement_6) ◽  
pp. vi199-vi199
Author(s):  
Ramin Morshed ◽  
Alexander Haddad ◽  
Saket Jain ◽  
Sabraj Gill ◽  
Jordan Spatz ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Gene Expression ◽  
Mouse Model ◽  
Tumor Cell ◽  
Expression Analysis ◽  
Gene Expression Analysis ◽  
Cytokine Expression ◽  
Metastatic Dissemination ◽  
Syngeneic Mouse ◽  
Syngeneic Mouse Model

Abstract Breast cancer is the most common malignancy in women in the United States, and brain metastases occur in almost a third of patients with metastatic dissemination. Immunoediting is a critical component of metastatic tumor cell elimination, and tumor clones that develop immune-escape mechanisms are associated with progression and metastatic dissemination. We hypothesized that breast cancer brain metastatic cells harbor immunomodulatory cytokine expression changes that promote an immunosuppressive environment to avoid immune cell-mediated elimination. To study this, a syngeneic mouse model of metastatic breast cancer was used. A brain metastatic line derived from the 4T1 breast cancer parental cell line was created by serially selecting brain metastatic populations of cells after intracardiac injection (4T1 BrM). A gene-expression analysis using an 800-gene cancer immunology-specific microarray panel was performed comparing the 4T1 parental and 4T1 BrM lines. 4T1 BrM cells demonstrate gene expression changes promoting immunosuppression including significant upregulation of IL18 and Lgals9 (Galectin-9) and downregulation of CD40, IL2rg, CCL2, and EOMES. When compared to 4T1 parental lines, the 4T1 BrM line demonstrated decreased expression of CCL2 and increased expression of GM-CSF on a cytokine array, corresponding to results obtained from gene expression analysis. These results suggest tumor-intrinsic cytokine expression changes that may mediate an immunosuppressive environment.

scholarly journals Gene Expression Analysis of Immune-Mediated Arrest of Tumorigenesis in a Transgenic Mouse Model of HER-2/neu-Positive Basal-Like Mammary Carcinoma

2005 ◽  
Vol 166 (4) ◽  
pp. 1205-1216 ◽  
Author(s):  
Annalisa Astolfi ◽  
Lorena Landuzzi ◽  
Giordano Nicoletti ◽  
Carla De Giovanni ◽  
Stefania Croci ◽  
...  
Keyword(s):  
Gene Expression ◽  
Mouse Model ◽  
Transgenic Mouse ◽  
Expression Analysis ◽  
Mammary Carcinoma ◽  
Gene Expression Analysis ◽  
Transgenic Mouse Model ◽  
Immune Mediated ◽  
Her 2

scholarly journals INPP5D Expression is Associated with Risk for Alzheimer’s Disease and Induced by Plaque-Associated Microglia

2020 ◽  
Author(s):  
Andy P Tsai ◽  
Peter Bor-Chian Lin ◽  
Chuanpeng Dong ◽  
Miguel Moutinho ◽  
Brad Casali ◽  
...  
Keyword(s):  
Gene Expression ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Differential Gene Expression ◽  
Expression Analysis ◽  
Gene Expression Analysis ◽  
Differential Gene Expression Analysis ◽  
Differential Gene ◽  
5Xfad Mice

Abstract Background Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by cognitive decline, robust microgliosis, neuroinflammation, and neuronal loss. Genome-wide association studies recently highlighted a prominent role for microglia in late-onset AD (LOAD). Specifically, inositol polyphosphate-5-phosphatase (INPP5D), also known as SHIP1, is selectively expressed in brain microglia and has been reported to be associated with LOAD. Although INPP5D is likely a crucial player in AD pathophysiology, its role in disease onset and progression remains unclear. Methods We performed differential gene expression analysis to investigate INPP5D expression in LOAD and its association with plaque density and microglial markers using transcriptomic (RNA-Seq) data from the Accelerating Medicines Partnership for Alzheimer’s Disease (AMP-AD) cohort. We also performed quantitative real-time PCR, immunoblotting, and immunofluorescence assays to assess INPP5D expression in the 5xFAD amyloid mouse model. Results Differential gene expression analysis found that INPP5D expression was upregulated in LOAD and positively correlated with amyloid plaque density. In addition, in 5xFAD mice, Inpp5d expression increased as the disease progressed, and selectively in plaque-associated microglia. Increased Inpp5d expression levels in 5xFAD mice were abolished entirely by depleting microglia with the colony-stimulating factor receptor-1 antagonist PLX5622. Conclusions Our findings show that INPP5D expression increases as AD progresses, predominantly in plaque-associated microglia. Importantly, we provide the first evidence that increased INPP5D expression might be a risk factor in AD, highlighting INPP5D as a potential therapeutic target. Moreover, we have shown that the 5xFAD mouse model is appropriate for studying INPP5D in AD.

scholarly journals INPP5D expression is associated with risk for Alzheimer’s disease and induced by plaque-associated microglia

2020 ◽  
Author(s):  
Andy P. Tsai ◽  
Peter Bor-Chian Lin ◽  
Chuanpeng Dong ◽  
Miguel Moutinho ◽  
Brad T. Casali ◽  
...  
Keyword(s):  
Gene Expression ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Differential Gene Expression ◽  
Expression Analysis ◽  
Gene Expression Analysis ◽  
Differential Gene Expression Analysis ◽  
Differential Gene ◽  
5Xfad Mice

AbstractBackgroundAlzheimer’s disease (AD) is a progressive neurodegenerative disorder characterized by cognitive decline, robust microgliosis, neuroinflammation, and neuronal loss. Genome-wide association studies recently highlighted a prominent role for microglia in late-onset AD (LOAD). Specifically, inositol polyphosphate-5-phosphatase (INPP5D), also known as SHIP1, is selectively expressed in brain microglia and has been reported to be associated with LOAD. Although INPP5D is likely a crucial player in AD pathophysiology, its role in disease onset and progression remains unclear.MethodsWe performed differential gene expression analysis to investigate INPP5D expression in LOAD and its association with plaque density and microglial markers using transcriptomic (RNA-Seq) data from the Accelerating Medicines Partnership for Alzheimer’s Disease (AMP-AD) cohort. We also performed quantitative real-time PCR, immunoblotting, and immunofluorescence assays to assess INPP5D expression in the 5xFAD amyloid mouse model.ResultsDifferential gene expression analysis found that INPP5D expression was upregulated in LOAD and positively correlated with amyloid plaque density. In addition, in 5xFAD mice, Inpp5d expression increased as the disease progressed, and selectively in plaque-associated microglia. Increased Inpp5d expression levels in 5xFAD mice were abolished entirely by depleting microglia with the colony-stimulating factor receptor-1 antagonist PLX5622.ConclusionsOur findings show that INPP5D expression increases as AD progresses, predominantly in plaque-associated microglia. Importantly, we provide the first evidence that increased INPP5D expression might be a risk factor in AD, highlighting INPP5D as a potential therapeutic target. Moreover, we have shown that the 5xFAD mouse model is appropriate for studying INPP5D in AD.

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