357 results on '"Nagae, Genta"'
Search Results
2. Single-cell multiomics reveals the interplay of clonal evolution and cellular plasticity in hepatoblastoma
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Roehrig, Amélie, Hirsch, Theo Z., Pire, Aurore, Morcrette, Guillaume, Gupta, Barkha, Marcaillou, Charles, Imbeaud, Sandrine, Chardot, Christophe, Gonzales, Emmanuel, Jacquemin, Emmanuel, Sekiguchi, Masahiro, Takita, Junko, Nagae, Genta, Hiyama, Eiso, Guérin, Florent, Fabre, Monique, Aerts, Isabelle, Taque, Sophie, Laithier, Véronique, Branchereau, Sophie, Guettier, Catherine, Brugières, Laurence, Fresneau, Brice, Zucman-Rossi, Jessica, and Letouzé, Eric
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- 2024
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3. Transcriptomic and epigenetic dissection of spinal ependymoma (SP-EPN) identifies clinically relevant subtypes enriched for tumors with and without NF2 mutation
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Neyazi, Sina, Yamazawa, Erika, Hack, Karoline, Tanaka, Shota, Nagae, Genta, Kresbach, Catena, Umeda, Takayoshi, Eckhardt, Alicia, Tatsuno, Kenji, Pohl, Lara, Hana, Taijun, Bockmayr, Michael, Kim, Phyo, Dorostkar, Mario M., Takami, Toshihiro, Obrecht, Denise, Takai, Keisuke, Suwala, Abigail K., Komori, Takashi, Godbole, Shweta, Wefers, Annika K., Otani, Ryohei, Neumann, Julia E., Higuchi, Fumi, Schweizer, Leonille, Nakanishi, Yuta, Monoranu, Camelia-Maria, Takami, Hirokazu, Engertsberger, Lara, Yamada, Keisuke, Ruf, Viktoria, Nomura, Masashi, Mohme, Theresa, Mukasa, Akitake, Herms, Jochen, Takayanagi, Shunsaku, Mynarek, Martin, Matsuura, Reiko, Lamszus, Katrin, Ishii, Kazuhiko, Kluwe, Lan, Imai, Hideaki, von Deimling, Andreas, Koike, Tsukasa, Benesch, Martin, Kushihara, Yoshihiro, Snuderl, Matija, Nambu, Shohei, Frank, Stephan, Omura, Takaki, Hagel, Christian, Kugasawa, Kazuha, Mautner, Viktor F., Ichimura, Koichi, Rutkowski, Stefan, Aburatani, Hiroyuki, Saito, Nobuhito, and Schüller, Ulrich
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- 2024
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4. Mutational signature, cancer driver genes mutations and transcriptomic subgroups predict hepatoblastoma survival
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Pire, Aurore, Hirsch, Theo Z., Morcrette, Guillaume, Imbeaud, Sandrine, Gupta, Barkha, Pilet, Jill, Cornet, Marianna, Fabre, Monique, Guettier, Catherine, Branchereau, Sophie, Brugières, Laurence, Guerin, Florent, Laithier, Véronique, Coze, Carole, Nagae, Genta, Hiyama, Eiso, Laurent-Puig, Pierre, Rebouissou, Sandra, Sarnacki, Sabine, Chardot, Christophe, Capito, Carmen, Faure-Conter, Cécile, Aerts, Isabelle, Taque, Sophie, Fresneau, Brice, and Zucman-Rossi, Jessica
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- 2024
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5. Multiancestry genomic and transcriptomic analysis of gastric cancer
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Totoki, Yasushi, Saito-Adachi, Mihoko, Shiraishi, Yuichi, Komura, Daisuke, Nakamura, Hiromi, Suzuki, Akihiro, Tatsuno, Kenji, Rokutan, Hirofumi, Hama, Natsuko, Yamamoto, Shogo, Ono, Hanako, Arai, Yasuhito, Hosoda, Fumie, Katoh, Hiroto, Chiba, Kenichi, Iida, Naoko, Nagae, Genta, Ueda, Hiroki, Shihang, Chen, Sekine, Shigeki, Abe, Hiroyuki, Nomura, Sachiyo, Matsuura, Tetsuya, Sakai, Eiji, Ohshima, Takashi, Rino, Yasushi, Yeoh, Khay Guan, So, Jimmy, Sanghvi, Kaushal, Soong, Richie, Fukagawa, Akihiko, Yachida, Shinichi, Kato, Mamoru, Seto, Yasuyuki, Ushiku, Tetsuo, Nakajima, Atsushi, Katai, Hitoshi, Tan, Patrick, Ishikawa, Shumpei, Aburatani, Hiroyuki, and Shibata, Tatsuhiro
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- 2023
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6. Identification of the ultrahigh-risk subgroup in neuroblastoma cases through DNA methylation analysis and its treatment exploiting cancer metabolism
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Watanabe, Kentaro, Kimura, Shunsuke, Seki, Masafumi, Isobe, Tomoya, Kubota, Yasuo, Sekiguchi, Masahiro, Sato-Otsubo, Aiko, Hiwatari, Mitsuteru, Kato, Motohiro, Oka, Akira, Koh, Katsuyoshi, Sato, Yusuke, Tanaka, Hiroko, Miyano, Satoru, Kawai, Tomoko, Hata, Kenichiro, Ueno, Hiroo, Nannya, Yasuhito, Suzuki, Hiromichi, Yoshida, Kenichi, Fujii, Yoichi, Nagae, Genta, Aburatani, Hiroyuki, Ogawa, Seishi, and Takita, Junko
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- 2022
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7. Multi-omics analysis defines highly refractory RAS burdened immature subgroup of infant acute lymphoblastic leukemia
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Isobe, Tomoya, Takagi, Masatoshi, Sato-Otsubo, Aiko, Nishimura, Akira, Nagae, Genta, Yamagishi, Chika, Tamura, Moe, Tanaka, Yosuke, Asada, Shuhei, Takeda, Reina, Tsuchiya, Akiho, Wang, Xiaonan, Yoshida, Kenichi, Nannya, Yasuhito, Ueno, Hiroo, Akazawa, Ryo, Kato, Itaru, Mikami, Takashi, Watanabe, Kentaro, Sekiguchi, Masahiro, Seki, Masafumi, Kimura, Shunsuke, Hiwatari, Mitsuteru, Kato, Motohiro, Fukuda, Shiro, Tatsuno, Kenji, Tsutsumi, Shuichi, Kanai, Akinori, Inaba, Toshiya, Shiozawa, Yusuke, Shiraishi, Yuichi, Chiba, Kenichi, Tanaka, Hiroko, Kotecha, Rishi S., Cruickshank, Mark N., Ishikawa, Fumihiko, Morio, Tomohiro, Eguchi, Mariko, Deguchi, Takao, Kiyokawa, Nobutaka, Arakawa, Yuki, Koh, Katsuyoshi, Aoki, Yuki, Ishihara, Takashi, Tomizawa, Daisuke, Miyamura, Takako, Ishii, Eiichi, Mizutani, Shuki, Wilson, Nicola K., Göttgens, Berthold, Miyano, Satoru, Kitamura, Toshio, Goyama, Susumu, Yokoyama, Akihiko, Aburatani, Hiroyuki, Ogawa, Seishi, and Takita, Junko
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- 2022
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8. Aberrant proximal tubule DNA methylation underlies phenotypic changes related to kidney dysfunction in patients with diabetes.
