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ABSTRACT:
PROVIDER: PRJNA140089 | ENA |
REPOSITORIES: ENA
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Project description:Gene expression in the the pancreatic lymph node of 4, 12, and 30 week old Deaf1-knockout (KO) mice compared to BALB/c littermate controls. Gene expression was measured in the pancreatic lymph nodes of 4 wk old Deaf1 KO mice (2 replicates), 12 wk old Deaf1-KO mice (3 replicates), and 30 wk old Deaf1-KO mice (3 replicates).
2011-08-31 | E-GEOD-29153 | biostudies-arrayexpress
Project description:This SuperSeries is composed of the following subset Series: GSE29152: Lymph node stromal cells: Control siRNA treated vs. Eif4g3 siRNA treated GSE29153: Differential gene expression in the Pancreatic lymph node of Deaf1 knockout mice vs. wild type littermate controls Refer to individual Series
2011-08-31 | E-GEOD-29167 | biostudies-arrayexpress
Project description:Gene expression in the the pancreatic lymph node of 4, 12, and 30 week old Deaf1-knockout (KO) mice compared to BALB/c littermate controls.
2011-09-01 | GSE29153 | GEO
Project description:A microarray study performed in the pancreatic lymph nodes of Deaf1 knock-out and BALB/c control mice to identify genes that are regulated by the transcriptional regulator Deaf1. These experiments constitute a portion of the study described below: Abstract: Type 1diabetes (T1D) can result from a breakdown in peripheral tolerance which is controlled by peripheral tissue antigen (PTA) expression in lymph nodes. Here, we identified a transcriptional regulator, deformed epidermal autoregulatory factor 1 (Deaf1), which regulates the expression of various PTAs in the pancreatic lymph node (PLN). We found, by microarray, that Deaf1 controls the expression of ~600 genes in the PLN. In the non-obese diabetic (NOD) mouse model of T1D, we identified a wild-type form of Deaf1 (DF1) and a truncated alternatively spliced variant (DF1-VAR1) that hetero-dimerizes with and decreases the transcriptional activity of DF1. The expression of DF1 correlates with the expression of various pancreatic PTAs such as insulin, and during the onset of destructive insulitis in NOD mice, DF1 expression is downregulated, while the DF1-VAR1 expression is upregulated in the PLN. A reduction in DF1-controlled PTA expression in the PLN, leading to decreased peripheral tolerance, could underlie the pathogenesis of NOD disease.
2009-07-15 | GSE13163 | GEO
Project description:A microarray study performed in the pancreatic lymph nodes of Deaf1 knock-out and BALB/c control mice to identify genes that are regulated by the transcriptional regulator Deaf1. These experiments constitute a portion of the study described below: Abstract: Type 1diabetes (T1D) can result from a breakdown in peripheral tolerance which is controlled by peripheral tissue antigen (PTA) expression in lymph nodes. Here, we identified a transcriptional regulator, deformed epidermal autoregulatory factor 1 (Deaf1), which regulates the expression of various PTAs in the pancreatic lymph node (PLN). We found, by microarray, that Deaf1 controls the expression of ~600 genes in the PLN. In the non-obese diabetic (NOD) mouse model of T1D, we identified a wild-type form of Deaf1 (DF1) and a truncated alternatively spliced variant (DF1-VAR1) that hetero-dimerizes with and decreases the transcriptional activity of DF1. The expression of DF1 correlates with the expression of various pancreatic PTAs such as insulin, and during the onset of destructive insulitis in NOD mice, DF1 expression is downregulated, while the DF1-VAR1 expression is upregulated in the PLN. A reduction in DF1-controlled PTA expression in the PLN, leading to decreased peripheral tolerance, could underlie the pathogenesis of NOD disease. Deaf1-KO mice (4 wk old) and age-matched BALB/c control mice were sacrificed, and the PLN were removed and immediately homogenized in Trizol Reagent. RNA was extracted in Trizol and then purified using the RNeasy kit (Qiagen). RNA quality was assessed using the Agilent RNA 6000 Nano Reagents, RNA Nano chips, and the Agilent 2100 bioanalyzer (Agilent Technologies), according to manufacturerâs instructions. Control and Deaf1-KO mouse RNA was amplified, labeled with Cy3 and Cy5, respectively, and combined with spike A and spike B mix, respectively, using the Agilent low RNA input fluorescence linear amplification kit (Agilent Technologies). The amplified cRNA was purified using the RNeasy kit (Qiagen), and specific activity was determined with the NanoDrop 1000 spectrophotometer (Thermo Scientific). Samples were prepared with the gene expression hybridization kit (Agilent Technologies) and two color microarrays were performed using the whole mouse genome (4x44K) Oligo microarray kit, according to manufacturerâs instructions. Microarray chips were washed and scanned using the DNA microarray scanner (Agilent Technologies). Data was processed with Feature Extraction Software (Agilent Technologies), and analyzed using GeneSpring GX 7.3 Software (Agilent Technologies). This submission shows the data obtained from two individual Deaf1 knockout mice measured against a pool of 4 BALB/c control mice.
2010-04-08 | E-GEOD-13163 | biostudies-arrayexpress
Project description:A total of 14 lymph node samples were collected from 7 mice, with 8 samples obtained from the MI group and 6 from the sham-operated group. Each mouse contributed two lymph node samples: the mediastinal lymph node, MedLN and the sub-iliac lymph node, siLN. Supplementary Table 1 provides a detailed breakdown of sample distribution across the experimental groups.
