Central to understanding the causes and mechanisms regulating cancer requires us to determine how cells grow and divide. Normal healthy cells have a limited life-span. Following a number of divisions, healthy aging cells will enter a protective arrested state, called senescence. Here they remain viable and metabolically active yet unable to grow and divide. Cells which become damaged or have inadequate growth conditions are also able to temporarily stop growing until the situation is repaired or the cell is removed from the healthy population. These are extremely important mechanisms in preserving genomic integrity, acting as a barrier in the pathway of malignancy. Determining how these barriers are overcome will reveal pivotal events in the earliest steps of cancer development. This project focuses on elucidating the role of a protein, Spy1A, in overcoming these protective cellular barriers. Spy1A is a protein known to play a role in cell growth and division and it has been found at high levels in some invasive forms of cancer. Our data demonstrates that when Spy1A levels are high, cells are no longer able to cease dividing and enter into senescence; hence these cells are at risk of becoming malignant. Understanding how the Spy1A protein regulates cellular decisions, during normal aging processes and following damage to the cell, will provide new promise toward understanding the development and progression of many forms of cancer, and may result in new drug design and/or new prognostic markers for treatment.