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Familial predisposition to Wilms' tumour does not map to the short arm of chromosome 11

Familial predisposition to Wilms' tumour does not map to the short arm of chromosome 11 Wilms9 tumour of the kidney usually occurs sporadically, but can also segregate as an autosomal dominant trait with incomplete penetrance1, 2. Patients with the WAGR syndrome of aniridia, genitourinary anomalies, mental retardation and high risk of Wilms' tumour have overlapping deletions of chromosome Hpl3 (ref. 3) which has suggested a possible location for a Wilms' tumour locus. Moreover, many sporadic tumours have lost a portion of chromosome lip (refs 4–8). A second locus at llplS is implicated by association of the tumour with the Wiedemann-Beckwith syndrome (refs 9–11) and by tumour-specific losses of chromosome 11 confined to lip 15 (ref. 12). Here we report a multipoint linkage analysis of a family segregating for Wilms' tumour, using polymorphic DNA markers mapped to chromosome lip. The results exclude the predisposing mutation from both locations. In a second family, the 11p15 alleles lost in the tumour were derived from the affected parent, thus precluding this region as the location of the inherited mutation. These findings imply an aetiological heterogeneity for Wilms' tumour and raise questions concerning the general applicability of the carcinogenesis model that has been useful in the understanding of retinoblastoma13, 14. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Nature Springer Journals

Familial predisposition to Wilms' tumour does not map to the short arm of chromosome 11

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References (36)

Publisher
Springer Journals
Copyright
Copyright © 1988 by Nature Publishing Group
Subject
Science, Humanities and Social Sciences, multidisciplinary; Science, Humanities and Social Sciences, multidisciplinary; Science, multidisciplinary
ISSN
0028-0836
eISSN
1476-4687
DOI
10.1038/336374a0
Publisher site
See Article on Publisher Site

Abstract

Wilms9 tumour of the kidney usually occurs sporadically, but can also segregate as an autosomal dominant trait with incomplete penetrance1, 2. Patients with the WAGR syndrome of aniridia, genitourinary anomalies, mental retardation and high risk of Wilms' tumour have overlapping deletions of chromosome Hpl3 (ref. 3) which has suggested a possible location for a Wilms' tumour locus. Moreover, many sporadic tumours have lost a portion of chromosome lip (refs 4–8). A second locus at llplS is implicated by association of the tumour with the Wiedemann-Beckwith syndrome (refs 9–11) and by tumour-specific losses of chromosome 11 confined to lip 15 (ref. 12). Here we report a multipoint linkage analysis of a family segregating for Wilms' tumour, using polymorphic DNA markers mapped to chromosome lip. The results exclude the predisposing mutation from both locations. In a second family, the 11p15 alleles lost in the tumour were derived from the affected parent, thus precluding this region as the location of the inherited mutation. These findings imply an aetiological heterogeneity for Wilms' tumour and raise questions concerning the general applicability of the carcinogenesis model that has been useful in the understanding of retinoblastoma13, 14.

Journal

Nature – Springer Journals

Published: Nov 24, 1988

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