Project description:We used gene expression data from Eµ-myc mouse lymphomas to test various genomic signatures and select lymphomas for further study When Eµ-myc mice had evidence of lymphoma and/or ill appearance, they were humanely sacrificed and dissected. Lymphoma tissue was obtained and flash frozen in liquid nitrogen. Lymphoma was dissociated into a single cell suspension, and cell pellets were frozen. Later, lymphoma tissue or cells were homogenized, and RNA was extracted. Gene expression microarrays were performed with the isolated RNA.
Project description:We used gene expression data from Eµ-myc mouse lymphomas to test various genomic signatures and select lymphomas for further study When Eµ-myc mice had evidence of lymphoma and/or ill appearance, they were humanely sacrificed and dissected. Lymphoma tissue was obtained and flash frozen in liquid nitrogen. Lymphoma and spleens were dissociated into single cell suspensions, and cell pellets were frozen. Later, lymphoma tissue or cells were homogenized, and RNA was extracted. Gene expression microarrays were performed with the isolated RNA.
Project description:We used gene expression data from Eµ-myc mouse lymphomas to perform unsupervised analyses that identified two lymphoma subgroups. We also used this data to develop a genomic signature to classify new lymphomas. When Eµ-myc mice had evidence of lymphoma and/or ill appearance, they were humanely sacrificed and dissected. Lymphoma tissue was obtained and flash frozen in liquid nitrogen. Later, lymphoma tissue was homogenized, and RNA was extracted. Gene expression microarrays were performed with the isolated RNA.
Project description:Impact of CDK4-deficiency on Eµ-myc driven B-lymphoma By crossing mating CDK4 Knockout mice with Eµ-myc mice,We found CDK4-deficiency enhances the Eµ-myc induced B-lymphoma.We further to discover the molecular mechanism
Project description:Purpose: In this study we sought to elucidate whether Gcn5 cooperates with Myc to induce the formation of lymphoma using an in vivo model, the Eµ-Myc mouse. In order to define the molecular mechanisms for how Gcn5 contributes to lymphoma development upon overexpression of Myc, we performed RNA-seq analyses on total RNA isolated from CD19+ B cells sorted from spleens of 5-6-week-old wild-type, Eµ-Myc, and Eµ-Myc; Gcn5Fx/Fx mice. Conclusions: Loss of Gcn5 not only ameliorates dysregulation of the cell cycle caused by Myc overexpression, but also affects Myc-induced pathways related to cancer cell growth.
