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Article ; Online: Precise characterization of somatic complex structural variations from tumor/control paired long-read sequencing data with nanomonsv.

Shiraishi, Yuichi / Koya, Junji / Chiba, Kenichi / Okada, Ai / Arai, Yasuhito / Saito, Yuki / Shibata, Tatsuhiro / Kataoka, Keisuke

Nucleic acids research

2023 Volume 51, Issue 14, Page(s) e74

Abstract: We present our novel software, nanomonsv, for detecting somatic structural variations (SVs) using tumor and matched control long-read sequencing data with a single-base resolution. The current version of nanomonsv includes two detection modules, ... ...

Abstract	We present our novel software, nanomonsv, for detecting somatic structural variations (SVs) using tumor and matched control long-read sequencing data with a single-base resolution. The current version of nanomonsv includes two detection modules, Canonical SV module, and Single breakend SV module. Using tumor/control paired long-read sequencing data from three cancer and their matched lymphoblastoid lines, we demonstrate that Canonical SV module can identify somatic SVs that can be captured by short-read technologies with higher precision and recall than existing methods. In addition, we have developed a workflow to classify mobile element insertions while elucidating their in-depth properties, such as 5' truncations, internal inversions, as well as source sites for 3' transductions. Furthermore, Single breakend SV module enables the detection of complex SVs that can only be identified by long-reads, such as SVs involving highly-repetitive centromeric sequences, and LINE1- and virus-mediated rearrangements. In summary, our approaches applied to cancer long-read sequencing data can reveal various features of somatic SVs and will lead to a better understanding of mutational processes and functional consequences of somatic SVs.
MeSH term(s)	Humans ; Genome, Human ; Genomic Structural Variation ; High-Throughput Nucleotide Sequencing/methods ; Mutation ; Neoplasms/genetics ; Sequence Analysis, DNA/methods ; Software
Language	English
Publishing date	2023-06-13
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	186809-3
ISSN	1362-4962 ; 1362-4954 ; 0301-5610 ; 0305-1048
ISSN (online)	1362-4962 ; 1362-4954
ISSN	0301-5610 ; 0305-1048
DOI	10.1093/nar/gkad526
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Article ; Online: Assessing the efficacy of target adaptive sampling long-read sequencing through hereditary cancer patient genomes.

NPJ genomic medicine

2024 Volume 9, Issue 1, Page(s) 11

Abstract: Innovations in sequencing technology have led to the discovery of novel mutations that cause inherited diseases. However, many patients with suspected genetic diseases remain undiagnosed. Long-read sequencing technologies are expected to significantly ... ...

Abstract	Innovations in sequencing technology have led to the discovery of novel mutations that cause inherited diseases. However, many patients with suspected genetic diseases remain undiagnosed. Long-read sequencing technologies are expected to significantly improve the diagnostic rate by overcoming the limitations of short-read sequencing. In addition, Oxford Nanopore Technologies (ONT) offers adaptive sampling and computationally driven target enrichment technology. This enables more affordable intensive analysis of target gene regions compared to standard non-selective long-read sequencing. In this study, we developed an efficient computational workflow for target adaptive sampling long-read sequencing (TAS-LRS) and evaluated it through application to 33 genomes collected from suspected hereditary cancer patients. Our workflow can identify single nucleotide variants with nearly the same accuracy as the short-read platform and elucidate complex forms of structural variations. We also newly identified several SINE-R/VNTR/Alu (SVA) elements affecting the APC gene in two patients with familial adenomatous polyposis, as well as their sites of origin. In addition, we demonstrated that off-target reads from adaptive sampling, which is typically discarded, can be effectively used to accurately genotype common single-nucleotide polymorphisms (SNPs) across the entire genome, enabling the calculation of a polygenic risk score. Furthermore, we identified allele-specific MLH1 promoter hypermethylation in a Lynch syndrome patient. In summary, our workflow with TAS-LRS can simultaneously capture monogenic risk variants including complex structural variations, polygenic background as well as epigenetic alterations, and will be an efficient platform for genetic disease research and diagnosis.
Language	English
Publishing date	2024-02-17
Publishing country	England
Document type	Journal Article
ZDB-ID	2813848-X
ISSN	2056-7944 ; 2056-7944
ISSN (online)	2056-7944
ISSN	2056-7944
DOI	10.1038/s41525-024-00394-z
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Article: [Successful treatment of pure red cell aplasia with cyclosporin in a patient with T-cell large granular lymphocytic leukemia harboring the STAT3 D661V mutation].

