Project description:KHR and KR tumors grow faster when deficient for Notch1. The hypothesis was to test for differences in gene expression between KHR and KHR oral tumors with intact or deficient Notch1 haplotypes. Total RNA was isolated for KHR (n=5), KHR-N+/- (n=4), KHR-N-/- (n=5), KR-N+/- (n=5), KR-N-/- (n=4) oral tumors. Expression profiling was performed using the Illumina MouseRef-8 v2 (GPL6885) array. Studies were conducted using tumors from C57BL/6 mice.
Project description:KHR and KR tumors grow faster when deficient for Notch1. The hypothesis was to test for differences in gene expression between KHR and KHR oral tumors with intact or deficient Notch1 haplotypes.
Project description:kRas (KR) tumors grow faster when expressing kRas and HPV E6E7 (KHR). The hypothesis was to test for differences in gene expression between KR and KHR oral tumors.
Project description:We created mice, which are deficient for Myc specifically in cardiac myocytes by crossing crossed Myc-floxed mice (Mycfl/fl) and MLC-2VCre/+ mice. Serial analysis of earlier stages of gestation revealed that Myc-deficient mice died prematurely at E13.5-14.5. Morphological analyses of E13.5 Myc-null embryos showed normal ventricular size and structure; however, decreased cardiac myocyte proliferation and increased apoptosis was observed. BrdU incorporation rates were also decreased significantly in Myc-null myocardium. Myc-null mice displayed a 3.67-fold increase in apoptotic cardiomyocytes by TUNEL assay. We examined global gene expression using oligonucleotide microarrays. Numerous genes involved in mitochondrial death pathways were dysregulated including Bnip3L and Birc2. Keywords: wildtype vs Myc-null