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Marumo, Takeshi, Yoshida, Naoto, Inoue, Noriko, Yamanouchi, Masayuki, Ubara, Yoshifumi, Urakami, Shinji, Fujii, Takeshi, Takazawa, Yutaka, Ohashi, Kenichi, Kawarazaki, Wakako, Nishimoto, Mitsuhiro, Ayuzawa, Nobuhiro, Hirohama, Daigoro, Nagae, Genta, Fujimoto, Mao, Arai, Eri, Kanai, Yae, Hoshino, Junichi, and Fujita, Toshiro
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PROXIMAL kidney tubules ,GLYCEMIC control ,DNA methylation ,DIABETIC nephropathies ,GLOMERULAR filtration rate ,DNA methyltransferases - Abstract
Epigenetic mechanisms are considered to contribute to diabetic nephropathy by maintaining memory of poor glycemic control during the early stages of diabetes. However, DNA methylation changes in the human kidney are poorly characterized, because of the lack of cell type-specific analysis. We examined DNA methylation in proximal tubules (PTs) purified from patients with diabetic nephropathy and identified differentially methylated CpG sites, given the critical role of proximal tubules in the kidney injury. Hypermethylation was observed at CpG sites annotated to genes responsible for proximal tubule functions, including gluconeogenesis, nicotinamide adenine dinucleotide synthesis, transporters of glucose, water, phosphate, and drugs, in diabetic kidneys, whereas genes involved in oxidative stress and the cytoskeleton exhibited demethylation. Methylation levels of CpG sites annotated to ACTN1, BCAR1, MYH9, UBE4B, AFMID, TRAF2, TXNIP, FOXO3, and HNF4A were correlated with the estimated glomerular filtration rate, whereas methylation of the CpG site in RUNX1 was associated with interstitial fibrosis and tubular atrophy. Hypermethylation of G6PC and HNF4A was accompanied by decreased expression in diabetic kidneys. Proximal tubule-specific hypomethylation of metabolic genes related to HNF4A observed in control kidneys was compromised in diabetic kidneys, suggesting a role for aberrant DNA methylation in the dedifferentiation process. Multiple genes with aberrant DNA methylation in diabetes overlapped genes with altered expressions in maladaptive proximal tubule cells, including transcription factors PPARA and RREB1. In conclusion, DNA methylation derangement in the proximal tubules of patients with diabetes may drive phenotypic changes, characterized by inflammatory and fibrotic features, along with impaired function in metabolism and transport. NEW & NOTEWORTHY: Cell type-specific DNA methylation patterns in the human kidney are not known. We examined DNA methylation in proximal tubules of patients with diabetic nephropathy and revealed that oxidative stress, cytoskeleton, and metabolism genes were aberrantly methylated. The results indicate that aberrant DNA methylation in proximal tubules underlies kidney dysfunction in diabetic nephropathy. Aberrant methylation could be a target for reversing memory of poor glycemic control. [ABSTRACT FROM AUTHOR]
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- 2024
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9. Region‐specific DNA hydroxymethylation along the malignant progression of IDH‐mutant gliomas
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Hana, Taijun, primary, Mukasa, Akitake, additional, Nomura, Masashi, additional, Nagae, Genta, additional, Yamamoto, Shogo, additional, Tatsuno, Kenji, additional, Ueda, Hiroki, additional, Fukuda, Shiro, additional, Umeda, Takayoshi, additional, Tanaka, Shota, additional, Nejo, Takahide, additional, Kitagawa, Yosuke, additional, Yamazawa, Erika, additional, Takahashi, Satoshi, additional, Koike, Tsukasa, additional, Kushihara, Yoshihiro, additional, Takami, Hirokazu, additional, Takayanagi, Shunsaku, additional, Aburatani, Hiroyuki, additional, and Saito, Nobuhito, additional
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- 2024
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10. RNA Oncological Therapeutics: Intracellular Hairpin RNA Assembly Enables MicroRNA-Triggered Anticancer Functionality
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Morihiro, Kunihiko, primary, Morita, Shunto, additional, Harada, Naoki, additional, Baba, Manami, additional, Yum, Jongmin, additional, Naito, Mitsuru, additional, Miyata, Kanjiro, additional, Nagae, Genta, additional, and Okamoto, Akimitsu, additional
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- 2024
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11. Genetic and epigenetic basis of hepatoblastoma diversity
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Nagae, Genta, Yamamoto, Shogo, Fujita, Masashi, Fujita, Takanori, Nonaka, Aya, Umeda, Takayoshi, Fukuda, Shiro, Tatsuno, Kenji, Maejima, Kazuhiro, Hayashi, Akimasa, Kurihara, Sho, Kojima, Masato, Hishiki, Tomoro, Watanabe, Kenichiro, Ida, Kohmei, Yano, Michihiro, Hiyama, Yoko, Tanaka, Yukichi, Inoue, Takeshi, Ueda, Hiroki, Nakagawa, Hidewaki, Aburatani, Hiroyuki, and Hiyama, Eiso
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- 2021
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12. BRCC3 mutations in myeloid neoplasms
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Huang, Dayong, Nagata, Yasunobu, Grossmann, Vera, Radivoyevitch, Tomas, Okuno, Yusuke, Nagae, Genta, Hosono, Naoko, Schnittger, Susanne, Sanada, Masashi, Przychodzen, Bartlomiej, Kon, Ayana, Polprasert, Chantana, Shen, Wenyi, Clemente, Michael J, Phillips, James G, Alpermann, Tamara, Yoshida, Kenichi, Nadarajah, Niroshan, Sekeres, Mikkael A, Oakley, Kevin, Nguyen, Nhu, Shiraishi, Yuichi, Shiozawa, Yusuke, Chiba, Kenichi, Tanaka, Hiroko, Koeffler, H Phillip, Klein, Hans-Ulrich, Dugas, Martin, Aburatani, Hiroyuki, Miyano, Satoru, Haferlach, Claudia, Kern, Wolfgang, Haferlach, Torsten, Du, Yang, Ogawa, Seishi, and Makishima, Hideki
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Human Genome ,Rare Diseases ,Cancer ,Genetics ,Hematology ,Stem Cell Research ,Stem Cell Research - Nonembryonic - Non-Human ,Aged ,Aged ,80 and over ,Alleles ,Animals ,BRCA1 Protein ,Chromosome Aberrations ,DNA Mutational Analysis ,Deubiquitinating Enzymes ,Female ,Gene Frequency ,Gene Knockdown Techniques ,Genetic Association Studies ,Genotype ,Humans ,Male ,Membrane Proteins ,Mice ,Middle Aged ,Mutation ,Myeloproliferative Disorders ,Phenotype ,RNA ,Small Interfering ,Immunology - Abstract
Next generation sequencing technologies have provided insights into the molecular heterogeneity of various myeloid neoplasms, revealing previously unknown somatic genetic events. In our cohort of 1444 cases analyzed by next generation sequencing, somatic mutations in the gene BRCA1-BRCA2-containing complex 3 (BRCC3) were identified in 28 cases (1.9%). BRCC3 is a member of the JAMM/MPN+ family of zinc metalloproteases capable of cleaving Lys-63 linked polyubiquitin chains, and is implicated in DNA repair. The mutations were located throughout its coding region. The average variant allelic frequency of BRCC3 mutations was 30.1%, and by a serial sample analysis at two different time points a BRCC3 mutation was already identified in the initial stage of a myelodysplastic syndrome. BRCC3 mutations commonly occurred in nonsense (n=12), frameshift (n=4), and splice site (n=5) configurations. Due to the marginal male dominance (odds ratio; 2.00, 0.84-4.73) of BRCC3 mutations, the majority of mutations (n=23; 82%) were hemizygous. Phenotypically, BRCC3 mutations were frequently observed in myelodysplastic syndromes and myelodysplastic/myeloproliferative neoplasms and associated with -Y abnormality (odds ratio; 3.70, 1.25-11.0). Clinically, BRCC3 mutations were also related to higher age (P=0.01), although prognosis was not affected. Knockdown of Brcc3 gene expression in murine bone marrow lineage negative, Sca1 positive, c-kit positive cells resulted in 2-fold more colony formation and modest differentiation defect. Thus, BRCC3 likely plays a role as tumor-associated gene in myelodysplastic syndromes and myelodysplastic/myeloproliferative neoplasms.
