This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Sanford, K. K. Articles by Tarone, R. E. Search for Related Content PubMed PubMed Citation Articles by Sanford, K. K. Articles by Tarone, R. E.

Chromosomal Radiosensitivity during the G₂ Cell Cycle Period and Cytopathology of Human Normal x Tumor Cell Hybrids¹

Laboratory of Cellular and Molecular Biology [K. K. S., G. M. J.] and Biostatistics Branch [R. E. T.], National Cancer Institute, Bethesda, Maryland 20892; Department of Pathology, Howard University College of Medicine, Washington, DC 20059 [R. P.]; Department of Microbiology, College of Medicine, University of California, Irvine, California 92717 [E. J. S., J. E. W.]; and Division of Cytopathology, Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205 [J. K. F.]

The relationship between tumorigenicity and enhanced chromosomal radiosensitivity during the G₂ cell cycle phase was examined through the use of nontumorigenic human cell hybrids and their nontumorigenic and tumorigenic segregants. The hybrid cells were produced by fusion of a normal and tumor cell. The parental lines, including HeLa and three fibroblast lines, one of skin and two of fetal lung origin, were also examined. The tumorigenic lines, which had cytological features associated with clinical cancer, showed a significantly higher incidence of chromatid breaks and gaps following X-irradiation during G₂ than the normal skin line or the nontumorigenic hybrids. The hybrids and their nontumorigenic subclones had cytological features which are predominantly found with a benign clinical course and had the G₂ chromosomal radiosensitivity more characteristic of the normal parental cells. Like tumorigenic cells, fetal cells exhibited enhanced G₂ chromosomal radiosensitivity which could be suppressed in fetal x tumor cell hybrids. This observation suggests that the molecular basis for radiosensitivity in fetal cells differs from that of tumor cells. The enhanced G₂ chromosomal radiosensitivity of a tumor cell, which appears to result from deficient DNA repair, is suppressed by fusion with a normal cell. Thus, the radiosensitivity, like tumorigenicity, behaves as a recessive trait. Although a Mendelian analysis is not possible with this material, the segregation of enhanced G₂ chromosomal radiosensitivity with the neoplastic phenotype suggests that the two may be genetically linked.

¹ The part of this project carried out at the University of California was supported by NIH Grant CA 19401.

Received 8/15/85. Revised 11/26/85. Accepted 12/11/85.