Association of CMYC polymorphisms with hepatoblastoma risk

Yang, Tianyou; Yang, Wen; Li, Jiahao; Tan, Tianbao; Yang, Jiliang; Pan, Jing; Hu, Chao; Yao, Yuxiao; Zhang, Jiao; Li, Suhong; Xia, Huimin; He, Jing; Zou, Yan

doi:10.21037/tcr.2019.12.19

Cited by 4 publications

(2 citation statements)

References 28 publications

(32 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…CMYC is also a critical oncogene and reported that the expression of c-Myc increased in hepatoblastoma tissue ( 106 ). However, Yang et al conducted a study in Chinese children and the result showed that CMYC rs4645943 and rs2070583 polymorphisms were not correlated with hepatoblastoma risk ( 107 ).…”

Section: Single Nucleotide Polymorphisms With Hepatoblastomamentioning

confidence: 99%

The Genetic Changes of Hepatoblastoma

Chen

Guan

et al. 2021

Front. Oncol.

View full text Add to dashboard Cite

Hepatoblastoma is the most common malignant liver cancer in childhood. The etiology of hepatoblastoma remains obscure. Hepatoblastoma is closely related to genetic syndromes, hinting that hepatoblastoma is a genetic predisposition disease. However, no precise exposures or genetic events are reported to hepatoblastoma occurrence. During the past decade, significant advances have been made in the understanding of etiology leading to hepatoblastoma, and several important genetic events that appear to be important for the development and progression of this tumor have been identified. Advances in our understanding of the genetic changes that underlie hepatoblastoma may translate into better patient outcomes. Single nucleotide polymorphisms (SNPs) have been generally applied in the research of etiology’s exploration, disease treatment, and prognosis assessment. Here, we reviewed and discussed the molecular epidemiology, especially SNPs progresses in hepatoblastoma, to provide references for future studies and promote the study of hepatoblastoma’s etiology.

show abstract

Section: Single Nucleotide Polymorphisms With Hepatoblastomamentioning

confidence: 99%

The Genetic Changes of Hepatoblastoma

Chen

Guan

et al. 2021

Front. Oncol.

View full text Add to dashboard Cite

show abstract

“…Two potential functional polymorphisms of CMYC (rs4645943 C>T and rs2070583 A>G) were selected from the NCBI dbSNP database (http://www.ncbi.nlm.nih.gov/projects/SNP) A c c e p t e d M a n u s c r i p t and SNPinfo (http://snpinfo.niehs.nih.gov/snpfunc.htm) [29][30][31]. rs4645943 may be linked to multiple SNPs.…”

Section: Polymorphism Selection and Genotypingmentioning

confidence: 99%

Investigation of the Relationship between CMYC Gene Polymorphisms and Glioma Susceptibility in Chinese Children

Lou

Huang

Tian

et al. 2021

Cancer Investigation

View full text Add to dashboard Cite

Glioma is a common central nervous system tumors in children. CMYC has a range of functions that are disrupted in various tumor cells, and may contribute to the occurrence and development of glioma. Two CMYC single nucleotide polymorphisms (rs4645943C>T and rs2070583 A>G) were genotyped in 190 cases and 248 controls from Wenzhou and Guangzhou hospitals. After adjusting for age and sex, odds ratio and 95% confidence interval values were calculated by logistic regression to evaluate the correlation between CMYC gene polymorphisms and glioma risk; no significant associations were detected. These results require future validation in a larger sample cohort.

show abstract

Insights into the Links between MYC and 3D Chromatin Structure and Epigenetics Regulation: Implications for Cancer Therapy

2021

View full text Add to dashboard Cite

MYC is embedded in the transcriptional oasis of the 8q24 gene desert. A plethora of genomic elements has roles in MYC aberrant expression in cancer development by interacting with transcription factors and epigenetics regulators as well as altering the structure of chromatin at the MYC locus and tissue-specific long-range enhancer–promoter contacts. Furthermore, MYC is a master regulator of several human cancers by modulating the transcription of numerous cancer-related genes through epigenetic mechanisms. This review provides a comprehensive overview of the three-dimensional genomic organization around MYC and the role of epigenetic machinery in transcription and function of MYC as well as discusses various epigenetic-targeted therapeutic strategies in MYC-driven cancers.

show abstract

Association of CMYC polymorphisms with hepatoblastoma risk

Cited by 4 publications

References 28 publications

The Genetic Changes of Hepatoblastoma

The Genetic Changes of Hepatoblastoma

Investigation of the Relationship between CMYC Gene Polymorphisms and Glioma Susceptibility in Chinese Children

Insights into the Links between MYC and 3D Chromatin Structure and Epigenetics Regulation: Implications for Cancer Therapy

Contact Info

Product

Resources

About