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- 2015
13. Integrated molecular profiling of juvenile myelomonocytic leukemia
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Murakami, Norihiro, Okuno, Yusuke, Yoshida, Kenichi, Shiraishi, Yuichi, Nagae, Genta, Suzuki, Kyogo, Narita, Atsushi, Sakaguchi, Hirotoshi, Kawashima, Nozomu, Wang, Xinan, Xu, Yinyan, Chiba, Kenichi, Tanaka, Hiroko, Hama, Asahito, Sanada, Masashi, Ito, Masafumi, Hirayama, Masashi, Watanabe, Arata, Ueno, Toshihide, Kojima, Seiji, Aburatani, Hiroyuki, Mano, Hiroyuki, Miyano, Satoru, Ogawa, Seishi, Takahashi, Yoshiyuki, and Muramatsu, Hideki
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- 2018
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14. Two distinct modes of DNMT1 recruitment ensure stable maintenance DNA methylation
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Nishiyama, Atsuya, Mulholland, Christopher B., Bultmann, Sebastian, Kori, Satomi, Endo, Akinori, Saeki, Yasushi, Qin, Weihua, Trummer, Carina, Chiba, Yoshie, Yokoyama, Haruka, Kumamoto, Soichiro, Kawakami, Toru, Hojo, Hironobu, Nagae, Genta, Aburatani, Hiroyuki, Tanaka, Keiji, Arita, Kyohei, Leonhardt, Heinrich, and Nakanishi, Makoto
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- 2020
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15. Comprehensive epigenome characterization reveals diverse transcriptional regulation across human vascular endothelial cells
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Nakato, Ryuichiro, Wada, Youichiro, Nakaki, Ryo, Nagae, Genta, Katou, Yuki, Tsutsumi, Shuichi, Nakajima, Natsu, Fukuhara, Hiroshi, Iguchi, Atsushi, Kohro, Takahide, Kanki, Yasuharu, Saito, Yutaka, Kobayashi, Mika, Izumi-Taguchi, Akashi, Osato, Naoki, Tatsuno, Kenji, Kamio, Asuka, Hayashi-Takanaka, Yoko, Wada, Hiromi, Ohta, Shinzo, Aikawa, Masanori, Nakajima, Hiroyuki, Nakamura, Masaki, McGee, Rebecca C., Heppner, Kyle W., Kawakatsu, Tatsuo, Genno, Michiru, Yanase, Hiroshi, Kume, Haruki, Senbonmatsu, Takaaki, Homma, Yukio, Nishimura, Shigeyuki, Mitsuyama, Toutai, Aburatani, Hiroyuki, Kimura, Hiroshi, and Shirahige, Katsuhiko
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- 2019
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16. Supplementary Figures and Legends from Reduced Neoantigen Expression Revealed by Longitudinal Multiomics as a Possible Immune Evasion Mechanism in Glioma
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Nejo, Takahide, primary, Matsushita, Hirokazu, primary, Karasaki, Takahiro, primary, Nomura, Masashi, primary, Saito, Kuniaki, primary, Tanaka, Shota, primary, Takayanagi, Shunsaku, primary, Hana, Taijun, primary, Takahashi, Satoshi, primary, Kitagawa, Yosuke, primary, Koike, Tsukasa, primary, Kobayashi, Yukari, primary, Nagae, Genta, primary, Yamamoto, Shogo, primary, Ueda, Hiroki, primary, Tatsuno, Kenji, primary, Narita, Yoshitaka, primary, Nagane, Motoo, primary, Ueki, Keisuke, primary, Nishikawa, Ryo, primary, Aburatani, Hiroyuki, primary, Mukasa, Akitake, primary, Saito, Nobuhito, primary, and Kakimi, Kazuhiro, primary
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- 2023
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17. Supplementary Tables from Reduced Neoantigen Expression Revealed by Longitudinal Multiomics as a Possible Immune Evasion Mechanism in Glioma
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Nejo, Takahide, primary, Matsushita, Hirokazu, primary, Karasaki, Takahiro, primary, Nomura, Masashi, primary, Saito, Kuniaki, primary, Tanaka, Shota, primary, Takayanagi, Shunsaku, primary, Hana, Taijun, primary, Takahashi, Satoshi, primary, Kitagawa, Yosuke, primary, Koike, Tsukasa, primary, Kobayashi, Yukari, primary, Nagae, Genta, primary, Yamamoto, Shogo, primary, Ueda, Hiroki, primary, Tatsuno, Kenji, primary, Narita, Yoshitaka, primary, Nagane, Motoo, primary, Ueki, Keisuke, primary, Nishikawa, Ryo, primary, Aburatani, Hiroyuki, primary, Mukasa, Akitake, primary, Saito, Nobuhito, primary, and Kakimi, Kazuhiro, primary
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- 2023
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18. Data from Reduced Neoantigen Expression Revealed by Longitudinal Multiomics as a Possible Immune Evasion Mechanism in Glioma
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Nejo, Takahide, primary, Matsushita, Hirokazu, primary, Karasaki, Takahiro, primary, Nomura, Masashi, primary, Saito, Kuniaki, primary, Tanaka, Shota, primary, Takayanagi, Shunsaku, primary, Hana, Taijun, primary, Takahashi, Satoshi, primary, Kitagawa, Yosuke, primary, Koike, Tsukasa, primary, Kobayashi, Yukari, primary, Nagae, Genta, primary, Yamamoto, Shogo, primary, Ueda, Hiroki, primary, Tatsuno, Kenji, primary, Narita, Yoshitaka, primary, Nagane, Motoo, primary, Ueki, Keisuke, primary, Nishikawa, Ryo, primary, Aburatani, Hiroyuki, primary, Mukasa, Akitake, primary, Saito, Nobuhito, primary, and Kakimi, Kazuhiro, primary
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- 2023
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19. Data from Three DNA Methylation Epigenotypes in Human Colorectal Cancer
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Yagi, Koichi, primary, Akagi, Kiwamu, primary, Hayashi, Hiroshi, primary, Nagae, Genta, primary, Tsuji, Shingo, primary, Isagawa, Takayuki, primary, Midorikawa, Yutaka, primary, Nishimura, Yoji, primary, Sakamoto, Hirohiko, primary, Seto, Yasuyuki, primary, Aburatani, Hiroyuki, primary, and Kaneda, Atsushi, primary
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- 2023
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20. Supplementary Data from Three DNA Methylation Epigenotypes in Human Colorectal Cancer
