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MiRNA expression profiling in a murine model of KrasG12D induced CMML-like MPD

ABSTRACT: miRNA expression profiling in a murine model of KrasG12D induced CMML-like MPD

PROVIDER: PRJNA605975 | ENA |

REPOSITORIES: ENA

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miRNA expression profiling in a murine model of KrasG12D induced CMML-like MPD

Project description:Mx1-Cre/KrasG12D mice were injected with pIpC to induce a myeloproliferative disease resembling human chronic myelomonocytic leukemia (CMML-like MPD). When the disease was fully developed, CD11b-/Ly6G-/c-Kit+ hematopoietic stem and progenitor cells (HSPCs) were isolated and subjected to miR-microarray expression profiling. pIpC-injected CD11b-/Ly6G-/c-Kit+ HSPCs of age matched wildytpe control mice were used as controls.

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Pancreatic tissue of 9 week old mice with genotypes Ptf1a-Cre;LSL-KrasG12D and Ptf1a-Cre;LSL-KrasG12D;Ptpn11fl/fl

Project description:To investigate the role of SHP2 (Ptpn11) in pancreatic carcinogenesis, murine pancreatic whole tissue RNA samples of 9 week old mice with the genotypes Ptf1a-Cre;LSL-KrasG12D (ID-labels Kxxx) and Ptf1a-Cre;LSL-KrasG12D;Ptpn11fl/fl (ID-labels Mxxxx) were analyzed by microarray.

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EGFR controls transcriptional and metabolic rewiring in KRASG12D colorectal cancer

Project description:We used RNA-Seq to profile APCmin, KRASG12D, TP53 murine organoids in the presence and absence of EGFR.

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The Transcriptome Of Cmml Monocytes Is Highly Inflammatory And Reflects Leukemia-Specific And Age-Related Alterations

Project description:Chronic myelomonocytic leukemia (CMML) is an aggressive myeloid neoplasm of older individuals characterized by persistent monocytosis. Somatic mutations in CMML are heterogeneous and only partially explain the variability in clinical outcomes. Recent data suggest that cardiovascular morbidity is increased in CMML and contributes to reduced survival. Clonal hematopoiesis of indeterminate potential (CHIP), the presence of mutated blood cells in hematologically normal individuals, is a precursor of age-related myeloid neoplasms and associated with increased cardiovascular risk. To isolate CMML-specific alterations from those related to aging, we performed RNA sequencing and DNA methylation profiling on purified monocytes from CMML patients and from age-matched (old) and young healthy controls. We found that the transcriptional signature of CMML monocytes is highly pro-inflammatory, with upregulation of multiple inflammatory pathways, including tumor necrosis factor, IL-6 and IL-17 signaling, while age per se does not significantly contribute to this pattern. We observed no consistent correlations between aberrant gene expression and CpG island methylation, suggesting that pro-inflammatory signaling in CMML monocytes is governed by multiple and complex regulatory mechanisms. We propose that pro-inflammatory monocytes may contribute to cardiovascular morbidity in CMML patients, and promote progression by selection of mutated cell clones. Our data raise questions whether asymptomatic CMML patients may benefit from monocyte-depleting or anti-inflammatory therapies.

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miRNA expression data from the hearts of murine myocardial infarction model

Project description:Sexual dimorphisms are well recognized in various cardiac diseases, including myocardial infarction (MI). MI develops later in women, but once established, it contributes more persistent symptoms and higher mortality than in men. Similar observations have been reported in murine model of MI. Although mRNA-level sexual dimorphism of MI have been reported, whether miRNA transcriptome also confers such dimorphism remains unknown. Comprehensive understanding of the mRNA- and miRNA-level genetic programs underlying the heart sexual dimorphisms will expectedly improve clinical outcome by facilitating the development of gender specific treatment strategies. Here, by conducting miRNA microarray analysis of murine MI model samples, we set out to characterize the heart sexual dimorphisms at the level of miRNA transcriptome

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Project description:We used RNA-Seq to profile APCmin, KRASG12D, TP53 murine organoids in the presence and absence of EGFR and additional deletion of SMOC2.

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NFATc1 cooperates with KrasG12D to promote pancreatic carcinogenesis.

Project description:Primary murine pancreatic cancer cells (referred to as NKC cells) derived from transgenic mice with pancreas-specific constitutive activation of NFATc1 and KrasG12D mutation in the presence or absence of NFATc1 expression were analyzed for target gene signatures.

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KRASG12D Transforms Murine B-Cell Progenitors and Causes Aggressive ALL in Vivo

Project description:KRASG12D Transforms Murine B-Cell Progenitors and Causes Aggressive ALL in Vivo

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