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Although success in treating intraocular retinoblastoma with radiation was first reported in 1903,1 all the eyes originally treated with radiation were lost as a result of radiation complications. Stallard in England2 and Reese in the USA3 recognised that by modifying the technique, it was possible to save the child's life, eye and in some cases vision. Stallard and Reese pioneered the use of external beam radiation, but it was Stallard who developed and perfected the use of brachytherapy for retinoblastoma in the 1930s.
Radiation was almost never used for unilateral cases, as they were all deemed too advanced to treat with anything but surgery. Thus, virtually all the eyes that received radiation were children with the germinal form of retinoblastoma. More than 50 years ago, it was recognised that some of these irradiated children subsequently went on and developed cancers outside the eye (called ‘second non-ocular cancers’). Reese believed that these second cancers were an unfortunate complication of radiation alone, as they only developed in irradiated children and in the field of radiation and after long latent periods. Subsequent work by Sagerman et al4 confirmed a lower incidence with lower doses, and in recent years a clear dose–response curve for sarcoma development in the field of radiation was demonstrated. In going from 35 Gy to 60 Gy, the incidence of sarcoma development is increased by eightfold.5
Even before the retinoblastoma gene was cloned in 1986,6 it was clear that genetics played an important role in the development of these cancers and that it was primarily the gene, not radiation, that was the cause of these cancers. By the 1990s, the most common cause of death of a retinoblastoma patient in the USA was not metastatic retinoblastoma, but rather these second (or third, fourth or fifth) cancers.7 …