Neuroblastoma

Colon, Nadja C.; Chung, Dai H.

doi:10.1016/j.yapd.2011.03.011

Cited by 161 publications

(150 citation statements)

References 43 publications

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“…Neuroblastoma most commonly occurs in the abdomen, particularly in the adrenal medulla, but also at other parts of the human body where sympathetic ganglia or other sympathetic nervous system components are present, such as chest, neck and pelvis [1,2]. Importantly, patients with neuroblastoma show poor prognosis, and neuroblastoma accounts for more than 10% cancer death in children [3,4].…”

Section: Introductionmentioning

confidence: 99%

Delineation of the frequency and boundary of chromosomal copy number variations in paediatric neuroblastoma

Peng

Mayoh

et al. 2018

Cell Cycle

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Neuroblastoma, the most common solid tumour in early childhood, is characterized by very frequent chromosomal copy number variations (CNVs). While chromosome 2p amplification, 17q gain, 1p and 11q deletion in human neuroblastoma tissues are well-known, the exact frequencies and boundaries of the chromosomal CNVs have not been delineated. We analysed the publicly available single nucleotide polymorphism (SNP) array data which were originally generated by the Therapeutically Applicable Research to Generate Effective Treatments (TARGET) initiative, defined the frequencies and boundaries of chromosomes 2p11.2 - 2p25.3 amplification, 17q11.1-17q25.3 gain, 1p13.3-1p36.33 deletion and 11q13.3-11q25 deletion in neuroblastoma tissues, and identified chromosome 7q14.1 (Chr7:38254795-38346971) and chromosome 14q11.2 (Chr14:21637401-22024617) deletion in blood and bone marrow samples from neuroblastoma patients, but not in tumour tissues. Kaplan Meier analysis showed that double deletion of Chr7q14.1 and Chr14q11.2 correlated with poor prognosis in MYCN gene amplified neuroblastoma patients. In conclusion, the oncogenes amplified or gained and tumour suppressor genes deleted within the boundaries of chromosomal CNVs in tumour tissues should be studied for their roles in tumourigenesis and as therapeutic targets. Focal deletions of Chr7q14.1 and Chr14q11.2 together in blood and bone marrow samples from neuroblastoma patients can be used as a marker for poorer prognosis and more aggressive therapies.

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Section: Introductionmentioning

confidence: 99%

Delineation of the frequency and boundary of chromosomal copy number variations in paediatric neuroblastoma

Peng

Mayoh

et al. 2018

Cell Cycle

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“…Familial neuroblastomas occur in 1–2%, with a mean age of 9 months at diagnosis 90 . Associations exist with neural crest disorders, such as Hirschsprung's disease, NF 1 and congenital central hypoventilation syndrome 91 …”

Section: Search Strategymentioning

confidence: 99%

Clinical and imaging overview of functional adrenal neoplasms

Low

Sahi

2012

Int J of Urology

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Abbreviations & AcronymsAbstract: Adrenal adenoma, adrenocortical carcinoma, pheochromocytoma and neuroblastoma are four discrete adrenal neoplasms that have the potential for functional activity. Functional adrenal neoplasms can secrete cortisol, aldosterone, sex hormones or catecholamines. These heterogeneous groups of tumors show varied biological behavior and clinical outcomes. These neoplasms are encountered with increasing clinical frequency as a result of an expansion in the volume of medical imaging carried out. The clinical presentation, including prognosis and treatment options, and the imaging features of these neoplasms are discussed. The key radiological observations of each of these neoplasms are shown using multimodality images. Familiarity with the clinical and imaging features of these neoplasms improves diagnosis, and facilitates appropriate clinical decision-making and patient management.

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“…Neuroblastoma is the most common solid tumor in children less than 5 years old, and is derived from primordial neural crest cells that eventually reside in the sympathetic nervous system (1,2). Amplification of a 130 kb core genomic DNA region containing the MYCN oncogene, the MYCN antisense NCYM gene and the long non-coding RNA lncUSMycN gene, occurs in more than a quarter of human neuroblastoma tissues (3).…”

Section: Introductionmentioning

confidence: 99%

NCYM is upregulated by lncUSMycN and modulates N-Myc expression

Liu

Atmadibrata

Mondal

et al. 2016

International Journal of Oncology

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Abstract. Neuroblastoma is the most common solid tumor in early childhood. Patients with neuroblastoma due to the amplification of a 130-kb genomic DNA region containing the MYCN, MYCN antisense NCYM and lncUSMycN genes show poor prognosis. BET bromodomain inhibitors show anticancer efficacy against neuroblastoma partly by reducing MYCN gene transcription and N-Myc mRNA and protein expression. We have previously shown that the long nocoding RNA lncUSMycN upregulates N-Myc mRNA expression by binding to the RNA-binding protein NonO. In this study, we found that lncUSMycN upregulated NCYM expression, and knockingdown lncUSMycN reduced histone H3 lysine 4 trimethylation, a marker for active gene transcription, at the NCYM gene promoter. NCYM upregulated N-Myc mRNA expression, NCYM RNA formed a complex with NonO protein, and knocking down NCYM expression reduced neuroblastoma cell proliferation. Importantly, treatment with BET bromodomain inhibitors reduced NCYM expression. In human neuroblastoma patients, high levels of NCYM expression in tumor tissues correlated with high levels of N-Myc, NonO and lncUSMycN expression as well as poor patient prognosis. Taken together, our findings suggest that lncUSMycN upregulates NCYM expression by activating its gene transcription, and that NCYM RNA upregulates N-Myc mRNA expression by binding to NonO. Our findings also provide further evidence for the application of BET bromodomain inhibitors for the therapy of neuroblastoma characterized by MYCN/ NCYM gene locus amplification.

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Neuroblastoma

Cited by 161 publications

References 43 publications

Delineation of the frequency and boundary of chromosomal copy number variations in paediatric neuroblastoma

Delineation of the frequency and boundary of chromosomal copy number variations in paediatric neuroblastoma

Clinical and imaging overview of functional adrenal neoplasms

NCYM is upregulated by lncUSMycN and modulates N-Myc expression

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