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Our research aims to determine the molecular mechanisms underlying the effects of aneuploidy (an abnormal number of chromosomes) on cellular physiology. The motivation to understand how cells respond to aneuploidy comes from the fact that cancer cells almost always harbor chromosome numbers higher than the normal count of 46. Despite aneuploidy being a hallmark feature of cancer cells, its role in tumorigenesis remains poorly understood. Recently, our studies showed that acquiring one extra copy of any chromosome lowers cellular fitness and proliferation. However, despite being aneuploid, a hallmark of cancer cells is unlimited proliferation potential. Therefore, we hypothesize that cancer cells must evolve and adapt to overcome the negative consequences of aneuploidy to cellular fitness. See our publications where we discovered that mutations in genes that regulate protein stability (Dephoure et al. 2014) or cellular metabolism (Hwang et al. 2017, 2019) improve aneuploid cells' cellular fitness.

Another reason why studying the consequences of aneuploidy is relevant to human health is that the most common genetic disease in humans is Down syndrome. Individuals born with an extra copy of chromosome 21 (a total of 47 chromosomes) have Down syndrome. Most research related to Down syndrome has focused on identifying the mechanisms by which a third copy of a given gene on chromosome 21 causes disease. We recently showed that cells with three copies of chromosome 21 have cellular defects associated with aneuploidy. These defects are present in human, mouse, or yeast cells that harbor an extra chromosome. Therefore, we hypothesize that in addition to increased activity of genes on chromosome 21, the consequences of aneuploidy on cellular physiology are essential to understand better how an extra copy of 21 causes Down syndrome. See our latest publication on this topic (Hwang et al. 2021)!