Radiosensitivity and early onset cancer

Abstract

The article is concerned with the radioprotection of a substantial radiosensitive population who present with cancer in early adulthood and will probably be treated with radiotherapy. A theory of radiation-induced health effects based on the induction of DNA double strand breaks is used to associate the radio-sensitivity of carriers of the BRCA1 and BRCA2 genes and the PALB2 gene with the defects in the homologous recombination repair of DNA damage found in the carriers. It is concluded that the defects in homologous recombination repair in these carriers will lead to an increased level of somatic mutations in all their cells and that this increased level of somatic mutations throughout their lifetime is, essentially, the reason that the carriers develop early onset cancer. This is a direct consequence of the more rapid accumulation of the cancer-inducing somatic mutations than the normal, slower accumulation in non-carriers. The radiotherapeutic treatment of these carriers needs to proceed with some care, taking account of their increased radio-sensitivity, and this suggests a need for international recognition and guidance of their radioprotection within the medical profession.