AI Article Synopsis

  • The study aimed to understand the molecular causes of pediatric germ cell tumors (GCTs) using various genomic analysis techniques on 51 tumor samples from both genders and different age groups.
  • Findings revealed that germinomas and embryonal carcinomas exhibited high levels of pluripotent gene expression, while yolk sac tumors showed signs of endodermal gene overexpression.
  • Researchers suggest potential treatment targets based on gene expression patterns: KIT for germinomas, TNFRSF8 for embryonal carcinomas, and ERBB4 for yolk sac tumors.

Article Abstract

To elucidate the molecular pathogenesis of pediatric germ cell tumors (GCTs), we performed DNA methylation array analysis, whole transcriptome sequencing, targeted capture sequencing, and single-nucleotide polymorphism array analysis using 51 GCT samples (25 female, 26 male), including 6 germinomas, 2 embryonal carcinomas, 4 immature teratomas, 3 mature teratomas, 30 yolk sac tumors, and 6 mixed germ cell tumors. Among the 51 samples, 11 were from infants, 23 were from young children, and 17 were from those aged ≥10 years. Sixteen of the 51 samples developed in the extragonadal regions. Germinomas showed upregulation of pluripotent genes and global hypomethylation. Pluripotent genes were also highly expressed in embryonal carcinomas. These genes may play essential roles in embryonal carcinomas given that their binding sites are hypomethylated. Yolk sac tumors exhibited overexpression of endodermal genes, such as GATA6 and FOXA2, the binding sites of which were hypomethylated. Interestingly, infant yolk sac tumors had different DNA methylation patterns from those observed in older children. Teratomas had higher expression of ectodermal genes, suggesting a tridermal nature. Based on our results, we suggest that KIT, TNFRSF8, and ERBB4 may be suitable targets for the treatment of germinoma, embryonal carcinomas, and yolk sac tumors, respectively.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7528104PMC
http://dx.doi.org/10.1038/s42003-020-01267-8DOI Listing

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