Carla Finkielstein, Ph.D.

When a cell’s repair system is impaired, cancerous mutations accumulate – particularly if those mutations involve the network of genes that regulate cellular repair and tumor suppression. These mutations disrupt the clock mechanism that keeps cells running in a 24-hour cycle and, as a result, cell division occurs at unscheduled times throughout the day. Left unchecked, cancerous cells are permitted to grow and divide at their own pace, resulting in tumors.

In a series of studies by the Finkielstein lab, her team reported the unexpected link between a key circadian protein responsible for keeping the cell’s molecular clock running, a tumor suppressor molecule that makes sure cells do not carry harmful mutations when they divide, and an oncogene that influences the speed of the cell’s clock. These findings emphasize the important relationship between the molecular circadian clock and key catalysts involved in cancer initiation and progression.

Finkielstein’s research offers a critical foundation for the emerging field of chronotherapeutics – the study of time-of-day medicine. This new discipline integrates the cellular and molecular biology of circadian rhythms to inform decision-making about when a therapeutic should be administered to yield the best results.