Author: Stallings, R. L.

Source: Current Pharmaceutical Design, Volume 15, Number 4, February 2009 , pp. 456-462(7)

Publisher: Bentham Science Publishers

Abstract:

Neuroblastoma arises from precursor cells of the sympathetic nervous system and presently accounts for 15% of all childhood cancer deaths. These tumors display remarkable heterogeneity in clinical behavior, ranging from spontaneous regression to rapid progression and resistance to therapy. The clinical behavior of these tumors is associated with many factors, including patient age, histopathology and genetic abnormalities such as MYCN amplification. More recently, the dysregulation of some miRNAs, including the miR-17-5p-92 cluster and miR-34a, has been implicated in the pathobiology of neuroblastoma. MiR-17-5p-92 family members act in an oncogenic manner while miR-34a has tumor suppressor functions. The evidence for the contribution of miRNAs in the aggressive neuroblastoma phenotype is reviewed in this article, along with exciting possibilities for miRNA mediated therapeutics.

Keywords: MicroRNA; neuroblastoma; MYCN; chromosomal imbalance

Document Type: Research article

DOI: http://dx.doi.org/10.2174/138161209787315837

Affiliations: 1: Royal College of Surgeons in Ireland, York House, York Street, Dublin 2, Ireland and Children's Research Centre, Our Lady's Children's Hospital, Crumlin, Dublin 12, Ireland.

Publication date: 2009-02-01

More about this publication?

• Current Pharmaceutical Design publishes timely in-depth reviews covering all aspects of current research in rational drug design. Each issue is devoted to a single major therapeutic area. A Guest Editor who is an acknowledged authority in a therapeutic field has solicits for each issue comprehensive and timely reviews from leading researchers in the pharmaceutical industry and academia.
  
  Each thematic issue of Current Pharmaceutical Design covers all subject areas of major importance to modern drug design, including: medicinal chemistry, pharmacology, drug targets and disease mechanism.

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