RASSF1A methylation may have two biological roles in neuroblastoma tumorigenesis depending on the ploidy status and age of patients

Masayuki Haruta; Takehiko Kamijo; Akira Nakagawara; Yasuhiko Kaneko

doi:10.1016/j.canlet.2014.03.022

RASSF1A methylation may have two biological roles in neuroblastoma tumorigenesis depending on the ploidy status and age of patients

Cancer Lett. 2014 Jun 28;348(1-2):167-76. doi: 10.1016/j.canlet.2014.03.022. Epub 2014 Mar 26.

Authors

Masayuki Haruta¹, Takehiko Kamijo², Akira Nakagawara², Yasuhiko Kaneko³

Affiliations

¹ Research Institute for Clinical Oncology, Saitama Cancer Center, Ina, Saitama, Japan.
² Research Institute, Chiba Cancer Center, Chiba, Japan.
³ Research Institute for Clinical Oncology, Saitama Cancer Center, Ina, Saitama, Japan. Electronic address: [email protected].

PMID: 24680815
DOI: 10.1016/j.canlet.2014.03.022

Abstract

RASSF1A methylation was frequent in neuroblastomas found in infants by mass-screening or infants and children diagnosed clinically, whereas CASP8 and DCR2 methylation was only frequent in tumors in children. When classified according to the ploidy status, RASSF1A and PCDHB methylation was only associated with MYCN amplification and poor outcomes in infants with a clinically diagnosed diploid, not triploid tumor. RASSF1A and PCDHB methylation was associated with poor outcomes in children with triploid and diploid tumors, respectively, and with MYCN amplification in children with diploid tumor. RASSF1A methylation may have two biological roles based on the ploidy status and patient's age.

Keywords: Diploid; Mass-screening; Neuroblastoma; RASSF1A methylation; Triploid.

MeSH terms

Age Factors
Caspase 8 / genetics
DNA Methylation*
Epigenesis, Genetic
Gene Amplification
Gene Expression Regulation, Neoplastic
Genetic Predisposition to Disease
Humans
Infant
Kaplan-Meier Estimate
Multivariate Analysis
N-Myc Proto-Oncogene Protein
Neoplasm Staging
Neuroblastoma / genetics*
Neuroblastoma / metabolism
Neuroblastoma / mortality
Neuroblastoma / pathology
Nuclear Proteins / genetics
Oncogene Proteins / genetics
Phenotype
Ploidies*
Prognosis
Proportional Hazards Models
Risk Factors
Time Factors
Tumor Necrosis Factor Decoy Receptors / genetics
Tumor Suppressor Proteins / genetics*

Substances

MYCN protein, human
N-Myc Proto-Oncogene Protein
Nuclear Proteins
Oncogene Proteins
RASSF1 protein, human
TNFRSF10D protein, human
Tumor Necrosis Factor Decoy Receptors
Tumor Suppressor Proteins
CASP8 protein, human
Caspase 8