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Cyclin-dependent kinase inhibitors play a critical role in regulating progression of the eukaryotic cell through the cell cycle by associating with protein complexes composed of cyclins and cyclin-dependent kinases and thus downmodulating the activity of the cyclindependent kinases(1). Pathways involving cyclin-dependent kinase inhibitors are frequently disrupted in cancer cells, and this disruption leads to abnormal regulation of the cell cycle. Overexpression of cyclin-dependent kinase inhibitors leads to the arrest of cells at one of the checkpoints in the cell cycle (2). Therefore, using cyclindependent kinase inhibitors for gene therapy of cancer is intuitively attractive because it has the potential to inhibit tumor growth(3). Thus far, adenoviral vectors expressing the cyclin-dependent kinase inhibitors p16 INK4A and p21 have been evaluated in preclinical models for their suitability for gene therapy of cancer (3–9). We have constructed an adenoviral vector expressing p27 Kip1 and observed that it is statistically significantly better at causing growth arrest in several breast cancer cell lines than is another adenoviral vector that expresses p21 waf1/cip1

Adenoviral Expression of the Cyclin-Dependent Kinase Inhibitor p27Kip1: a Strategy for Breast Cancer Gene Therapy