Adachi, Masaaki / Yoshida, Kenichi / Shiraishi, Yuichi / Chiba, Kenichi / Miyano, Satoru / Ogawa, Seishi

Rinsho ketsueki] The Japanese journal of clinical hematology

2019 Volume 60, Issue 1, Page(s) 39–45

Abstract: T-cell large granular lymphocyte (T-LGL) leukemia is a chronic T-cell monoclonal disease that is occasionally associated with pure red cell aplasia (PRCA). A 71-year-old previously healthy man complained of physical fatigue and exhibited anemia ( ... ...

Abstract	T-cell large granular lymphocyte (T-LGL) leukemia is a chronic T-cell monoclonal disease that is occasionally associated with pure red cell aplasia (PRCA). A 71-year-old previously healthy man complained of physical fatigue and exhibited anemia (hemoglobin, 10.5 g/dl) with lymphocytosis (76%) showing LGL. The LGL cells expressed CD3, CD7, CD8, and T-cell receptor (TCR) -α/β. TCR-β/γ gene rearrangement was positive. He was thus diagnosed with CD8
MeSH term(s)	Aged ; Cyclosporine/therapeutic use ; Humans ; Leukemia, Large Granular Lymphocytic/complications ; Lymphocytosis ; Male ; Mutation ; Red-Cell Aplasia, Pure/drug therapy ; STAT3 Transcription Factor/genetics
Chemical Substances	STAT3 Transcription Factor ; STAT3 protein, human ; Cyclosporine (83HN0GTJ6D)
Language	Japanese
Publishing date	2019-02-06
Publishing country	Japan
Document type	Case Reports ; Journal Article
ZDB-ID	390900-1
ISSN	0485-1439
ISSN	0485-1439
DOI	10.11406/rinketsu.60.39
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Zs.A 1175: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MO 535: Show issues

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Article ; Online: Systematic identification of intron retention associated variants from massive publicly available transcriptome sequencing data.

Shiraishi, Yuichi / Okada, Ai / Chiba, Kenichi / Kawachi, Asuka / Omori, Ikuko / Mateos, Raúl Nicolás / Iida, Naoko / Yamauchi, Hirofumi / Kosaki, Kenjiro / Yoshimi, Akihide

Nature communications

2022 Volume 13, Issue 1, Page(s) 5357

Abstract: Many disease-associated genomic variants disrupt gene function through abnormal splicing. With the advancement of genomic medicine, identifying disease-associated splicing associated variants has become more important than ever. Most bioinformatics ... ...

Abstract	Many disease-associated genomic variants disrupt gene function through abnormal splicing. With the advancement of genomic medicine, identifying disease-associated splicing associated variants has become more important than ever. Most bioinformatics approaches to detect splicing associated variants require both genome and transcriptomic data. However, there are not many datasets where both of them are available. In this study, we develop a methodology to detect genomic variants that cause splicing changes (more specifically, intron retention), using transcriptome sequencing data alone. After evaluating its sensitivity and precision, we apply it to 230,988 transcriptome sequencing data from the publicly available repository and identified 27,049 intron retention associated variants (IRAVs). In addition, by exploring positional relationships with variants registered in existing disease databases, we extract 3,000 putative disease-associated IRAVs, which range from cancer drivers to variants linked with autosomal recessive disorders. The in-silico screening framework demonstrates the possibility of near-automatically acquiring medical knowledge, making the most of massively accumulated publicly available sequencing data. Collections of IRAVs identified in this study are available through IRAVDB ( https://iravdb.io/ ).
MeSH term(s)	Introns/genetics ; Levamisole/analogs & derivatives ; Mutation ; RNA Splicing/genetics ; Transcriptome/genetics ; Whole Exome Sequencing
Chemical Substances	Levamisole (2880D3468G) ; 3-aminolevamisole (43081-63-6)
Language	English
Publishing date	2022-09-29
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-022-32887-9
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Article ; Online: OVarCall: Bayesian Mutation Calling Method Utilizing Overlapping Paired-End Reads.

