Bulent Cetin

Bulent Cetin


University of Oxford (Ph.D); Bogazici University (B.Sc.)

Aneuploidy (chromosomal abnormalities) and centrosome copy number abnormalities (often as centrosome amplification) are among the common features cancer cells. Yet duplication of centrosomes and chromosomes strictly once per cell division cycle and equal partitioning of duplicates to daughter cells during mitosis is essential for health and life. Whether aneuploidy and centrosome amplification is a cause or a consequence of cellular transformation is a matter of active debate and research. On the other hand, introducing chromosomal or centrosomal abnormality to otherwise normal cells causes activation of checkpoints that lead to senescence or apoptosis. Cancer cells possess additional mutations that silence such checkpoint signals for their uninhibited growth.

What if cancer cells are challenged further with additional chromosomal abnormalities and centrosome amplification?

I am using small molecule inhibitors against mitotic kinases such as Plk4 and Aurora B, which further complicate mitoses of cancer cells, in other words, fooling them in their own game. In addition I am using other small molecule inhibitors to target their pro-survival strategies, which effectively kill these mitotically challenged cancer cells.