Alterations in growth properties of human papilloma virus type 16 immortalised human cervical keratinocyte cell line correlate with amplification and overexpression of c-myc oncogene.

Clinical and epidemiological data support a role for human papilloma virus (HPV) type 16 in the pathogenesis of cervical carcinoma. The W12 cell line contains HPV16 sequences, predominantly as a high copy number episome, and is immortalised in vitro, but non-tumourigenic. A morphologically distinct sub-line of the parental W12 cell line was isolated which displayed increased growth rate, increased capacity for self-renewal and increased resistance to differentiation in comparison with the parental W12 cell line. The structure and expression of the HPV16 sequences was virtually identical in the two cell lines. However, expression of the c-myc proto-oncogene was elevated in the morphologically distinct sub-line, and this was associated with amplification, but not rearrangement, of the c-myc locus. Karyotype analysis demonstrated that amplification of the c-myc locus was a result of duplication of the long arm of chromosome eight.