A key hallmark of colorectal cancer progression is genomic instability, with chromosomal aneuploidy frequently observed. Based on previous work in our laboratory and elsewhere, specific aneuploidy has been shown to occur before the transition to invasive disease. These genomic imbalances are maintained when cells metastasize and are conserved in cells lines derived from primary tumors. A constant selective pressure to maintain these specific aneuploid cells suggests a vital role in cancer tumorigenesis. However, it remains unknown what impact these genomic balances have on the transcriptome of cancer cells.

In order to address the question of aneuploidy, our lab has generated artificial trisomies to determine what effect these would have on the transcriptome. We are interested in further utilizing these cell lines in our studies to identify the role of aneuploidy-driven gene expression changes in tumorigenesis. We are also interested in elucidating the consequences of tumorigenesis on the 3D architecture of chromosomes and exploring its impact on transcriptional activity.