A novel and promising target for cancer therapy is the ribonucleoprotein molecule, telomerase, which functions to maintain the ends of chromosomes. Normally, human telomeres shorten with each round of cell division ultimately resulting in chromosome instability and cellular senescence. Not typically observed in human somatic tissue, the vast majority of human cancers have been shown to express telomerase. It is believed that this is why cancerous cells are able to undergo an infinite number of divisions, while normal cells have a finite replicative potential. Although telomerase expression is associated with malignancy it is remains unknown whether telomerase expression is critical for malignant conversion. In the present experiment it was hypothesized that telomerase activation is an important step in malignant transformation and therefore should occur early in carcinogenesis. To test this the development of lung cancer was modeled by inducing carcinogenesis in cultured human lung fibroblast cells through exposure to a potent lung carcinogen, benzo [a] pyrene (BaP) for a period of six weeks during which both telomerase activity and the expression of a molecular marker (p53) associated with the early stages of cancer were assayed on a weekly basis. Controls included both BaP treated malignant, as well as untreated normal and malignant human lung fibroblasts. It was predicted that levels of p53 would increase in normal human lung fibroblast cells treated with BaP, but not in control cultures unexposed to the carcinogen. It was further expected that telomerase activity would be induced in BaP treated normal human lung fibroblast cells, but not in untreated control cultures. Results, however, for both the p53 and telomerase assays were ambiguous making it impossible to determine whether or not carcinogesis was induced, and whether telomerase activation is associated with this process. Due to the lack of valid data, the hypothesis was not tested and no interpretation or inferences relative to telomerase excision early in carcinogenesis could be made.