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Yagi, Koichi, primary, Akagi, Kiwamu, primary, Hayashi, Hiroshi, primary, Nagae, Genta, primary, Tsuji, Shingo, primary, Isagawa, Takayuki, primary, Midorikawa, Yutaka, primary, Nishimura, Yoji, primary, Sakamoto, Hirohiko, primary, Seto, Yasuyuki, primary, Aburatani, Hiroyuki, primary, and Kaneda, Atsushi, primary
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- 2023
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21. Supplementary Data from Accumulation of Molecular Aberrations Distinctive to Hepatocellular Carcinoma Progression
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Midorikawa, Yutaka, primary, Yamamoto, Shogo, primary, Tatsuno, Kenji, primary, Renard-Guillet, Claire, primary, Tsuji, Shingo, primary, Hayashi, Akimasa, primary, Ueda, Hiroki, primary, Fukuda, Shiro, primary, Fujita, Takanori, primary, Katoh, Hiroto, primary, Ishikawa, Shumpei, primary, Covington, Kyle R., primary, Creighton, Chad J., primary, Sugitani, Masahiko, primary, Wheeler, David A., primary, Shibata, Tatsuhiro, primary, Nagae, Genta, primary, Takayama, Tadatoshi, primary, and Aburatani, Hiroyuki, primary
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- 2023
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22. Supplementary Figures from Fusion Kinases Identified by Genomic Analyses of Sporadic Microsatellite Instability–High Colorectal Cancers
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Sato, Kazuhito, primary, Kawazu, Masahito, primary, Yamamoto, Yoko, primary, Ueno, Toshihide, primary, Kojima, Shinya, primary, Nagae, Genta, primary, Abe, Hiroyuki, primary, Soda, Manabu, primary, Oga, Takafumi, primary, Kohsaka, Shinji, primary, Sai, Eirin, primary, Yamashita, Yoshihiro, primary, Iinuma, Hisae, primary, Fukayama, Masashi, primary, Aburatani, Hiroyuki, primary, Watanabe, Toshiaki, primary, and Mano, Hiroyuki, primary
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- 2023
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23. Supplementary Tables from Fusion Kinases Identified by Genomic Analyses of Sporadic Microsatellite Instability–High Colorectal Cancers
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Sato, Kazuhito, primary, Kawazu, Masahito, primary, Yamamoto, Yoko, primary, Ueno, Toshihide, primary, Kojima, Shinya, primary, Nagae, Genta, primary, Abe, Hiroyuki, primary, Soda, Manabu, primary, Oga, Takafumi, primary, Kohsaka, Shinji, primary, Sai, Eirin, primary, Yamashita, Yoshihiro, primary, Iinuma, Hisae, primary, Fukayama, Masashi, primary, Aburatani, Hiroyuki, primary, Watanabe, Toshiaki, primary, and Mano, Hiroyuki, primary
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- 2023
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24. Supplementary Figure from Accumulation of Molecular Aberrations Distinctive to Hepatocellular Carcinoma Progression
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Midorikawa, Yutaka, primary, Yamamoto, Shogo, primary, Tatsuno, Kenji, primary, Renard-Guillet, Claire, primary, Tsuji, Shingo, primary, Hayashi, Akimasa, primary, Ueda, Hiroki, primary, Fukuda, Shiro, primary, Fujita, Takanori, primary, Katoh, Hiroto, primary, Ishikawa, Shumpei, primary, Covington, Kyle R., primary, Creighton, Chad J., primary, Sugitani, Masahiko, primary, Wheeler, David A., primary, Shibata, Tatsuhiro, primary, Nagae, Genta, primary, Takayama, Tadatoshi, primary, and Aburatani, Hiroyuki, primary
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- 2023
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25. Supplementary Data from Impact of AAV2 and Hepatitis B Virus Integration Into Genome on Development of Hepatocellular Carcinoma in Patients with Prior Hepatitis B Virus Infection
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Tatsuno, Kenji, primary, Midorikawa, Yutaka, primary, Takayama, Tadatoshi, primary, Yamamoto, Shogo, primary, Nagae, Genta, primary, Moriyama, Mitsuhiko, primary, Nakagawa, Hayato, primary, Koike, Kazuhiko, primary, Moriya, Kyoji, primary, and Aburatani, Hiroyuki, primary
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- 2023
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26. Supplementary Table from Accumulation of Molecular Aberrations Distinctive to Hepatocellular Carcinoma Progression
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Midorikawa, Yutaka, primary, Yamamoto, Shogo, primary, Tatsuno, Kenji, primary, Renard-Guillet, Claire, primary, Tsuji, Shingo, primary, Hayashi, Akimasa, primary, Ueda, Hiroki, primary, Fukuda, Shiro, primary, Fujita, Takanori, primary, Katoh, Hiroto, primary, Ishikawa, Shumpei, primary, Covington, Kyle R., primary, Creighton, Chad J., primary, Sugitani, Masahiko, primary, Wheeler, David A., primary, Shibata, Tatsuhiro, primary, Nagae, Genta, primary, Takayama, Tadatoshi, primary, and Aburatani, Hiroyuki, primary
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- 2023
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27. Supplementary Methods, Tables 1-5, Figures 1-4 from Classification of Epstein–Barr Virus–Positive Gastric Cancers by Definition of DNA Methylation Epigenotypes
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Matsusaka, Keisuke, primary, Kaneda, Atsushi, primary, Nagae, Genta, primary, Ushiku, Tetsuo, primary, Kikuchi, Yasuko, primary, Hino, Rumi, primary, Uozaki, Hiroshi, primary, Seto, Yasuyuki, primary, Takada, Kenzo, primary, Aburatani, Hiroyuki, primary, and Fukayama, Masashi, primary
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- 2023
