Elevated frequencies of spontaneous chromosome breakage and hypersensitivity to radiation induced chromosome damage are characteristic findings in cultured lymphocytes and skin fibroblasts of patients with ataxia telangiectasia (AT). To determine whether long-term AT lymphoblastoid cells (B-lymphocytes) which do not express spontaneous chromosomal instability, exhibit increased chromosomal radiation sensitivity, four AT lymphoblastoid cell lines were exposed to various doses of 250 kVp X-rays during G2. At doses of 25 and 50 rad, the AT cells exhibited a 2–3 fold increase in radiation damage relative to that observed in B-cell lines or PHA stimulated lymphocytes from normal donors, while at 100 rad, the AT cells demonstrated approximately 1.5 times more lesions. These findings suggest that the genetic (or other) factors responsible for increased chromosomal radiation sensitivity in AT lymphocytes and fibroblasts also operate in long-term lymphoblastoid AT cell