Moriyama, Takuya / Shiraishi, Yuichi / Chiba, Kenichi / Yamaguchi, Rui / Imoto, Seiya / Miyano, Satoru

IEEE transactions on nanobioscience

2017 Volume 16, Issue 2, Page(s) 116–122

Abstract: Detection of somatic mutations from tumor and matched normal sequencing data has become a standard approach in cancer research. Although a number of mutation callers have been developed, it is still difficult to detect mutations with low allele frequency ...

Abstract	Detection of somatic mutations from tumor and matched normal sequencing data has become a standard approach in cancer research. Although a number of mutation callers have been developed, it is still difficult to detect mutations with low allele frequency even in exome sequencing. We expect that overlapping paired-end read information is effective for this purpose, but no mutation caller has modeled overlapping information statistically in a proper form in exome sequence data. Here, we develop a Bayesian hierarchical method, OVar- Call (https://github.com/takumorizo/OVarCall), where overlapping paired-end read information improves the accuracy of low allele frequency mutation detection. Firstly, we construct two generative models: one is for reads with somatic variants generated from tumor cells and the other is for reads that does not have somatic variants but potentially includes sequence errors. Secondly, we calculate marginal likelihood for each model using a variational Bayesian algorithm to compute Bayes factor for the detection of somatic mutations. We empirically evaluated the performance of OVarCall and confirmed its better performance than other existing methods.
Language	English
Publishing date	2017-03-01
Publishing country	United States
Document type	Journal Article
ISSN	1558-2639
ISSN (online)	1558-2639
DOI	10.1109/TNB.2017.2670601
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Article ; Online: Inter- and intra-tumor heterogeneity of genetic and immune profiles in inherited renal cell carcinoma.

Cell reports

2023 Volume 42, Issue 7, Page(s) 112736

Abstract: Patients with von Hippel-Lindau disease (vHL) are at risk of developing spatially and temporally multiple clear cell renal cell carcinomas (ccRCCs), which offers a valuable opportunity to analyze inter- and intra-tumor heterogeneity of genetic and immune ...

Abstract	Patients with von Hippel-Lindau disease (vHL) are at risk of developing spatially and temporally multiple clear cell renal cell carcinomas (ccRCCs), which offers a valuable opportunity to analyze inter- and intra-tumor heterogeneity of genetic and immune profiles within the same patient. Here, we perform whole-exome and RNA sequencing, digital gene expression, and immunohistochemical analyses for 81 samples from 51 ccRCCs of 10 patients with vHL. Inherited ccRCCs are clonally independent and have less genomic alterations than sporadic ccRCCs. Hierarchical clustering of transcriptome profiles shows two clusters with distinct immune signatures: immune hot and cold clusters. Interestingly, not only samples from the same tumors but also different tumors from the same patients tend to show a similar immune signature, whereas samples from different patients frequently exhibit different signatures. Our findings reveal the genetic and immune landscape of inherited ccRCCs, demonstrating the relevance of host factors in shaping anti-tumor immunity.
MeSH term(s)	Humans ; Carcinoma, Renal Cell/genetics ; Carcinoma, Renal Cell/pathology ; Kidney Neoplasms/genetics ; Kidney Neoplasms/pathology ; Von Hippel-Lindau Tumor Suppressor Protein/genetics ; Von Hippel-Lindau Tumor Suppressor Protein/metabolism ; von Hippel-Lindau Disease/genetics ; von Hippel-Lindau Disease/pathology ; Base Sequence ; Carcinoma/genetics ; Mutation
Chemical Substances	Von Hippel-Lindau Tumor Suppressor Protein (EC 2.3.2.27)
Language	English
Publishing date	2023-07-04
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2023.112736
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Article ; Online: Genetic Analysis of Pheochromocytoma and Paraganglioma Complicating Cyanotic Congenital Heart Disease.

Ogasawara, Tatsuki / Fujii, Yoichi / Kakiuchi, Nobuyuki / Shiozawa, Yusuke / Sakamoto, Ryuichi / Ogawa, Yoshihiro / Ootani, Katsuki / Ito, Etsuro / Tanaka, Tomoaki / Watanabe, Kenichiro / Yoshida, Yusaku / Kimura, Noriko / Shiraishi, Yuichi / Chiba, Kenichi / Tanaka, Hiroko / Miyano, Satoru / Ogawa, Seishi

The Journal of clinical endocrinology and metabolism

2022 Volume 107, Issue 9, Page(s) 2545–2555

Abstract: Context: Pheochromocytoma and paraganglioma (PPGL) may appear as a complication of cyanotic congenital heart disease (CCHD-PPGL) with frequent EPAS1 mutations, suggesting a close link between EPAS1 mutations and tissue hypoxia in CCHD-PPGL pathogenesis.! ...