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28. Data from Classification of Epstein–Barr Virus–Positive Gastric Cancers by Definition of DNA Methylation Epigenotypes
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Matsusaka, Keisuke, primary, Kaneda, Atsushi, primary, Nagae, Genta, primary, Ushiku, Tetsuo, primary, Kikuchi, Yasuko, primary, Hino, Rumi, primary, Uozaki, Hiroshi, primary, Seto, Yasuyuki, primary, Takada, Kenzo, primary, Aburatani, Hiroyuki, primary, and Fukayama, Masashi, primary
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- 2023
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29. Publisher Correction: DNA demethylation is associated with malignant progression of lower-grade gliomas
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Nomura, Masashi, Saito, Kuniaki, Aihara, Koki, Nagae, Genta, Yamamoto, Shogo, Tatsuno, Kenji, Ueda, Hiroki, Fukuda, Shiro, Umeda, Takayoshi, Tanaka, Shota, Takayanagi, Shunsaku, Otani, Ryohei, Nejo, Takahide, Hana, Taijun, Takahashi, Satoshi, Kitagawa, Yosuke, Omata, Mayu, Higuchi, Fumi, Nakamura, Taishi, Muragaki, Yoshihiro, Narita, Yoshitaka, Nagane, Motoo, Nishikawa, Ryo, Ueki, Keisuke, Saito, Nobuhito, Aburatani, Hiroyuki, and Mukasa, Akitake
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- 2019
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30. DNA demethylation is associated with malignant progression of lower-grade gliomas
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Nomura, Masashi, Saito, Kuniaki, Aihara, Koki, Nagae, Genta, Yamamoto, Shogo, Tatsuno, Kenji, Ueda, Hiroki, Fukuda, Shiro, Umeda, Takayoshi, Tanaka, Shota, Takayanagi, Shunsaku, Otani, Ryohei, Nejo, Takahide, Hana, Taijun, Takahashi, Satoshi, Kitagawa, Yosuke, Omata, Mayu, Higuchi, Fumi, Nakamura, Taishi, Muragaki, Yoshihiro, Narita, Yoshitaka, Nagane, Motoo, Nishikawa, Ryo, Ueki, Keisuke, Saito, Nobuhito, Aburatani, Hiroyuki, and Mukasa, Akitake
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- 2019
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31. Loss of Viral Genome with Altered Immune Microenvironment During Tumour Progression of Epstein‐Barr Virus‐Associated Gastric Carcinoma
- Author
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Kondo, Atsushi, primary, Shinozaki‐Ushiku, Aya, additional, Rokutan, Hirofumi, additional, Kunita, Akiko, additional, Ikemura, Masako, additional, Yamashita, Hiroharu, additional, Seto, Yasuyuki, additional, Nagae, Genta, additional, Tatsuno, Kenji, additional, Aburatani, Hiroyuki, additional, Koinuma, Daizo, additional, and Ushiku, Tetsuo, additional
- Published
- 2023
- Full Text
- View/download PDF
32. A deep learning system accurately classifies primary and metastatic cancers using passenger mutation patterns
- Author
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Jiao, Wei, Atwal, Gurnit, Polak, Paz, Karlic, Rosa, Cuppen, Edwin, Al-Shahrour, Fatima, Bailey, Peter J, Biankin, Andrew V, Boutros, Paul C, Campbell, Peter J, Chang, David K, Cooke, Susanna L, Deshpande, Vikram, Faltas, Bishoy M, Faquin, William C, Garraway, Levi, Getz, Gad, Grimmond, Sean M, Haider, Syed, Hoadley, Katherine A, Kaiser, Vera B, Kato, Mamoru, Kübler, Kirsten, Lazar, Alexander J, Li, Constance H, Louis, David N, Margolin, Adam, Martin, Sancha, Nahal-Bose, Hardeep K, Nielsen, G Petur, Nik-Zainal, Serena, Omberg, Larsson, P’ng, Christine, Perry, Marc D, Rheinbay, Esther, Rubin, Mark A, Semple, Colin A, Sgroi, Dennis C, Shibata, Tatsuhiro, Siebert, Reiner, Smith, Jaclyn, Stein, Lincoln D, Stobbe, Miranda D, Sun, Ren X, Thai, Kevin, Wright, Derek W, Wu, Chin-Lee, Yuan, Ke, Zhang, Junjun, Danyi, Alexandra, de Ridder, Jeroen, van Herpen, Carla, Lolkema, Martijn P, Steeghs, Neeltje, Morris, Quaid D, Aaltonen, Lauri A, Abascal, Federico, Abeshouse, Adam, Aburatani, Hiroyuki, Adams, David J, Agrawal, Nishant, Ahn, Keun Soo, Ahn, Sung-Min, Aikata, Hiroshi, Akbani, Rehan, Akdemir, Kadir C, Al-Ahmadie, Hikmat, Al-Sedairy, Sultan T, Alawi, Malik, Albert, Monique, Aldape, Kenneth, Alexandrov, Ludmil B, Ally, Adrian, Alsop, Kathryn, Alvarez, Eva G, Amary, Fernanda, Amin, Samirkumar B, Aminou, Brice, Ammerpohl, Ole, Anderson, Matthew J, Ang, Yeng, Antonello, Davide, Anur, Pavana, Aparicio, Samuel, Appelbaum, Elizabeth L, Arai, Yasuhito, Aretz, Axel, Arihiro, Koji, Ariizumi, Shun-ichi, Armenia, Joshua, Arnould, Laurent, Asa, Sylvia, Assenov, Yassen, Aukema, Sietse, Auman, J Todd, Aure, Miriam RR, Awadalla, Philip, Aymerich, Marta, Bader, Gary D, Baez-Ortega, Adrian, Bailey, Matthew H, Balasundaram, Miruna, Balu, Saianand, Bandopadhayay, Pratiti, Banks, Rosamonde E, Barbi, Stefano, Barbour, Andrew P, Barenboim, Jonathan, Barnholtz-Sloan, Jill, Barr, Hugh, Barrera, Elisabet, Bartlett, John, Bartolome, Javier, Bassi, Claudio, Bathe, Oliver F, Baumhoer, Daniel, Bavi, 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Francesco, Fayzullaev, Nodirjon, Felau, Ina, Fereday, Sian, Ferguson, Martin L, Ferretti, Vincent, Feuerbach, Lars, Field, Matthew A, Fink, J Lynn, Finocchiaro, Gaetano, Fisher, Cyril, Fittall, Matthew W, Fitzgerald, Anna, Fitzgerald, Rebecca C, Flanagan, Adrienne M, Fleshner, Neil E, Flicek, Paul, Foekens, John A, Fong, Kwun M, Fonseca, Nuno A, Foster, Christopher S, Fox, Natalie S, Fraser, Michael, Frazer, Scott, Frenkel-Morgenstern, Milana, Friedman, William, Frigola, Joan, Fronick, Catrina C, Fujimoto, Akihiro, Fujita, Masashi, Fukayama, Masashi, Fulton, Lucinda A, Fulton, Robert S, Furuta, Mayuko, Futreal, P Andrew, Füllgrabe, Anja, Gabriel, Stacey B, Gallinger, Steven, Gambacorti-Passerini, Carlo, Gao, Jianjiong, Gao, Shengjie, Garred, Øystein, Garrison, Erik, Garsed, Dale W, Gehlenborg, Nils, Gelpi, Josep