Expression of the human apurinic endonuclease gene (ape) in normal and malignant-tissues

Apurinic/apyrimidinic endonucleases initiate repair at sites of base loss produced by many carcinogens and maintain genetic stability by repairing abasic sites produced spontaneously. We examined whether expression of the main apurinic endonuclease of human cells, encoded by the APE gene, might be decreased in malignant cells and thus potentiate an elevated mutation rate. Northern blotting and in situ hybridisation were used to quantitate the level of APE mRNA in various normal tissues and in 24 different brain tumors. There were no differences in APE expression among the normal tissues, or between malignant astrocytomas and meningiomas and the surrounding normal brain tissues. This suggests that diminished expression of the apurinic endonuclease does not underly the induction of these cancers, or explain clinical variations in presentation and response to treatment.