Chromosomal radiosensitivity during the G2 cell cycle period and cytopathology of human normal x tumor cell hybrids

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....

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Veröffentlicht in:Cancer research (Chicago, Ill.) Ill.), 1986-04, Vol.46 (4 Pt 2), p.2045-2049
Hauptverfasser: Sanford, K K, Parshad, R, Stanbridge, E J, Frost, J K, Jones, G M, Wilkinson, J E, Tarone, R E
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container_end_page 2049
container_issue 4 Pt 2
container_start_page 2045
container_title Cancer research (Chicago, Ill.)
container_volume 46
creator Sanford, K K
Parshad, R
Stanbridge, E J
Frost, J K
Jones, G M
Wilkinson, J E
Tarone, R E
description 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.
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source MEDLINE; American Association for Cancer Research; EZB Electronic Journals Library
subjects Cell Line
Chromatids - radiation effects
Chromosomes, Human - radiation effects
HeLa Cells
Humans
Hybrid Cells - pathology
Hybrid Cells - ultrastructure
Interphase
Neoplasms - genetics
Neoplasms - pathology
title Chromosomal radiosensitivity during the G2 cell cycle period and cytopathology of human normal x tumor cell hybrids
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