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Genetics and the Etiology of Childhood Cancer

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Genetics and the Etiology of Childhood Cancer Pediat. Res. 10: 513-517 (1976) Genetics and the Etiology of Childhood Cancer ALFRED G. KNUDSON, JR.13" Graduate School of Biomedical Sciences, University of Texas Health Science Center, Housron, Texas, USA In developed nations cancer is now the principal cause of death had bilateral disease; in fact, in the latter case, transmission fits a from disease between infancy and adulthood, yet little is known of dominant gene model. However, the affected offspring of unilat- its etiology. The most uniquely childhood tumors occur so soon eral cases are more often bilaterally affected than not, as with the after birth in many instances that prenatal initiation becomes affected offspring of bilateral cases. The simplest model which suspect. In all parts of the world, each form is uncommon, and, explains these observations is one which estimates that approxi- with a few notable exceptions, there is no region with a unique or mately 40% of cases are attributable to a dominant gene which very unusual incidence of a particular form. In studying the produces a mean number of 3 retinoblastomas/gene carrier, and etiology of childhood cancer we, begin by suspecting rather that it is a matter of chance whether a given individual acquires universal agents and processes. bilateral or unilateral disease, or, in fact, no disease, as an estimated 5% of carriers seem to do (9). On the other hand, 60% of WILMS' TUMOR cases occur in children who do not carry such a dominant gene; for these, tumor is a very improbable event and would virtually never Of all the childhood cancers none has a more uniform incidence occur bilaterally. in the world than Wilms' tumor of the kidney. In fact its incidence These are then two main groups of children who acquire of approximately 1/15,000 births is so uniform that its use as an retinoblastoma. One group, with an incidence of about 21 100,000 index reference cancer has been proposed (2). It is obviously has a 95% chance of developing this tumor, and on average unpromising to suppose that locally occurring causative factors develops 3 of them. The other group, which includes essentially all may be significant contributors to the origin of Wilms' tumor. other children, has a probability of about 3/ 100,000 of developing Still, we are not entirely without etiologic evidence; some high retinoblastoma. The dominant gene for the tumor increases the risk groups have been identified. A particularly high risk group is number of tumors per individual from 1 primary tumor/30,000 the category of children with sporadic aniridia and various subjects to 3 primaries in one patient; i.e., it increases the risk of congenital anomalies (25). In at least one case of such a tumor approximately 100,000 times-a potent carcinogen indeed. coincidence a chromosomal abnormality (translocation of part of By way of comparing retinoblastoma and Wilms' tumor we the long arm of a number I I chromosome to the short arm of a should note that if there were no successful treatment for chromosome number 8, with a deletion in the latter) was found retinoblastoma, as has nearly been the case for Wilms' tumor until (16). It will be of great interest to discover whether all such cases recent times, the dominant subgroup of retinoblastoma would have have some feature of this chromosomal abnormality in common. been obscured. The clue to heritability would have been the Another predisposing condition is hemihypertrophy (25), which occurrence of the tumor in identical twins, in sibs, and, very may also be associated with adrenocortical carcinoma and/or occasionally, in more than one generation. These familial cases hepatoblastoma. Anomalies of the genitourinary system without would have been more frequently bilateral than usual and would hemihypertrophy seem to be associated with Wilms' tumor more have occurred at earlier ages on average. These expectations often than expected by chance. accord precisely with the observations reported on Wilms' tumor. Familial cases of Wilms' tumor have also been reported (14) Even retinoblastoma has been curable only in modern times. In and, in one remarkable family, in association with hemihypertro- the past most gene carriers died. Their continued appearance has phy in a parent (22). The familial cases are more often bilateral becn due to recurrent mutations in parental germ cells. Even now than usual and are diagnosed at earlier age than is normally the most cases do not have a positive family history. An important case. The pattern of familial cases is very similar to that which implication for counseling is that all bilateral cases should be would be expected from retinoblastoma if few affected individuals considered heritable regardless of family history. For unilateral survived to reproduce; the familial cases are usually twins or other cases the problem is very difficult; only about 10-15% are sibs and in only a few instances is more than