One of the main properties of cancer cells is their increased and deregulat
ed proliferative activity. It is now well known that abnormalities in many
positive and negative modulators of the cell cycle are frequent in many can
cer types, including breast carcinomas. Abnormalities such as defective fun
ction of the retinoblastoma gene and cyclin-dependent kinase inhibitors (fo
r example, p16, p21, and p27), as well as upregulation of cyclins, are ofte
n seen in breast tumours. These abnormalities are sometimes coincidental, a
nd newly described interplays between them suggest the existence of a compl
ex regulatory web in the cell cycle.