Publications by authors named "M Suyama"
Background: The placenta is essential for nutrient exchange and hormone production between the mother and the developing fetus and serves as an invaluable model for epigenetic research. Most epigenetic studies of the human placenta have used whole placentas from term pregnancies and have identified the presence of partially methylated domains (PMDs). However, the origin of these domains, which are typically absent in most somatic cells, remains unclear in the placental context.
View Article and Find Full Text PDFMagnetoencephalography (MEG) conventionally operates within high-performance magnetic shields due to the extremely weak magnetic field signals from the measured objects and the narrow dynamic range of the magnetic sensors employed for detection. This limitation results in elevated equipment costs and restricted usage. Additionally, the information obtained from MEG is functional images, and to analyze from which part of the brain the signals are coming, it is necessary to capture morphological images separately.
View Article and Find Full Text PDFThe search for genetic variants that act as causative factors in human diseases by disrupting the normal splicing process has primarily focused on single nucleotide variants (SNVs). It is worth noting that insertions or deletions (indels) have also been sporadically reported as causative disease variants through their potential impact on the splicing process. In this study, to perform identification of indels inducing exon extension/shrinkage events, we used individual-specific genomes and RNA sequencing (RNA-seq) data pertaining to the corresponding individuals and identified 12 exon extension/shrinkage events that were potentially induced by indels that disrupted authentic splice sites or created novel splice sites in 235 normal individuals.
View Article and Find Full Text PDFArticle Synopsis
- Trifluridine (FTD) is a chemotherapy drug used for cancer treatment, but its cytotoxic mechanism is not fully understood, particularly in relation to mutations in the TP53 gene, which are known to impact cancer progression and drug resistance.
- This study uncovered that FTD leads to DNA damage and abnormal cell division (mitosis) in both cells lacking p53 and those with gain-of-function TP53 mutations, though it failed to enforce a proper cell cycle checkpoint during G2/M transition.
- The research indicates that FTD's effectiveness as an anti-tumor agent operates independently of p53 functionality, suggesting that it can be effective even in the presence of the mutant forms of p53 that typically enhance resistance to chemotherapy