The molecular and cytogenetic properties of renal neoplasms have been studied extensively
with the consequent identification of several genes that are involved in the development
and progression of these tumors. Ideally, a multi-step model of tumor progression
from benign to malignant, as demonstrated for colorectal carcinomas by Fearon and
Vogelstein [
[1]
] would be discovered for each type of renal epithelial neoplasm; however, the genetics
of renal tumors are extremely complex and heterogeneous and, as a result, do not lend
themselves easily to this type of model. Solid renal parenchymal tumors are a heterogeneous
group of neoplasms in terms of their clinical behavior and biologic properties [
2
,
3
]. Cytogenetic and molecular genetic analyses showed that each histologic type of renal
cortical tumor is characterized by specific genetic alterations (See later discussion)
[
4
,
5
,
6
,
7
,
8
,
9
,
10
,
11
]. Bugert and Kovacs [
[8]
] analyzed 82 renal tumors by way of loss of heterozygosity (LOH) analysis and were
able to classify most of these tumors correctly based solely on these results. Similarly,
Wilhelm et al [
[7]
] were able to classify 33 of 34 renal tumors correctly using only array-based comparative
genomic hybridization (CGH). In addition to allelic loss analysis and CGH, techniques,
such as fluorescent in situ hybridization (FISH) and classical cytogenetics and karyotyping,
have been used extensively to study renal neoplasia.To read this article in full you will need to make a payment
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