Conclusions

Development of neuroblastoma may be triggered by a genetic event(s) that leads to chromosome and/or the genomic DNA abnormalities such as amplification of the MYCN gene and deletions or gains in chromosomal regions including 1p, 11q, and 17q. Together with other epigenetic mechanisms of gene activation or gene silencing, they affect gene and protein expression which in turn deregulate cellular signaling. In neuroblastoma the normal biology of developing neuronal cells and cancer biology appear to overlap. A further understanding of the mechanisms involved in the transformation of progenitors or the stem cells into neuroblasto-ma with significant cellular heterogeneity may provide clues for the development of novel therapeutic strategies for this often aggressive lethal disease.

Acknowledgements. I thank M. Ohira and T. Ozaki for reading the manuscript. I also thank K. Yagyu for preparing the figures.

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