The increased HPRT mutation frequency is more reminiscent of data from patients with xeroderma pigmentosum, a disease characterized by UV sensitivity and deficiency in the nucleotide excision pathway of DNA repair.
Circulating lymphocytes from patients with the DNA-repair-deficient disorders, xeroderma pigmentosum (XP) and ataxia telangiectasia (A-T) have elevated frequencies of mutants at the hypoxanthine-guanine phosphoribosyltransferase (hprt) locus.