LL, George, Joshy, Gerhard, Daniela S, Gerhauser, Clarissa, Gershenwald, Jeffrey E, Gerstein, Mark, Gerstung, Moritz, Ghori, Mohammed, Ghossein, Ronald, Giama, Nasra H, Gibbs, 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Karaszi, Katalin, Karlan, Beth, Karlić, Rosa, Karsch, Dennis, Kasaian, Katayoon, Kassahn, Karin S, Katai, Hitoshi, Katoh, Hiroto, Kawakami, Yoshiiku, Kay, Jonathan D, Kazakoff, Stephen H, Kazanov, Marat D, Keays, Maria, Kebebew, Electron, Kefford, Richard F, Kellis, Manolis, Kench, James G, Kennedy, Catherine J, Kerssemakers, Jules NA, Khoo, David, Khoo, Vincent, Khuntikeo, Narong, Khurana, Ekta, Kilpinen, Helena, Kim, Hark Kyun, Kim, Hyung-Lae, Kim, Hyung-Yong, Kim, Hyunghwan, Kim, Jaegil, Kim, Jihoon, Kim, Jong K, Kim, Youngwook, King, Tari A, Klapper, Wolfram, Kleinheinz, Kortine, Klimczak, Leszek J, Knappskog, Stian, Kneba, Michael, Knoppers, Bartha M, Koh, Youngil, Komorowski, Jan, Komura, Daisuke, Komura, Mitsuhiro, Kong, Gu, Kool, Marcel, Korbel, Jan O, Korchina, Viktoriya, Korshunov, Andrey, Koscher, Michael, Koster, Roelof, Kote-Jarai, Zsofia, Koures, Antonios, Kovacevic, Milena, Kremeyer, Barbara, Kretzmer, Helene, Kreuz, Markus, Krishnamurthy, Savitri, Kube, Dieter, Kumar, 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Johan, Stadler, Peter F, Staib, Peter, Stark, Stefan G, Stebbings, Lucy, Stefánsson, Ólafur Andri, Stegle, Oliver, Stenhouse, Alasdair, Stewart, Chip, Stilgenbauer, Stephan, Stratton, Michael R, Stretch, Jonathan R, Struck, Adam J, Stuart, Joshua M, Stunnenberg, Henk G, Su, Hong, Su, Xiaoping, Sungalee, Stephanie, Susak, Hana, Suzuki, Akihiro, Sweep, Fred, Szczepanowski, Monika, Sültmann, Holger, Yugawa, Takashi, Tam, Angela, Tamborero, David, Tan, Benita Kiat Tee, Tan, Donghui, Tan, Patrick, Tanaka, Hiroko, Taniguchi, Hirokazu, Tanskanen, Tomas J, Tarabichi, Maxime, Tarnuzzer, Roy, Tarpey, Patrick, Taschuk, Morgan L, Tatsuno, Kenji, Tavaré, Simon, Taylor, Darrin F, Taylor-Weiner, Amaro, Teague, Jon W, Teh, Bin Tean, Tembe, Varsha, Temes, Javier, Thayer, Sarah P, Thiessen, Nina, Thomas, Gilles, Thomas, Sarah, Thompson, Alan, Thompson, Alastair M, Thompson, John FF, Thompson, R Houston, Thorne, Heather, Thorne, Leigh B, Thorogood, Adrian, Tiao, Grace, Tijanic, Nebojsa, Timms, Lee E, 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Paresh, Vázquez-García, Ignacio, Waddell, Nick M, Waddell, Nicola, Wadelius, Claes, Wadi, Lina, Wagener, Rabea, Wala, Jeremiah A, Wang, Jian, Wang, Jiayin, Wang, Linghua, Wang, Qi, Wang, Wenyi, Wang, Yumeng, Wang, Zhining, Waring, Paul M, Warnatz, Hans-Jörg, Warrell, Jonathan, Warren, Anne Y, Waszak, Sebastian M, Wedge, David C, Weichenhan, Dieter, Weinberger, Paul, Weinstein, John N, Weischenfeldt, Joachim, Weisenberger, Daniel J, Welch, Ian, Wendl, Michael C, Werner, Johannes, Whalley, Justin P, Wheeler, David A, Whitaker, Hayley C, Wigle, Dennis, Wilkerson, Matthew D, Williams, Ashley, Wilmott, James S, Wilson, Gavin W, Wilson, Julie M, Wilson, Richard K, Winterhoff, Boris, Wintersinger, Jeffrey A, Wiznerowicz, Maciej, Wolf, Stephan, Wong, Bernice H, Wong, Tina, Wong, Winghing, Woo, Youngchoon, Wood, Scott, Wouters, Bradly G, Wright, Adam J, Wright, Mark H, Wu, Dai-Ying, Wu, Guanming, Wu, Jianmin, Wu, Kui, Wu, Yang, Wu, Zhenggang, Xi, Liu, Xia, Tian, Xiang, Qian, Xiao, Xiao, Xing, Rui, Xiong, Heng, Xu, Qinying, Xu, Yanxun, Xue, Hong, Yachida, Shinichi, Yakneen, Sergei, Yamaguchi, Rui, Yamaguchi, Takafumi N, Yamamoto, Masakazu, Yamamoto, Shogo, Yamaue, Hiroki, Yang, Fan, Yang, Huanming, Yang, Jean Y, Yang, Liming, Yang, Lixing, Yang, Shanlin, Yang, Tsun-Po, Yang, Yang, Yao, Xiaotong, Yaspo, Marie-Laure, Yates, Lucy, Yau, Christina, Ye, Chen, Ye, Kai, Yellapantula, Venkata D, Yoon, Christopher J, Yoon, Sung-Soo, Yousif, Fouad, Yu, Jun, Yu, Kaixian, Yu, Willie, Yu, Yingyan, Yuan, Yuan, Yuen, Denis, Yung, Christina K, Zaikova, Olga, Zamora, Jorge, Zapatka, Marc, Zenklusen, Jean C, Zenz, Thorsten, Zeps, Nikolajs, Zhang, Cheng-Zhong, Zhang, Fan, Zhang, Hailei, Zhang, Hongwei, Zhang, Hongxin, Zhang, Jiashan, Zhang, Jing, Zhang, Xiuqing, Zhang, Xuanping, Zhang, Yan, Zhang, Zemin, Zhao, Zhongming, Zheng, Liangtao, Zheng, Xiuqing, Zhou, Wanding, Zhou, Yong, Zhu, Bin, Zhu, Hongtu, Zhu, Jingchun, Zhu, Shida, Zou, Lihua, Zou, Xueqing, deFazio, Anna, van As, Nicholas, van Deurzen, Carolien HM, van de Vijver, Marc J, Veer, L van’t, and von Mering, Christian
- Subjects
Human Biology & Physiology ,Ecology,Evolution & Ethology ,Tumour Biology ,Genetics & Genomics ,Structural Biology & Biophysics ,Computational & Systems Biology - Abstract
In cancer, the primary tumour’s organ of origin and histopathology are the strongest determinants of its clinical behaviour, but in 3% of cases a patient presents with a metastatic tumour and no obvious primary. Here, as part of the ICGC/TCGA Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium, we train a deep learning classifier to predict cancer type based on patterns of somatic passenger mutations detected in whole genome sequencing (WGS) of 2606 tumours representing 24 common cancer types produced by the PCAWG Consortium. Our classifier achieves an accuracy of 91% on held-out tumor samples and 88% and 83% respectively on independent primary and metastatic samples, roughly double the accuracy of trained pathologists when presented with a metastatic tumour without knowledge of the primary. Surprisingly, adding information on driver mutations reduced accuracy. Our results have clinical applicability, underscore how patterns of somatic passenger mutations encode the state of the cell of origin, and can inform future strategies to detect the source of circulating tumour DNA.
