Human papillomavirus (HPV), especially HPV types 16, 18, and 33, play an important role in the development of cervical cancer.^1–3 We,^4,5 as well as others,^6–9 have shown that DNA from these HPV types immortalize cultured human foreskin keratinocytes (HKc) and human cervical cells. HPV 16-immortalized HKc (HKc/HPV16) represent an attractive in vitro model system to study the process of multistep carcinogenesis in human cells, and for identifying agents that can modify or prevent HPV-induced transformation, since they undergo malignant conversion through four phenotypically defined “steps” or stages. Although immortal, HKc/HPV 16 are not tumorigenic and retain many features characteristic of normal HKc, including a requirement for epidermal growth factor (EGF) and bovine pituitary extract (BPE) for proliferation.^4,5 In the next step of this progression model, growth factor independent sublines, HKc/GFI, that no longer require EGF and BPE for proliferation, are selected from HKc/HPV16.^5,10 Next, sublines that no longer respond to calcium and serum-induced differentiation, HKc/DR, are selected from HKc/GFI.⁵ In the final step, malignant conversion of HKc/DR is achieved by transfection with viral Harvey ras (v-Ha-ras) or herpes simplex virus type 2 DNA.^11,12 The steps from immortalized HKc/HPV16 to malignant conversion are highly reproducible and at each step the cells progressively acquire phenotypic and biochemical characteristics similar to those found in cell lines established from human tumors.¹⁰