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Please use this identifier to cite or link to this item: http://hdl.handle.net/1993/3187

Title: Mechanisms of c-Myc dependent genomic instability
Authors: Louis, Sherif
Supervisor: Mai, Sabine (Physiology, Medicine)
Examining Committee: Duckworth, Mary Lynn (Physiology), Severini, Alberto (Medical Microbiology), Shiu, Bob (Physiology), Drouin, Regen (Genetics, U of Sherbrook)
Graduation Date: October 2009
Keywords: Genomic instability
Gene amplification
Oncoproteins
Telomeres
Issue Date: 3-Sep-2009
Citation: Louis, SF (2005). c-Myc induces chromosomal rearrangements through telomere and chromosome remodeling in the interphase nucleus 102(27):9613-8
Abstract: Cancer is a disease that involves genomic instability, to which c-Myc contributes during its initiation and progression. Over 70% of all human cancers show deregulated levels of c-Myc protein. The term genomic instability refers to genetic and/or epigenetic changes that alter the normal organization and function of genes and chromosomes. Genomic instability is a hallmark of cancer and often is associated with cancer. Deregulated c-Myc expression generates genomic instability by initiating intra- and extrachromosomally locus-specific gene amplification, gene rearrangements and karyotypic instability that includes translocations, fusions, insertions and deletions. Out of the several outlined pathways by which deregulated levels of c-Myc can lead to genomic instability, the work described in this thesis focuses on three with direct relevance to tumorigenesis; gene amplification (increase in gene copy number), remodeling of the chromosomal and telomeric structures in the interphase nucleus and comparing the effect of Myc to that of Epstein Bar virus (EBV) infection in remodeling the nuclear structure that may lead to genomic instability.
URI: http://hdl.handle.net/1993/3187
Appears in Collection(s):FGS - Electronic Theses & Dissertations (Public)

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