Project description:Transcriptional profiling Myc-driven lymphomas to determine pathways by which Wrn deficiency impairs tumor development Total RNA isolated from Eµ-Myc and Eµ-Myc Wrn Δhel/Δhel murine B-cell lymphomas (n=4)
Project description:Therapy-induced senescence associates with expression of lineage-aberrant transcript profiles. Spi1, Cebpb and Jun encode important hematopoietic transcription factors. To investigate their impact on lineage-adherence in therapy-induced senescence of B-cell lymphomas, we engineered several senescence-susceptible and senescence-deficient individual primary, murine Eµ-myc lymphomas overexpressing Bcl2, in which each target gene has been knocked down by shRNA. We then treated lymphomas with adriamycin (doxorubicin) to induce senescence and performed gene expression analysis using data obtained from RNA-seq of the individual lymphoma samples.
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:Induction of apoptosis by the tumor suppressor p53 is known to protect from Myc-driven lymphomagenesis. The p53 family member p73 is also a pro-apoptotic protein, which is activated in response to oncogenes like Myc. We therefore investigated whether p73 provides a similar protection from Myc-driven lymphomas as p53. To generate B-cell lymphomas with defined genetic alterations in p53 or p73, we crossed the Eµ-Myc transgenic to mice heterozygous for germ-line deletions in p53 (p53+/) or p73 (p73+/-). Lymphomas which have spontaneously developed in Eµ-Myc transgenic animals with the genotypes p53+/+, p53+/-, p73+/+, p73+/- or p73-/- were isolated when the animals were moribund and further processed for gene expression profiling with 22.5K cDNA microarrays.
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.
Project description:Smchd1 appears to act as a tumour suppressor in the Eµ-Myc B cell lymphoma model. We find gene expression differences are most pronounced in the premalignant cells, and observe more variability in end stage lymphomas. We always detect a small number of clustered genes and imprinted genes as differentially expressed, along with others involved in tumorigenesis. The microarrays compared Smchd1 null and Smchd1 wildtype samples from end stage lymphomas. All lymphomas are on the C57BL/6 background and carry the Eµ-Myc transgene, and Smchd1 null samples are additionally homozygous for a Smchd1 genetrap allele.
