Project description:Neuroblastoma is an embryonal tumor arising from the neural crest. It can be mimicked in mice by neural crest-specific overepxression of oncogenes such as MYCN or mutated ALK. Expression profiling of murine neuroblastoma driven by MYCN were compared to those driven by mutated ALK and to mouse normal adrenal tissue.
Project description:Transcriptional profiling of mouse Prostate cancer cells comparing Pbsn-Cre LSL-KrasG12D P53L/L cells with Pbsn-Cre LSL-BrafV600E P53L/L cells, and to determine the effects of Kras or Braf mutantion on murine PCa gene expression.
Project description:Pediatric glioma of the subclass MYCN are highly aggressive tumors frequently carrying MYCN amplifications, TP53 mutations, or both alterations. In order to understand the biology of these tumors better and to improve treatment options, we generated a genetically engineered model by breeding hGFAP-cre::TP53Fl/Fl::lsl-MYCN mice. All such mice developed aggressive forebrain tumors early in lifetime that mimic their human counterparts regarding histology, DNA methylation, and gene expression.
Project description:Pediatric glioma of the subclass MYCN are highly aggressive tumors frequently carrying MYCN amplifications, TP53 mutations, or both alterations. In order to understand the biology of these tumors better and to improve treatment options, we generated a genetically engineered model by breeding hGFAP-cre::TP53Fl/Fl::lsl-MYCN mice. All such mice developed aggressive forebrain tumors early in lifetime that mimic their human counterparts regarding histology, DNA methylation, and gene expression.
Project description:Pediatric glioma of the subclass MYCN are highly aggressive tumors frequently carrying MYCN amplifications, TP53 mutations, or both alterations. In order to understand the biology of these tumors better and to improve treatment options, we generated a genetically engineered model by breeding hGFAP-cre::TP53Fl/Fl::lsl-MYCN mice. All such mice developed aggressive forebrain tumors early in lifetime that mimic their human counterparts regarding histology, DNA methylation, and gene expression.
Project description:Pediatric glioma of the subclass MYCN are highly aggressive tumors frequently carrying MYCN amplifications, TP53 mutations, or both alterations. In order to understand the biology of these tumors better and to improve treatment options, we generated a genetically engineered model by breeding hGFAP-cre::TP53Fl/Fl::lsl-MYCN mice. All such mice developed aggressive forebrain tumors early in lifetime that mimic their human counterparts regarding histology, DNA methylation, and gene expression.
Project description:Pediatric glioma of the subclass MYCN are highly aggressive tumors frequently carrying MYCN amplifications, TP53 mutations, or both alterations. In order to understand the biology of these tumors better and to improve treatment options, we generated a genetically engineered model by breeding hGFAP-cre::TP53Fl/Fl::lsl-MYCN mice. All such mice developed aggressive forebrain tumors early in lifetime that mimic their human counterparts regarding histology, DNA methylation, and gene expression.
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.
Project description:Notch intracellular domain (NICD) is the active form of the Notch receptor. In this mouse model, NICD is inserted in the Rosa26 locus downstream of a loxP-STOP-LoxP (lsl) sequence and therefore NICD expression is dependant on Cre recombinase expression (Mono transgenic control Rosa26-lsl-NICD) . These mice are crossed with the AFP-Cre strain that expresses Cre in hepatoblasts due to its regulation by the AFP promoter and albumin enhancer (Double transgenic mutant AFP-Cre/Rosa26-lsl-NICD). Newborn mice at day 0 and day 2 are sacrificed and liver RNA samples from control monotransgenic Rosa26-lsl-NICD and from bitransgenic AFP-Cre/Rosa26-lsl-NICD (AFP-NICD) are obtained. Whole genome expression profiling of these samples is submitted.
