DNA repair in tumor cells from the variant form of xeroderma pigmentosum.
Cells from most patients with xeroderma pigmentosum (XP) can be shown to be defective in repairing ultraviolet (UV) light-induced damage to their DNA, for they have a reduced rate of UV-induced thymidine incorporation.  XP variants, however, have clinical manifestations of XP, but all their tissues tested to date have a normal rate of UV-induced 3H-thymidine incorporation. We have now tested tumor cells from an XP variant and from a typical XP patient.  The variant's tumor cells, in contrast to those of the typical patient, had no detectable defect in their UV-induced thymidine corporation.  We conclude, therefore, that the cells that formed tumors in this XP variant resemble his other cells in DNA repair capacity, and do not represent a minor cell population with the kind of DNA repair defect that is reflected in reduced UV-induced thymidine incorporation.
D001345:Autoradiography; D002280:Basal Cell Carcinoma / Q000378:metabolism*; D002478:Cells, Cultured; D004247:DNA / Q000528:radiation effects*; D004260:DNA Repair; D006801:Humans; D011830:Radiation Effects; D012878:Skin Neoplasms / Q000378:metabolism*; D013936:Thymidine / Q000378:metabolism; D014316:Tritium; D014466:Ultraviolet Rays; D014983:Xeroderma Pigmentosum / Q000378:metabolism*
D014316:Tritium; D004247:DNA; D013936:Thymidine