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p16(CDKN2/INK4a) in Neuroblastoma:An Enigma of Expressive Proportions

Issue: Vol.6, No.1 - January 2007

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  1. Dr Mitchell B Diccianni
    PhD
    University of California at San Diego, Department of Pediatric Hematology/Oncology

Neuroblastoma is one of most common solid tumors of young children and has a wide spectrum of clinical and biological features. Most patients with localized disease (stage 1 and 2) and stage 4s survive the disease while patients with advanced disease (stage 3 and 4) have a poor prognosis. A number of molecular alterations have been associated with a poor prognosis in neuroblastoma, including amplification of N-myc proto-oncogene and deletion of a portion of the short arm of chromosome 1. Though the exact mechanism by which these alterations influence outcome remains elusive, they are known to act through cell cycle deregulation. Cyclin dependent kinase inhibitors such as p16, p18 and p27 also regulate the cell cycle. Deletions, mutations, promoter hypermethylation or translational inactivation of these genes being very common in most cancers, with p16 appearing to be almost universally inactivated in many cancer types. However, neuroblastoma is a notable exception. In contrast to inactivation, the p16 gene is paradoxically highly expressed in many advanced neuroblastoma and associated with a poor outcome. In this review, I will offer an overview of the status of the CDKI p16 in neuroblastoma, and offer some insights into the role p16 and two other CDKIs, p18 and p27, may play in this disease.

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