- Published
- 2023
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33. Combined burden and functional impact tests for cancer driver discovery using DriverPower
- Author
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Human Biology & Physiology ,Ecology,Evolution & Ethology ,Tumour Biology ,Genetics & Genomics ,Structural Biology & Biophysics ,Computational & Systems Biology - Abstract
The discovery of driver mutations is one of the key motivations for cancer genome sequencing. Here, as part of the ICGC/TCGA Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium, which aggregated whole genome sequencing data from 2658 cancers across 38 tumour types, we describe DriverPower, a software package that uses mutational burden and functional impact evidence to identify driver mutations in coding and non-coding sites within cancer whole genomes. Using a total of 1373 genomic features derived from public sources, DriverPower’s background mutation model explains up to 93% of the regional variance in the mutation rate across multiple tumour types. By incorporating functional impact scores, we are able to further increase the accuracy of driver discovery. Testing across a collection of 2583 cancer genomes from the PCAWG project, DriverPower identifies 217 coding and 95 non-coding driver candidates. Comparing to six published methods used by the PCAWG Drivers and Functional Interpretation Working Group, DriverPower has the highest F1 score for both coding and non-coding driver discovery. This demonstrates that DriverPower is an effective framework for computational driver discovery.
- Published
- 2023
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34. Integrative pathway enrichment analysis of multivariate omics data
- Author
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Vijver, Marc J, and Veer, L van’t
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Human Biology & Physiology ,Ecology,Evolution & Ethology ,Tumour Biology ,Genetics & Genomics ,Structural Biology & Biophysics ,Computational & Systems Biology - Abstract
Multi-omics datasets represent distinct aspects of the central dogma of molecular biology. Such high-dimensional molecular profiles pose challenges to data interpretation and hypothesis generation. ActivePathways is an integrative method that discovers significantly enriched pathways across multiple datasets using statistical data fusion, rationalizes contributing evidence and highlights associated genes. As part of the ICGC/TCGA Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium, which aggregated whole genome sequencing data from 2658 cancers across 38 tumor types, we integrated genes with coding and non-coding mutations and revealed frequently mutated pathways and additional cancer genes with infrequent mutations. We also analyzed prognostic molecular pathways by integrating genomic and transcriptomic features of 1780 breast cancers and highlighted associations with immune response and anti-apoptotic signaling. Integration of ChIP-seq and RNA-seq data for master regulators of the Hippo pathway across normal human tissues identified processes of tissue regeneration and stem cell regulation. ActivePathways is a versatile method that improves systems-level understanding of cellular organization in health and disease through integration of multiple molecular datasets and pathway annotations.
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- 2023
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35. Pathway and network analysis of more than 2500 whole cancer genomes
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Human Biology & Physiology ,Ecology,Evolution & Ethology ,Tumour Biology ,Genetics & Genomics ,Structural Biology & Biophysics ,Computational & Systems Biology - Abstract
The catalog of cancer driver mutations in protein-coding genes has greatly expanded in the past decade. However, non-coding cancer driver mutations are less well-characterized and only a handful of recurrent non-coding mutations, most notably TERT promoter mutations, have been reported. Here, as part of the ICGC/TCGA Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium, which aggregated whole genome sequencing data from 2658 cancer across 38 tumor types, we perform multi-faceted pathway and network analyses of non-coding mutations across 2583 whole cancer genomes from 27 tumor types compiled by the ICGC/TCGA PCAWG project that was motivated by the success of pathway and network analyses in prioritizing rare mutations in protein-coding genes. While few non-coding genomic elements are recurrently mutated in this cohort, we identify 93 genes harboring non-coding mutations that cluster into several modules of interacting proteins. Among these are promoter mutations associated with reduced mRNA expression in TP53, TLE4, and TCF4. We find that biological processes had variable proportions of coding and non-coding mutations, with chromatin remodeling and proliferation pathways altered primarily by coding mutations, while developmental pathways, including Wnt and Notch, altered by both coding and non-coding mutations. RNA splicing is primarily altered by non-coding mutations in this cohort, and samples containing non-coding mutations in well-known RNA splicing factors exhibit similar gene expression signatures as samples with coding mutations in these genes. These analyses contribute a new repertoire of possible cancer genes and mechanisms that are altered by non-coding mutations and offer insights into additional cancer vulnerabilities that can be investigated for potential therapeutic treatments.
- Published
- 2023
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36. Divergent mutational processes distinguish hypoxic and normoxic tumours
- Author
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Bhandari, Vinayak, Li, Constance H, Bristow, Robert G, Boutros, Paul C, Aaltonen, Lauri A, Abascal, Federico, Abeshouse, Adam, Aburatani, Hiroyuki, Adams, David J, Agrawal, Nishant, Ahn, Keun Soo, Ahn, Sung-Min, Aikata, Hiroshi, Akbani, Rehan, Akdemir, Kadir C, Al-Ahmadie, Hikmat, Al-Sedairy, Sultan T, Al-Shahrour, Fatima, Alawi, Malik, Albert, Monique, Aldape, Kenneth, Alexandrov, Ludmil B, Ally, Adrian, Alsop, Kathryn, Alvarez, Eva G, Amary, Fernanda, Amin, Samirkumar B, Aminou, Brice, Ammerpohl, Ole, Anderson, Matthew J, Ang, Yeng, Antonello, Davide, Anur, Pavana, Aparicio, Samuel, Appelbaum, Elizabeth L, Arai, Yasuhito, Aretz, Axel, Arihiro, Koji, Ariizumi, Shun-ichi, Armenia, Joshua, Arnould, Laurent, Asa, Sylvia, Assenov, Yassen, Atwal, Gurnit, Aukema, Sietse, Auman, J Todd, Aure, Miriam RR, Awadalla, Philip, Aymerich, Marta, Bader, Gary D, Baez-Ortega, Adrian, Bailey, Matthew H, Bailey, Peter J, Balasundaram, Miruna, Balu, Saianand, Bandopadhayay, Pratiti, Banks, Rosamonde E, 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Human Biology & Physiology ,Ecology,Evolution & Ethology ,Tumour Biology ,Genetics & Genomics ,Structural Biology & Biophysics ,Computational & Systems Biology - Abstract
Many primary tumours have low levels of molecular oxygen (hypoxia), and hypoxic tumours respond poorly to therapy. Pan-cancer molecular hallmarks of tumour hypoxia remain poorly understood, with limited comprehension of its associations with specific mutational processes, non-coding driver genes and evolutionary features. Here, as part of the ICGC/TCGA Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium, which aggregated whole genome sequencing data from 2658 cancers across 38 tumour types, we quantify hypoxia in 1188 tumours spanning 27 cancer types. Elevated hypoxia associates with increased mutational load across cancer types, irrespective of underlying mutational class. The proportion of mutations attributed to several mutational signatures of unknown aetiology directly associates with the level of hypoxia, suggesting underlying mutational processes for these signatures. At the gene level, driver mutations in TP53, MYC and PTEN are enriched in hypoxic tumours, and mutations in PTEN interact with hypoxia to direct tumour evolutionary trajectories. Overall, hypoxia plays a critical role in shaping the genomic and evolutionary landscapes of cancer.