Abstract	Context: Pheochromocytoma and paraganglioma (PPGL) may appear as a complication of cyanotic congenital heart disease (CCHD-PPGL) with frequent EPAS1 mutations, suggesting a close link between EPAS1 mutations and tissue hypoxia in CCHD-PPGL pathogenesis. Objective: Our aim is to further investigate the role of EPAS1 mutations in the hypoxia-driven mechanism of CCHD-PPGL pathogenesis, particularly focusing on metachronous and/or multifocal CCHD-PPGL tumors. Methods: We performed whole-exome sequencing (WES) for somatic and germline mutations in 15 PPGL samples from 7 CCHD patients, including 3 patients with metachronous and/or multifocal tumors, together with an adrenal medullary hyperplasia (AMH) sample. Results: We detected EPAS1 mutations in 15 out of 16 PPGL/AMH samples from 7 cases. Conspicuously, all EPAS1 mutations in each of 3 cases with multifocal or metachronous tumors were mutually independent and typical examples of parallel evolution, which is suggestive of strong positive selection of EPAS1-mutated clones. Compared to 165 The Cancer Genome Atlas non-CCHD-PPGL samples, CCHD-PPGL/AMH samples were enriched for 11p deletions (13/16) and 2p amplifications (4/16). Of particular note, the multiple metachronous PPGL tumors with additional copy number abnormalities developed 18 to 23 years after the resolution of hypoxemia, suggesting that CCHD-induced hypoxic environments are critical for positive selection of EPAS1 mutants in early life, but may no longer be required for development of PPGL in later life. Conclusion: Our results highlight a key role of activated hypoxia-inducible factor 2α due to mutated EPAS1 in positive selection under hypoxic environments, although hypoxemia itself may not necessarily be required for the EPAS1-mutated clones to progress to PPGL.
MeSH term(s)	Adrenal Gland Neoplasms/complications ; Adrenal Gland Neoplasms/genetics ; Adrenal Gland Neoplasms/pathology ; Heart Defects, Congenital/complications ; Heart Defects, Congenital/genetics ; Humans ; Hypoxia/genetics ; Paraganglioma/complications ; Paraganglioma/genetics ; Paraganglioma/pathology ; Pheochromocytoma/complications ; Pheochromocytoma/genetics ; Pheochromocytoma/pathology
Language	English
Publishing date	2022-06-22
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3029-6
ISSN	1945-7197 ; 0021-972X
ISSN (online)	1945-7197
ISSN	0021-972X
DOI	10.1210/clinem/dgac362
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Article ; Online: KRAS G12 mutations as adverse prognostic factors in KMT2A-rearranged acute myeloid leukemia.

Iyoda, Shinju / Yoshida, Kenichi / Shoji, Kota / Ito, Nana / Tanaka, Miu / Nannya, Yasuhito / Yamato, Genki / Tsujimoto, Shinichi / Shiba, Norio / Hayashi, Yasuhide / Shiozawa, Yusuke / Shiraishi, Yuichi / Chiba, Kenichi / Okada, Ai / Tanaka, Hiroko / Miyano, Satoru / Koga, Yuhki / Goto, Hiroaki / Moritake, Hiroshi /

Terui, Kiminori / Ito, Etsuro / Kiyokawa, Nobutaka / Tomizawa, Daisuke / Taga, Takashi / Tawa, Akio / Takita, Junko / Nishikori, Momoko / Adachi, Souichi / Ogawa, Seishi / Matsuo, Hidemasa

Leukemia

2024

Language	English
Publishing date	2024-04-18
Publishing country	England
Document type	Journal Article
ZDB-ID	807030-1
ISSN	1476-5551 ; 0887-6924
ISSN (online)	1476-5551
ISSN	0887-6924
DOI	10.1038/s41375-024-02244-4
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Article ; Online: A comprehensive characterization of

Shiraishi, Yuichi / Kataoka, Keisuke / Chiba, Kenichi / Okada, Ai / Kogure, Yasunori / Tanaka, Hiroko / Ogawa, Seishi / Miyano, Satoru

Genome research

2018 Volume 28, Issue 8, Page(s) 1111–1125

Abstract: Although many driver mutations are thought to promote carcinogenesis via abnormal splicing, the landscape of splicing-associated variants (SAVs) remains unknown due to the complexity of splicing abnormalities. Here, we developed a statistical framework ... ...

