Purpose: To determine if cells from the cancer-prone autosomal recessive disorder ataxia telangiectasia (A-T) are defective in responding to stimuli other than ionizing-radiation (IR) damage.
Materials and methods: The induction of c-jun transcripts by IR, by phorbol 12-myristate 13-acetate (PMA), interleukin 1 (IL-1) and epidermal growth factor (EGF) in normal and A-T lymphoblasts was measured.
Results: Treatment with PMA increased c-jun transcripts in a dose- and time-dependent manner two- to three-fold more in A-T than in normal cells. Similarly, treatment with EGF and IL-1 also increased c-jun transcripts more in A-T than in normal lymphoblasts. In contrast, exposure to gamma-radiation increased c-jun transcripts at least twofold more in normal than in A-T lymphoblasts.
Conclusions: These findings indicate that A-T cells are not only defective in responding to IR damage, but also in responding to mitogenic stimuli like IL-1 and EGF. Furthermore, these findings implicate ATM, the gene responsible for the A-T disorder, in the induction of c-jun transcripts by PMA, EGF or IL-1.