PRECURSOR LESIONS OF WILMS-TUMOR IN INDIAN CHILDREN - A MULTIINSTITUTIONAL STUDY

Citation
K. Mishra et al., PRECURSOR LESIONS OF WILMS-TUMOR IN INDIAN CHILDREN - A MULTIINSTITUTIONAL STUDY, Cancer, 83(10), 1998, pp. 2228-2232
Citations number
18
Categorie Soggetti
Oncology
Journal title
CancerACNP
ISSN journal
0008543X
Volume
83
Issue
10
Year of publication
1998
Pages
2228 - 2232
Database
ISI
SICI code
0008-543X(1998)83:10<2228:PLOWII>2.0.ZU;2-V
Abstract
BACKGROUND, Studies regarding different ethnic populations of children with Wilms' tumor (WT) in the U. S. have shown differences between ag e and gender incidence and the type of its precursor lesions (nephroge nic rests). To the authors' knowledge there are few reports in the lit erature regarding nephrogenic rests in a large number of cases from ot her parts of the world. METHODS. In this study, histopathology section s from 127 WTs were pooled from the archives of 4 institutions in nort hern India and studied for the incidence of nephrogenic rests. Their i ncidence also was cross-correlated with patient age gender, and tumor morphology. RESULTS. Significantly, the complete absence of perilobar nephrogenic rests was observed in all cases. Intralobar rests were ass ociated with 45.3% of WTs and were observed predominantly with a triph asic histologic pattern and a relatively lower incidence of anaplasia compared with reports in the Western literature (1.5% vs. 4.5%). A low er median age of 2.5 years with a peak in the first 2 years of life wa s consistent with reported studies in Asian children. The male gender preponderance was in contrast to the equal male to female ratio report ed in Western cases. CONCLUSIONS. The type of nephrogenic rests presen t in Indian children was noted to be different from that in children r eported in the Western literature. Differences also existed with regar d to the age and gender incidence of children with WT and its morpholo gic pattern, possibly due to the different genetic nature of the tumor . However, this theory requires confirmation by large epidemiologic an d genetic studies. Cancer 1998;83:2228-32. (C) 1998 American Cancer So ciety.