G(2) RADIOSENSITIVITY OF CELLS DERIVED FROM CANCER-PRONE INDIVIDUALS

The potential of enhanced chromatid damage, observed after X-irradiation of G(2) phase, has been used to detect individuals genetically predisposed to cancer, utilising fibroblasts/lymphocytes from these patients as well as fibroblasts derived from human tumours. Fibroblasts and/or lymphocyte samples of two autosomal recessive syndromes (xeroderma pigmentosum (XP), Fanconi's anaemia (FA)) and one congenital or acquired disorder, aplastic anaemia (AA), were employed for the G(2) radiosensitivity assay. In addition, we have estimated the frequencies of spontaneously occurring chromosomal aberrations as well as G(2) radiosensitivity of eight samples of fibroblasts/fibroblast-like cells (two normal, two colorectal carcinoma, two Wilms' tumour, one retinoblastoma and one polyposis coli), and three samples of lymphocytes (two normal and one from a lymphoma patient). The results obtained indicate that there were no differences between fibroblast cells derived from patients or tumours, except FA patients, in the frequency of spontaneously occurring chromosomal aberrations when compared to normal cells. Following X-irradiation we did not observe any significantly increased G(2) radiosensitivity in FA and XP cells. Lymphocytes from AA and lymphoma patients, and all tumour cell lines except retinoblastoma, responded with increased frequencies of aberrations following G(2) X-irradiation in comparison to cells derived from normal individuals. In our hands, the G(2) sensitivity assay could not always discriminate cells from cancer-prone individuals from those of controls.