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Toxicologic Pathology
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In Vitro Models for Studying the Molecular Biology of Carcinogenesis

Joseph A. DiPaolo

Laboratory of Biology, Division of Cancer Etiology, National Cancer Institute, Bethesda, Maryland 20892

Anne Burkhardt

Laboratory of Biology, Division of Cancer Etiology, National Cancer Institute, Bethesda, Maryland 20892

Jay Doniger

Laboratory of Biology, Division of Cancer Etiology, National Cancer Institute, Bethesda, Maryland 20892

Lucia Pirisi

Laboratory of Biology, Division of Cancer Etiology, National Cancer Institute, Bethesda, Maryland 20892

Nicholas C. Popescu

Laboratory of Biology, Division of Cancer Etiology, National Cancer Institute, Bethesda, Maryland 20892

Shigeru Yasumoto

Laboratory of Biology, Division of Cancer Etiology, National Cancer Institute, Bethesda, Maryland 20892

Although carcinogens cause various similar deleterious effects on rodent and human cells, only rodent cells can convert to malignancy in a quantitative, predictable fashion. Therefore, the control mechanisms involving indefinite proliferation and tumorigenicity are different. Human cell lines may exhibit normal or aneuploid chromosome constitutions with numerical or structural alterations frequently involving proto-oncogene loci, but fail to produce progressively growing tumors in nude mice. A new approach for obtaining human cells susceptible to malignant transformation by chemical or physical carcinogens is to use DNA from a cancer associated virus. Transfection of human papilloma virus (HPV) DNA associated with genital cancer can extend life-span of human cells; post-X-irradiated cells grow in agar suspension. Southern blot analysis of extracted DNA indicates that HPV sequences persist. Similar results are obtained with human fibroblast and epithelial cells.

Toxicologic Pathology, Vol. 14, No. 4, 417-423 (1986)
DOI: 10.1177/019262338601400406
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