May 2013

Document Type


Degree Name



Dept. of Cell and Developmental Biology


Oregon Health & Science University


The majority of human cancers display a wide range of genetic abnormalities, including changes in chromosome number and structure, that are essentially nonexistent in normal tissue. While some of these abnormalities directly affect genes involved in cell growth and survival, the vast majority play an unknown role in carcinogenesis. It has been shown that certain chromosomal rearrangements present in tumor cells display a significant delay in replication timing (DRT) and a subsequent delay in mitotic chromosome condensation (DMC). Importantly, these chromosomes are very unstable and undergo frequent rearrangements, resulting in an overall increase in the rate of mutagenesis. The Thayer lab has proposed that DRT/DMC is caused by the disruption of a cis-acting ‘inactivation/stability center’ (I/S center) that functions to maintain proper replication timing, mitotic chromosome condensation, monoallelic gene expression and stability of individual chromosomes. To date, two chromosomal loci,




School of Medicine



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