Specialized proteins called cell cycle regulators, such as p$53$ and p$21,$ regulate the progression of the cell cycle from one phase to the next. This progression through the checkpoints is strictly regulated and usually works without error. When errors do occur, they can have catastrophic consequences, including cancer.

How did this study lend new evidence to our understanding of how genes regulate the cell cycle, giving us a better chance of developing successful cancer treatments?

Mutations in the $p53$ and $p21$ genes play a crucial role at the $S$ checkpoint of the cell cycle, preventing cells with DNA damage from entering mitosis. Targeting therapies to these proteins could improve efficacy of treatment.

All cells deficient in p $53$ and p$21$ proteins proceed to mitosis after radiation exposure, and the cells have a DNA content that differs from what would be expected. This chromosomal abnormality can be exploited in the development of targeted treatments.

Mutations in the $p53$ and $p21$ genes lead to checkpoint deficits, specifically the $G_2-M$ checkpoint, linked to multiple types of cancer. These checkpoint deficits can be exploited in the development of targeted treatments.