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Your search keyword '"Shunsaku Takayanagi"' showing total 3 results
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3 results on '"Shunsaku Takayanagi"'

1. Early prediction of functional prognosis in neurofibromatosis type 2 patients based on genotype–phenotype correlation with targeted deep sequencing

Author

Yu Teranishi, Satoru Miyawaki, Hirofumi Nakatomi, Kenta Ohara, Hiroki Hongo, Shogo Dofuku, Atsushi Okano, Shunsaku Takayanagi, Takahiro Ota, Jun Yoshimura, Wei Qu, Jun Mitsui, Shinichi Morishita, Shoji Tsuji, and Nobuhito Saito

Subjects
Medicine, Science
Abstract

Abstract Regardless of treatment, the clinical progression of neurofibromatosis type 2 (NF2), particularly in terms of hearing, swallowing, and gait, tend to worsen throughout the patients’ lives. We performed a retrospective analysis of functional outcomes in Japanese NF2 patients to predict their functional prognosis. We analyzed genotype–phenotype correlation based on genetic data from a cohort of 57 patients with a mean follow-up of 14.5 ± 6.0 years. Their functional outcomes, including hearing, swallowing, and ambulation, were reviewed. Performing a targeted deep sequencing, germline NF2 mutations were identified in 28 patients (49.1%), and mosaic NF2 was identified in 20 patients (20, 35.0%). The functional preservation period and outcome differed significantly depending on clinical/genetic factors. Among these factors, “Truncating”, “Mosaic”, and “Age of symptom onset ≥ 25” had the most significant effects on functional disability. By applying a combination of an NF2 mutation type/location, and age of symptom onset, we classified different degrees of functional preservation and progression, schwannoma growth rate and total interventions per year per patient. The prediction of detailed functional outcomes in NF2 patients can plan better strategies for life-long disease management and social integration.

Published
2022
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2. DNA demethylation is associated with malignant progression of lower-grade gliomas

Author

Yoshihiro Muragaki, Mayu Omata, Nobuhito Saito, Motoo Nagane, Yosuke Kitagawa, Ryohei Otani, Fumi Higuchi, Genta Nagae, Taishi Nakamura, Takahide Nejo, Taijun Hana, Koki Aihara, Ryo Nishikawa, Hiroki Ueda, Keisuke Ueki, Hiroyuki Aburatani, Masashi Nomura, Satoshi Takahashi, Shogo Yamamoto, Akitake Mukasa, Shiro Fukuda, Yoshitaka Narita, Kenji Tatsuno, Shota Tanaka, Shunsaku Takayanagi, Takayoshi Umeda, and Kuniaki Saito

Subjects
0301 basic medicine, Oncogene Proteins, Fusion, lcsh:Medicine, Cell Cycle Proteins, Kaplan-Meier Estimate, Biology, Article, Malignant transformation, 03 medical and health sciences, 0302 clinical medicine, Glioma, medicine, Humans, Promoter Regions, Genetic, lcsh:Science, neoplasms, Demethylation, Multidisciplinary, CpG Island Methylator Phenotype, Brain Neoplasms, lcsh:R, RNA-Binding Proteins, Methylation, medicine.disease, Publisher Correction, Isocitrate Dehydrogenase, Up-Regulation, DNA Demethylation, 030104 developmental biology, DNA demethylation, CpG site, Mutation, DNA methylation, Disease Progression, Cancer research, CpG Islands, lcsh:Q, Neoplasm Grading, 030217 neurology & neurosurgery
Abstract

To elucidate the mechanisms of malignant progression of lower-grade glioma, molecular profiling using methylation array, whole-exome sequencing, and RNA sequencing was performed for 122, 36 and 31 gliomas, respectively. This cohort included 24 matched pairs of initial lower-grade gliomas and recurrent tumors, most of which showed malignant progression. Nearly half of IDH-mutant glioblastomas that had progressed from lower-grade gliomas exhibited characteristic partial DNA demethylation in previously methylated genomic regions of their corresponding initial tumors, which had the glioma CpG island methylator phenotype (G-CIMP). In these glioblastomas, cell cycle-related genes, RB and PI3K-AKT pathway genes were frequently altered. Notably, late-replicating domain was significantly enriched in the demethylated regions that were mostly located in non-regulatory regions, suggesting that the loss of DNA methylation during malignant transformation may involve mainly passive demethylation due to a delay in maintenance of methylation during accelerated cell division. Nonetheless, a limited number of genes including IGF2BP3, which potentially drives cell proliferation, were presumed to be upregulated due to demethylation of their promoter. Our data indicated that demethylation of the G-CIMP profile found in a subset of recurrent gliomas reflects accelerated cell divisions accompanied by malignant transformation. Oncogenic genes activated by such epigenetic change represent potential therapeutic targets.

Published
2019

3. Publisher Correction: DNA demethylation is associated with malignant progression of lower-grade gliomas

Author

Fumi Higuchi, Ryohei Otani, Kuniaki Saito, Takayoshi Umeda, Koki Aihara, Motoo Nagane, Kenji Tatsuno, Shota Tanaka, Akitake Mukasa, Taijun Hana, Mayu Omata, Shunsaku Takayanagi, Yoshitaka Narita, Yosuke Kitagawa, Masashi Nomura, Hiroki Ueda, Nobuhito Saito, Ryo Nishikawa, Yoshihiro Muragaki, Shiro Fukuda, Hiroyuki Aburatani, Takahide Nejo, Shogo Yamamoto, Taishi Nakamura, Keisuke Ueki, Genta Nagae, and Satoshi Takahashi

Subjects
Lower grade, Multidisciplinary, DNA demethylation, business.industry, lcsh:R, Cancer research, ComputingMethodologies_DOCUMENTANDTEXTPROCESSING, Medicine, lcsh:Medicine, lcsh:Q, Malignant progression, business, lcsh:Science
Abstract

A correction to this article has been published and is linked from the HTML and PDF versions of this paper. The error has been fixed in the paper.

Published
2019

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