2025-06-18 | MSV000098260 | MassIVE
Project description:A total of 14 lymph node samples were collected from 7 mice, with 8 samples obtained from the MI group and 6 from the sham-operated group. Each mouse contributed two lymph node samples: the mediastinal lymph node, MedLN and the sub-iliac lymph node, siLN. Supplementary Table 1 provides a detailed breakdown of sample distribution across the experimental groups.
2025-06-16 | MSV000098224 | MassIVE
Project description:Purpose: Lymph node invasion is a hallmark of breast cancer disease progression, but current treatment strategies lack guidance from lymph node biomarkers. We investigated JAGGED1 (JAG1) as a promoter of lymph node metastasis and a prognostic biomarker in metastatic lymph node specimens. Experimental Design: We used mouse models to assess the role of JAG1 expression in human and mouse breast cancer cells on lymphovascular invasion, lymph node metastatic potential, transcriptional profiles, and tumor interactions with lymphatic endothelium. We examined breast and lymph node samples from 284 breast cancer patients to determine the correlative and prognostic value of tumoral JAG1 expression in the lymph node. Results: In matched human breast tumor and lymph node samples, tumor cells that invaded lymph nodes showed higher JAG1 expression than their associated primary tumors (P value < 0.0001). In multiple models, breast cancer cells with high JAG1 expression showed increased lymphovascular invasion, lymph node metastasis, lymph node metastatic outgrowth, and migration through lymphatic endothelium. Transcriptomic analysis indicated that tumoral JAG1 regulates both juxtacrine and paracrine signaling pathways that induce inflammatory and pro-metastatic genes in lymphatic endothelium. When examining patients with identical surgical treatments, patients with lymph node JAG1 H-scorelow showed increased 5-year recurrence free survival rates than patients with lymph node JAG1 H-scorehi (87% vs 70%, P=0.016). Conclusions: JAG1 expression promotes lymphovascular invasion and lymph node metastasis in murine models. In patients, high expression of JAG1 in tumor cells in lymph node metastases predicts reduced recurrence free survival.
2026-07-27 | GSE253035 | GEO
Project description:Purpose: Lymph node invasion is a hallmark of breast cancer disease progression, but current treatment strategies lack guidance from lymph node biomarkers. We investigated JAGGED1 (JAG1) as a promoter of lymph node metastasis and a prognostic biomarker in metastatic lymph node specimens. Experimental Design: We used mouse models to assess the role of JAG1 expression in human and mouse breast cancer cells on lymphovascular invasion, lymph node metastatic potential, transcriptional profiles, and tumor interactions with lymphatic endothelium. We examined breast and lymph node samples from 284 breast cancer patients to determine the correlative and prognostic value of tumoral JAG1 expression in the lymph node. Results: In matched human breast tumor and lymph node samples, tumor cells that invaded lymph nodes showed higher JAG1 expression than their associated primary tumors (P value < 0.0001). In multiple models, breast cancer cells with high JAG1 expression showed increased lymphovascular invasion, lymph node metastasis, lymph node metastatic outgrowth, and migration through lymphatic endothelium. Transcriptomic analysis indicated that tumoral JAG1 regulates both juxtacrine and paracrine signaling pathways that induce inflammatory and pro-metastatic genes in lymphatic endothelium. When examining patients with identical surgical treatments, patients with lymph node JAG1 H-scorelow showed increased 5-year recurrence free survival rates than patients with lymph node JAG1 H-scorehi (87% vs 70%, P=0.016). Conclusions: JAG1 expression promotes lymphovascular invasion and lymph node metastasis in murine models. In patients, high expression of JAG1 in tumor cells in lymph node metastases predicts reduced recurrence free survival.
2026-07-27 | GSE252953 | GEO
Project description:Purpose: Lymph node invasion is a hallmark of breast cancer disease progression, but current treatment strategies lack guidance from lymph node biomarkers. We investigated JAGGED1 (JAG1) as a promoter of lymph node metastasis and a prognostic biomarker in metastatic lymph node specimens. Experimental Design: We used mouse models to assess the role of JAG1 expression in human and mouse breast cancer cells on lymphovascular invasion, lymph node metastatic potential, transcriptional profiles, and tumor interactions with lymphatic endothelium. We examined breast and lymph node samples from 284 breast cancer patients to determine the correlative and prognostic value of tumoral JAG1 expression in the lymph node. Results: In matched human breast tumor and lymph node samples, tumor cells that invaded lymph nodes showed higher JAG1 expression than their associated primary tumors (P value < 0.0001). In multiple models, breast cancer cells with high JAG1 expression showed increased lymphovascular invasion, lymph node metastasis, lymph node metastatic outgrowth, and migration through lymphatic endothelium. Transcriptomic analysis indicated that tumoral JAG1 regulates both juxtacrine and paracrine signaling pathways that induce inflammatory and pro-metastatic genes in lymphatic endothelium. When examining patients with identical surgical treatments, patients with lymph node JAG1 H-scorelow showed increased 5-year recurrence free survival rates than patients with lymph node JAG1 H-scorehi (87% vs 70%, P=0.016). Conclusions: JAG1 expression promotes lymphovascular invasion and lymph node metastasis in murine models. In patients, high expression of JAG1 in tumor cells in lymph node metastases predicts reduced recurrence free survival.
2026-07-27 | GSE252952 | GEO