| Literature DB >> 33801456 |
Ritsuko Kimata Pooh1,2, Megumi Machida1, Issei Imoto3, Eri Noel Arai4, Hiroyasu Ohashi2, Masayoshi Takeda2, Osamu Shimokawa2, Kaori Fukuta4, Arihiro Shiozaki4, Shigeru Saito4, Hideaki Chiyo1.
Abstract
The phosphatase and tensin homolog (PTEN) gene is a tumor-suppressor gene located on 10q22-23. Since the introduction of molecular genetics in prenatal diagnostics, various birth defects associated with gene mutations have been diagnosed. However, no reports on fetal cases related to PTEN mutation have been found, so far. We encountered a rare case of fetal PTEN mutation. Fetal macrocephaly was noted at 16 weeks. At 18 and 20 weeks, neurosonography revealed megalencephaly with an asymmetrical structure and multifocal polygyria. The head circumference (HC) was +6.2 SD at 18 weeks and +8.1 SD at 20 weeks. The parents opted for pregnancy termination, and the male fetus was delivered at 21 weeks, with HC +9.3 SD. Single-nucleotide polymorphism (SNP) array for amniotic cells showed paternal uniparental disomy (UPD) 10q mosaicism, and the mosaic ratio was calculated as 56% from B-allele frequency. Exome sequencing revealed the pathogenic PTEN mutation with mosaicism. The heterozygous PTEN mutation may not cause early manifestations from the fetal period, and an abnormal phenotype may appear after birth. This may be the reason why fetal defects associated with PTEN mutation are not detected. Since this case had homozygous and heterozygous mutations, survival was possible, exhibiting an incredibly huge head with cortical dysplasia from early pregnancy.Entities:
Keywords: BAF; PTEN; SNP; cortical dysplasia; fetus; megalencephaly; microarray; mosaicism; uniparental disomy
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Year: 2021 PMID: 33801456 PMCID: PMC7999901 DOI: 10.3390/genes12030358
Source DB: PubMed Journal: Genes (Basel) ISSN: 2073-4425 Impact factor: 4.096