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Open AccessJournal ArticleDOI

Neuroblastoma and MYCN

TLDR
Roles for MYCN in neuroblastoma are reviewed and recent identification of other driver mutations are highlighted, as well as strategies to target MYCN at the level of protein stability and transcription.
Abstract
Neuroblastoma, the most common extracranial solid tumor of childhood, is thought to originate from undifferentiated neural crest cells. Amplification of the MYC family member, MYCN, is found in ∼25% of cases and correlates with high-risk disease and poor prognosis. Currently, amplification of MYCN remains the best-characterized genetic marker of risk in neuroblastoma. This article reviews roles for MYCN in neuroblastoma and highlights recent identification of other driver mutations. Strategies to target MYCN at the level of protein stability and transcription are also reviewed.

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Journal ArticleDOI

Neuroblastoma

TL;DR: Neuroblastoma is a type of cancer that most often affects children and can spread to other parts of the body such as the bones, liver, or skin.
Journal ArticleDOI

The bright side of dark matter: lncRNAs in cancer

TL;DR: The traditional view of genome organization has been upended in the last decade with the discovery of vast amounts of non-protein-coding transcription; it is apparent that a subset of these noncoding RNAs are functional.
Journal ArticleDOI

An Overview of MYC and Its Interactome

TL;DR: A view of MYC as a sensor that integrates multiple cellular signals to mediate a broad transcriptional response controlling many aspects of cell behavior is presented and evidence that the network has evolved for millions of years, dating back to the emergence of animals is discussed.
Journal ArticleDOI

Neuroblastoma: Paradigm for Precision Medicine

TL;DR: Current clinical trials have continued to reduce therapy for patients with non-high-risk NB, including the most favorable subsets who are often followed with observation approaches, and high-risk patients are treated aggressively with chemotherapy, radiation, surgery, and myeloablative and immunotherapies.
References
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Journal ArticleDOI

Induction of apoptosis in fibroblasts by c-myc protein

TL;DR: It is demonstrated that deregulated c-myc expression induces apoptosis in cells growth arrested by a variety of means and at various points in the cell cycle.
Journal ArticleDOI

Amplification of N-myc in untreated human neuroblastomas correlates with advanced disease stage

TL;DR: N-myc amplification is highly correlated with advanced stages of disease (P less than 0.001) and with the ability to grow in vitro as an established cell line, both of which are associated with a poor prognosis.
Journal ArticleDOI

Driver mutations in histone H3.3 and chromatin remodelling genes in paediatric glioblastoma

Jeremy Schwartzentruber, +66 more
- 09 Feb 2012 - 
TL;DR: The presence of H3F3A/ATRX-DAXX/TP53 mutations was strongly associated with alternative lengthening of telomeres and specific gene expression profiles, suggesting that defects of the chromatin architecture underlie paediatric and young adult GBM pathogenesis.
Journal ArticleDOI

Association of multiple copies of the N-myc oncogene with rapid progression of neuroblastomas.

TL;DR: The results suggest that genomic amplification of N-myc may have a key role in determining the aggressiveness of neuroblastomas.
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