one generation heritable, but that subgroup is not identifiable except in the affected. It has been deduced that there are two large groups of presence of a positive family history. Means for identifying the Wilms' tumor patients, one with a hereditary (autosomal domi- hereditary unilateral group are sorely needed. nant) form of the tumor and one with a nonhereditary form (14). In rare instances retinoblastoma has been associated with other An estimate of the fraction of the hereditary form was 38%. The tumors or with congenital defects. Other tumors are reported at a relationship between the two forms was concluded to be similar to generally low rate, probably of the order of magnitude of 1 or 2% that found in retinoblastoma. The prediction was made that as (8). However, one tumor, osteogenic sarcoma, dominates this more and more patients survive to adulthood and reproduce there group and seems to occur in about 1% of persons who carry the will be more examples of vertical transmission from generation to dominant retinoblastoma gene. If these individuals receive x- generation, just as has happened with retinoblastoma. irradiation in an attempt to save useful vision, the risk increases. In fact, it has been estimated that with high doses of irradiation the incidence of osteogenic sarcoma of the orbit may rise to 30% (29); RETINOBLASTOMA an already greatly increased risk of this tumor is still further Retinoblastoma is distributed on a world-wide basis with an increased. incidence of approximately 1/20,000 births (6). This tumor has Congenital defects have also been associated with retinoblas- long been known to be transmissible in autosomal dominant toma, but one cluster of defects is particularly outstanding in this fashion, but it has also been known that transmission by survivors respect, viz., those linked with a deletion of the long arm of who had unilateral tumor is much less frequent than by those who chromosome 13, formerly referred to as the D-deletion syndrome. 5 1 5 14 KNUDSION, JR. The diverse anomalies may reasonably be attributed to deletions of times. Hepatic tumors of childhood have a low incidence, as does various gene loci, the variability in expression of defects being in Ewing's sarcoma. Osteogenic sarcoma and other connective tissue large part due to variability in the chormosomal segment which is sarcomas have a peak incidence in adolescence and continue to deleted. Among children with this syndrome there is a high risk of occur in adults. Even so, there are enough published reports to retinoblastoma, and its occurrence is most often bilateral. The suggest that the same pattern of two groups, one attributable to a simplest hypothesis is that the gene for retinoblastoma is located in dominant gene and one nonhereditary, is operative for these the q21 band of the long arm of chromosome 13, that in some cases tumors also (15). of the 13-deletion syndrome it is deleted, and that its deletion The occurrence of brain tumors in sibs is not a common event, results in a risk of retinoblastoma identical with that of the usual but it greatly exceeds the expectation of chance (23). Brain tumors dominant mutation (27). The latter is evidently not generally the have also been reported in more than one generation and, although result of deletion, since cases unassociated with congenital defects no characteristic dominantly inherited forms have emerged, me- generally have normal karyotypes, whether they are unilateral or dulloblastoma has an excessive incidence among individuals with bilateral (17). Presumably retinoblastoma can ensue whether the the dominantly inherited basal cell nevus syndrome (26). gene is changed microscopically (deletion) or not (point mutation Rhabdomyosarcoma has also been reported in sibs and in more or other submicroscopic change). In both cases the gene change is than one generation, but here a new factor is introduced. dominantly heritable in the next generation. This same relation- Rhabdomyosarcoma has been found in several pedigrees in which ship between microscopic and submicroscopic change may be breast cancer, and perhaps certain other cancers, have been operating in Wilms' tumor, the chromosomal group being com- transmitted through multiple generations (19). These pedigrees prised of those with aniridia and congenital defects. deviate from others discussed so far in that the tumor gene is not primarily specific for a childhood tumor. NEUROBLASTOMA Deviating even further from this pattern are other somatic tissue sarcomas, including osteogenic sarcoma, fibrosarcoma, and neuro- A third important tumor of children which shares many of these fibrosarcoma (4). As noted for retinoblastoma, osteogenic sar- features is neuroblastoma. It too is distributed on a world-wide coma may be an associated tumor. It has also been found as a basis, with an incidence of nearly 1/10,000 births. One anomaly in second tumor, either within or outside radiation fields, associated its distribution is a significantly decreased incidence in troprical with several other tumors.
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