Radiation Induced Neoplasia Following External Beam Therapy for Children With Retinoblastoma

Second primary neoplasms in patients with retinoblastoma

“…The largest reported series of patients is that from Columbia Presbyterian Medical Center, New York, which has been analysed in a number of papers by Abramson et al (1976Abramson et al ( , 1984, Jensen and Miller (1971), Sagarman et al (1969) and Kitchin and Ellsworth (1974). In one of these papers the series was analysed jointly with that from the American Forces Institute of Pathology (Abramson et al, 1976) giving a total of 2300 cases, though it appears that there is some duplication of patients between the two series and that the true total is less than this.…”

Second Malignancies in Retinoblastoma: The Real Problem

“…Mortality has also been reported to occur earlier as irradiated hereditary retinoblastoma patients died sooner than their non-irradiated counterparts with a median age of death of 20.5 years and 40 years, respectively (Yu et al, 2009). The dose-dependent relationship of radiation administration and the development of second malignancies was established over 40 years ago, (Sagerman et al, 1969) and more recent studies have confirmed this analysis (Kleinerman et al, 2005;Wong et al, 1997). The age at which radiation therapy is administered seems to influence the incidence of second tumor development, as patients treated under the age of 1 year were twice as likely to develop a second malignancy than those radiated after the age of 1 year (Abramson & Frank, 1998).…”

Similar Histological Patterns in a Bilateral Malignant Teratoma of the Ovary and a Previous Retinoblastoma in a Girl

“…The latter tumors are re garded as germinal mutations and hereditary, whereas this is assumed only in 10-15% of patients with unilateral affec tion [1,12]. At first glance Knudson's hypothesis of a two step mutation in pathogenesis of retinoblastoma could perhaps theoretical ly explain the similar histological features in the different neoplasms, if one could imagine that proliferation of germ cells is generally stimulated by an early mutation and the sec ond steps are delayed in different organic systems [13,14], This imagination would be supported by the clinical findings that the mean latent period to manifestation of second tu mors after cured retinoblastoma is 13 years and the highest incidence of germ cell malignancies of the ovary is noted in the second decade of life [8,15], But, in contradiction, germ cell malignancies in children previously treated for retino blastoma are a very rare event [1,7,8,16]. As a chromosomal deletion can be detected in about 10% in patients affected by retinoblastoma, we performed chromo somal analysis of blood lymphocytes with banding technique, which did not reveal any abnormal structure [17].…”