The genetics of retinoblastoma

Jk, Cowell

doi:10.1038/bjc.1991.79

Cited by 25 publications

(12 citation statements)

References 42 publications

(35 reference statements)

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“…Cowell (1991) in a review of the molecular genetics of retinoblastoma stated that identification of all gene carriers in retinoblastoma families will soon be possible. This would mean that the frequent ophthalmological examinations under anaesthetic of all children of affected parents and other relatives of retinoblastoma patients would no longer be necessary, and clinical resources could be concentrated on patients who are carriers.…”

Section: Genetic Counsellingmentioning

confidence: 99%

Patterns of risk of hereditary retinoblastoma and applications to genetic counselling

Draper

Sanders²,

Brownbill³

et al. 1992

Br J Cancer

148

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A registry including information about nearly 1,600 cases of retinoblastoma diagnosed in Britain has been created at the Childhood Cancer Research Group. Cases have been classified as 'old germ cell mutation', 'new germ cell mutation' or 'sporadic non-hereditary'. For a population-based group of 918 cases diagnosed between 1962 and 1985 we have calculated the proportions of unilateral/bilateral and hereditary/non-hereditary cases. Bilateral cases represent 40% of the total number over this period; the proportion known to be hereditary is 44%, a higher proportion than has been reported elsewhere. By following up selected groups of cases, an estimate has been made of the proportions of siblings of retinoblastoma patients and offspring of survivors from retinoblastoma who are themselves affected with the disease. Where there is no previous family history, the risk for siblings of retinoblastoma patients of developing the disease is approximately 2% if the disease in the affected child is bilateral and 1% if it is unilateral, assuming that there are no other siblings; if there are unaffected siblings the risks for subsequent children are lower. Children of patients with hereditary retinoblastoma have a one in two chance of carrying the germ cell mutation and for those who are carriers the probability of developing retinoblastoma is very close to the accepted figure of 90% if the parents have bilateral retinoblastoma but probably less if they have the unilateral form. For children of patients not known to be carriers, the probability of developing retinoblastoma is estimated to be about 1%, considerably lower than the previously accepted figure of about 5%. Retinoblastoma kindreds consist mainly of bilateral cases but there is evidence that some kindreds have a high proportion of unilateral cases. The ways in which these findings may be used in conjunction with modern techniques of molecular biology for prenatal and postnatal genetic counselling are discussed.

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Section: Genetic Counsellingmentioning

confidence: 99%

Patterns of risk of hereditary retinoblastoma and applications to genetic counselling

Draper

Sanders²,

Brownbill³

et al. 1992

Br J Cancer

148

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“…Retinoblastoma is a classic example of a cancer for which a genetic aetiology has been identified in a sizeable proportion of cases 34 . It essentially occurs in two forms, heritable and non-heritable.…”

Section: Retinoblastomamentioning

confidence: 99%

Geographic and ethnic variations in the incidence of childhood cancer

Stiller

Parkin

1996

British Medical Bulletin

251

156

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The total incidence of childhood cancer varies rather little between different regions of the world, with cumulative risk to age 15 nearly always in the range 1.0-2.5 per thousand. Acute h/mphoblastic leukaemia, especially in early childhood, is most common in populations of high socio-economic status and is the most frequent childhood cancer in all industrialised countries. The risk of Burkitt's lymphoma is highest in tropical Africa and Papua New Guinea; it is strongly associated with Epstein-Barr virus infection and intense immune stimulation by malaria. Other rymphomas are also relatively common in developing countries. Non-heritable retinoblastoma has a higher incidence among less affluent populations, suggesting an association with poor living conditions and maybe an infectious aetiology. In contrast, the incidence of Wilms' tumour and Ewing's sarcoma varies largely on ethnic lines, indicating a strong role for genetic predisposition. Much of the variation in recorded incidence of brain tumours and neuroblastoma may be due to varying levels of case ascertainment. Recently the incidence of childhood Kaposi's sarcoma has risen substantially in parts of Africa severely affected by the AIDS epidemic. Geographic and ethnic variations in the incidence of childhood cancerCompared with the very large variations in cancer incidence among adults between different regions of the world, the total incidence of childhood cancer is relatively constant. The cumulative incidence to age 15 is nearly always in the range 1.0-2.5 per thousand and age-_ , . standardised annual incidence rates (ASR) calculated using the world

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“…Few risk factors have been established for childhood cancers other than ionizing radiation (2,3), chemotherapy agents (2), and certain inherited genetic disorders (4,5). Positive associations have been observed in case-control studies between pesticide use in the home or garden and childhood leukemia (6-9) and brain cancer (10,11).…”

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confidence: 99%

Childhood cancer and agricultural pesticide use: an ecologic study in California.

Reynolds

Behren

Gunier

et al. 2002

Environ Health Perspect

105

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We analyzed population-based childhood cancer incidence rates throughout California in relation to agricultural pesticide use. During 1988-1994, a total of 7,143 cases of invasive cancer were diagnosed among children under 15 years of age in California. Building on the availability of high-quality population-based cancer incidence information from the California Cancer Registry, population data from the U.S. Census, and uniquely comprehensive agricultural pesticide use information from California's Department of Pesticide Regulation, we used a geographic information system to assign summary population, exposure, and outcome attributes at the block group level. We used Poisson regression to estimate rate ratios (RRs) by pesticide use density adjusted for race/ethnicity, age, and sex for all types of childhood cancer combined and separately for the leukemias and central nervous system cancers. We generally found no association between pesticide use density and childhood cancer incidence rates. The RR for all cancers was 0.95 [95% confidence interval (CI), 0.80-1.13] for block groups in the 90th percentile and above for use of pesticides classified as probable carcinogens, compared to the block groups with use of < 1 lb/mi(2). The RRs were similar for leukemia and central nervous system cancers. Childhood leukemia rates were significantly elevated (RR = 1.48; 95% CI, 1.03-2.13) in block groups with the highest use of propargite, although we saw no dose-response trend with increasing exposure categories. Results were unchanged by further adjustment for socioeconomic status and urbanization.

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The genetics of retinoblastoma

Cited by 25 publications

References 42 publications

Patterns of risk of hereditary retinoblastoma and applications to genetic counselling

Patterns of risk of hereditary retinoblastoma and applications to genetic counselling

Geographic and ethnic variations in the incidence of childhood cancer

Childhood cancer and agricultural pesticide use: an ecologic study in California.

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