A number of genes have been identified as inducible in mammalian cells by agents that cause DNA damage and growth arrest.

Spiro speculated that the embryonic muscle development he had seen in the boy was due to growth arrest during the myotubular phase, causing the myopathy.

This differentiation process does not require the addition of retinoic acid, but takes place spontaneously when cultures are grown to high density and undergo growth arrest.

Violation during reconstruction can lead to growth arrest or asymmetric growth.

But the interpretation of these findings was not straightforward, because high levels of p53 induce growth arrest without apoptosis in other cells.

Sulforaphane and its metabolite mediate growth arrest and apoptosis in human prostate cancer cells.

Once growth arrest has been achieved, it is irreversible.

The over-expression of p73 in cultured cells promotes a growth arrest and/or apoptosis similarly to p53.

The activation of p53 by these diverse stimuli can initiate either growth arrest or apoptosis depending on the cellular context [ 1, 2, 3].

By inducing normally untreatable malignant cells into growth arrest, the patient would be able to survive in a chronic asymptomatic condition.