Abstract	Although many driver mutations are thought to promote carcinogenesis via abnormal splicing, the landscape of splicing-associated variants (SAVs) remains unknown due to the complexity of splicing abnormalities. Here, we developed a statistical framework to systematically identify SAVs disrupting or newly creating splice site motifs and applied it to matched whole-exome and transcriptome sequencing data from 8976 samples across 31 cancer types, generating a catalog of 14,438 SAVs. Such a large collection of SAVs enabled us to characterize their genomic features, underlying mutational processes, and influence on cancer driver genes. In fact, ∼50% of SAVs identified were those disrupting noncanonical splice sites (non-GT-AG dinucleotides), including the third and fifth intronic bases of donor sites, or newly creating splice sites. Mutation signature analysis revealed that tobacco smoking is more strongly associated with SAVs, whereas ultraviolet exposure has less impact. SAVs showed remarkable enrichment of cancer-related genes, and as many as 14.7% of samples harbored at least one SAVs affecting them, particularly in tumor suppressors. In addition to intron retention, whose association with tumor suppressor inactivation has been previously reported, exon skipping and alternative splice site usage caused by SAVs frequently affected tumor suppressors. Finally, we described high-resolution distributions of SAVs along the gene and their splicing outcomes in commonly disrupted genes, including
MeSH term(s)	Female ; Gene Expression Regulation, Neoplastic ; Humans ; Male ; Neoplasm Proteins/biosynthesis ; Neoplasm Proteins/genetics ; RNA Splice Sites ; RNA Splicing ; RNA, Neoplasm/biosynthesis ; RNA, Neoplasm/genetics
Chemical Substances	Neoplasm Proteins ; RNA Splice Sites ; RNA, Neoplasm
Language	English
Publishing date	2018-07-16
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1284872-4
ISSN	1549-5469 ; 1088-9051 ; 1054-9803
ISSN (online)	1549-5469
ISSN	1088-9051 ; 1054-9803
DOI	10.1101/gr.231951.117
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Article ; Online: Genomon ITDetector: a tool for somatic internal tandem duplication detection from cancer genome sequencing data.

Chiba, Kenichi / Shiraishi, Yuichi / Nagata, Yasunobu / Yoshida, Kenichi / Imoto, Seiya / Ogawa, Seishi / Miyano, Satoru

Bioinformatics (Oxford, England)

2015 Volume 31, Issue 1, Page(s) 116–118

Abstract: Summary: Somatic internal tandem duplications (ITDs) are known to play important roles in cancer pathogenesis. Although recent advances in high-throughput sequencing technologies have enabled genome-wide detection of various types of genomic mutations, ... ...

Abstract	Summary: Somatic internal tandem duplications (ITDs) are known to play important roles in cancer pathogenesis. Although recent advances in high-throughput sequencing technologies have enabled genome-wide detection of various types of genomic mutations, including single nucleotide variants, indels and structural variations, only a few studies have focused on ITDs. We have developed an analytical tool called 'Genomon ITDetector' for genome-wide detection of somatic ITDs. After evaluating the sensitivity and precision of the proposed approach using synthetic data, we have demonstrated that it can successfully detect not only common ITDs involving FLT3, but also a number of ITDs affecting other putative driver genes in acute myeloid leukemia exome sequencing data. Availability and implementaion: Genomon ITDetector is freely available at https://github.com/ken0-1n/Genomon-ITDetector.
MeSH term(s)	Computational Biology/methods ; DNA Mutational Analysis/methods ; Exome/genetics ; High-Throughput Nucleotide Sequencing/methods ; Humans ; Leukemia, Myeloid, Acute/diagnosis ; Leukemia, Myeloid, Acute/genetics ; Mutation/genetics ; Tandem Repeat Sequences/genetics ; fms-Like Tyrosine Kinase 3/genetics
Chemical Substances	FLT3 protein, human (EC 2.7.10.1) ; fms-Like Tyrosine Kinase 3 (EC 2.7.10.1)
Language	English
Publishing date	2015-01-01
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1422668-6
ISSN	1367-4811 ; 1367-4803
ISSN (online)	1367-4811
ISSN	1367-4803
DOI	10.1093/bioinformatics/btu593
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