Areas of Expertise (8)
Institute of Cancer Research, University of London: PhD, Cancer Biology: The Role of c-Myb During T Cell Activation
University of Cambridge: MA, Biological Natural Sciences, Biochemistry, Chemistry, Molecular Biology, Pathology and Physiology
- Dr Bessie F Lawrence International Summer Science Institute Alumna
Media Appearances (1)
Toronto scientist creates first living 3D pancreas model
The Toronto Star print
The goal of the research, funded by a $200,000 grant from the Canadian Cancer Society, is to eventually find clues for early detection.
Unlike breast cancer, there is no way to screen for pancreatic cancer. And because the vast majority of patients don’t survive, few people are around to campaign for more research and funding, said Dr. Mary Argent-Katwala, director of research at the Canadian Cancer Society.
“It’s a vicious cycle,” she said. “It has been very challenging to crack the science behind the tumor.”
Important biological and pathological properties are often conserved across species. Although several mouse leukemia models have been well established, the genes deregulated in both human and murine leukemia cells have not been studied systematically. We performed a serial analysis of gene expression (SAGE) analysis on gene expression in both human and murine MLL-ELL or MLL-ENL leukemia cells, and identified 88 genes that appeared to be significantly deregulated in both types of leukemia cells, including 57 genes not reported previously as being deregulated in MLL-associated leukemias...
The c-myb gene encodes a transcription factor required for the normal development of T cells in the thymus, and for subsequent peripheral T-cell activation and survival. However, the profile of genes known to be transcriptionally regulated by c-Myb in T cells does not adequately explain the pleiotrophic nature of the effects of c-Myb. We present here a detailed molecular characterization of the regulation of a novel target gene, the histone variant H2A.Z. We show that c-Myb is able to bind to and activate the H2A.Z promoter in T cells both in vitro and in vivo, and present evidence that perturbation of Myb activity during T-cell development results in reduced H2A.Z expression. As H2A.Z is absolutely required for the early stages of mammalian development, and plays essential roles in the regulation of chromatin structure in gene promoters in yeast, its regulation by c-Myb is likely to be of some importance during T-cell development.