By selecting focal regions commonly involved in chromosomal anomalies, we identified genes with a possible role in WT development, based on the prior knowledge of their biological relevance, including <i>MYCN, DIS3L2, MIR562</i>, <i>HACE1</i>, <i>GLI3</i>, <i>CDKN2A</i> and <i>CDKN2B</i>, <i>PALB2</i>, and <i>CHEK2</i>.
Although the WT1 gene, located at 11p13, has been proven to be implicated in the development of Wilms tumor, other genes such as MYCN are also involved.
A higher occurrence of 1q gain and MYCN gain and a lack of difference in the distribution of variations among survivors and those with a relapse suggest a different molecular profile of Wilms tumor in Indian children.
Reduced RA pathway activity and MYCN overexpression were found in high risk tumors as opposed to tumors with low/intermediate risk, suggesting a beneficial impact of RA especially on advanced WT.
DNA, extracted from tumours arising in 29 paediatric patients [14 neuroblastoma, 9 Wilms tumour (nephroblastoma), 6 miscellaneous] was investigated for evidence of N-myc amplification, using pNb-1, a recombinant plasmid containing a 1.0 Kb fragment homologous to the 5' end of the human N-myc gene.
Similarly, the human N-myc gene was transcribed at an equivalent rate in HeLa cells, which do not accumulate this RNA in the cytoplasm, and cell lines G401 (a Wilms tumor-derived cell line) and SKNMc (established from a primitive neuroepithelioma), which do express N-myc RNA.
Adjusted odds ratios (AORs) and 95% confidence intervals (CIs) were calculated to evaluate the association between MYCN gene polymorphisms and Wilms tumor susceptibility.