- Published
- 2023
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37. Genomic footprints of activated telomere maintenance mechanisms in cancer
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Prinz, Manuel, Pritchard, Antonia L, Prokopec, Stephenie D, Provenzano, Elena, Puente, Xose S, Puig, Sonia, Pulido-Tamayo, Sergio, Pupo, Gulietta M, Purdie, Colin A, Quinn, Michael C, Rabionet, Raquel, Rader, Janet S, Radlwimmer, Bernhard, Radovic, Petar, Raeder, Benjamin, Raine, Keiran M, Ramakrishna, Manasa, Ramakrishnan, Kamna, Ramalingam, Suresh, Raphael, Benjamin J, Rathmell, W Kimryn, Rausch, Tobias, Reifenberger, Guido, Reimand, Jüri, Reis-Filho, Jorge, Reuter, Victor, Reyes-Salazar, Iker, Reyna, Matthew A, Reynolds, Sheila M, Rheinbay, Esther, Riazalhosseini, Yasser, Richardson, Andrea L, Richter, Julia, Ringel, Matthew, Ringnér, Markus, Rino, Yasushi, Roach, Jeffrey, Roberts, Lewis R, Robertson, A Gordon, Robertson, Alan J, Rodriguez, Javier Bartolomé, Rodríguez-González, F Germán, Roehrl, Michael HA, Rohde, Marius, Rokutan, Hirofumi, Romieu, Gilles, Rooman, Ilse, Roques, Tom, Rosebrock, Daniel, Rosenberg, Mara, Rosenstiel, Philip C, Rosenwald, Andreas, Rowe, Edward W, Royo, Romina, Rozen, Steven G, Rubanova, Yulia, Rubin, Mark A, Rubio-Perez, Carlota, Rudneva, Vasilisa A, Rusev, Borislav C, Ruzzenente, Andrea, Rätsch, Gunnar, Sabarinathan, Radhakrishnan, Sabelnykova, Veronica Y, Sadeghi, Sara, Sahinalp, S Cenk, Saini, Natalie, Saito-Adachi, Mihoko, Saksena, Gordon, Salcedo, Adriana, Salgado, Roberto, Salichos, Leonidas, Sallari, Richard, Saller, Charles, Salvia, Roberto, Sam, Michelle, Samra, Jaswinder S, Sanchez-Vega, Francisco, Sander, Chris, Sanders, Grant, Sarin, Rajiv, Sarrafi, Iman, Sasaki-Oku, Aya, Sauer, Torill, Sauter, Guido, Saw, Robyn PM, Scardoni, Maria, Scarlett, Christopher J, Scarpa, Aldo, Scelo, Ghislaine, Schadendorf, Dirk, Schein, Jacqueline E, Schilhabel, Markus B, Schlomm, Thorsten, Schmidt, Heather K, Schramm, Sarah-Jane, Schreiber, Stefan, Schultz, Nikolaus, Schwarz, Roland F, Scolyer, Richard A, Scott, David, Seethala, Raja, Segre, Ayellet V, Selander, Iris, Semple, Colin A, Senbabaoglu, Yasin, Sengupta, Subhajit, Sereni, Elisabetta, Serra, Stefano, Sgroi, Dennis C, Shah, Nimish C, Shahabi, Sagedeh, Shang, Catherine A, Shang, Ping, Shapira, Ofer, Shelton, Troy, Shen, Ciyue, Shen, Hui, Shepherd, Rebecca, Shi, Ruian, Shi, Yan, Shiah, Yu-Jia, Shibata, Tatsuhiro, Shih, Juliann, Shimizu, Eigo, Shimizu, Kiyo, Shin, Seung Jun, Shiraishi, Yuichi, Shmaya, Tal, Shmulevich, Ilya, Shorser, Solomon I, Short, Charles, Shrestha, Raunak, Shringarpure, Suyash S, Shriver, Craig, Shuai, Shimin, Siebert, Reiner, Sieuwerts, Anieta M, Signoretti, Sabina, Sikora, Katarzyna O, Simbolo, Michele, Simon, Ronald, Simons, Janae V, Simpson, Jared T, Simpson, Peter T, Singer, Samuel, Sinnott-Armstrong, Nasa, Sipahimalani, Payal, Skelly, Tara J, Smid, Marcel, Smith, Jaclyn, Smith-McCune, Karen, Socci, Nicholas D, Sofia, Heidi J, Soloway, Matthew G, Song, Lei, Sood, Anil K, Sothi, Sharmila, Sotiriou, Christos, Soulette, Cameron M, Span, Paul N, Spellman, Paul T, Sperandio, Nicola, Spillane, Andrew J, Spiro, Oliver, Spring, Jonathan, Staaf, Johan, Stadler, Peter F, Staib, Peter, Stark, Stefan G, Stebbings, Lucy, Stefánsson, Ólafur Andri, Stegle, Oliver, Stein, Lincoln D, Stenhouse, Alasdair, Stilgenbauer, Stephan, Stobbe, Miranda D, Stratton, Michael R, Stretch, Jonathan R, Struck, Adam J, Stuart, Joshua M, Stunnenberg, Henk G, Su, Hong, Su, Xiaoping, Sun, Ren X, Sungalee, Stephanie, Susak, Hana, Suzuki, Akihiro, Sweep, Fred, Szczepanowski, Monika, Sültmann, Holger, Yugawa, Takashi, Tam, Angela, Tamborero, David, Tan, Benita Kiat Tee, Tan, Donghui, Tan, Patrick, Tanaka, Hiroko, Taniguchi, Hirokazu, Tanskanen, Tomas J, Tarabichi, Maxime, Tarnuzzer, Roy, Tarpey, Patrick, Taschuk, Morgan L, Tatsuno, Kenji, Tavaré, Simon, Taylor, Darrin F, Taylor-Weiner, Amaro, Teague, Jon W, Teh, Bin Tean, Tembe, Varsha, Temes, Javier, Thai, Kevin, Thayer, Sarah P, Thiessen, Nina, Thomas, Gilles, Thomas, Sarah, Thompson, Alan, Thompson, Alastair M, Thompson, John FF, Thompson, R Houston, Thorne, Heather, Thorne, Leigh B, Thorogood, Adrian, Tiao, Grace, Tijanic, Nebojsa, Timms, Lee E, Tirabosco, Roberto, Tojo, Marta, Tommasi, Stefania, Toon, Christopher W, Toprak, Umut H, Tortora, Giampaolo, Tost, Jörg, Totoki, Yasushi, Townend, David, Traficante, Nadia, Treilleux, Isabelle, Trotta, Jean-Rémi, Trümper, Lorenz HP, Tsao, Ming, Tsunoda, Tatsuhiko, Tucker, Olga, Turkington, Richard, Turner, Daniel J, Tutt, Andrew, Ueno, Masaki, Ueno, Naoto T, Umbricht, Christopher, Umer, Husen M, Underwood, Timothy J, Urban, Lara, Urushidate, Tomoko, Ushiku, Tetsuo, Uusküla-Reimand, Liis, Valencia, Alfonso, Van Den Berg, David J, Van Laere, Steven, Van Loo, Peter, Van Meir, Erwin G, Van den Eynden, Gert G, Van der Kwast, Theodorus, Vasudev, Naveen, Vazquez, Miguel, Vedururu, Ravikiran, Veluvolu, Umadevi, Vembu, Shankar, Verbeke, Lieven PC, Vermeulen, Peter, Verrill, Clare, Viari, Alain, Vicente, David, Vicentini, Caterina, VijayRaghavan, K, Viksna, Juris, Vilain, Ricardo E, Vincent-Salomon, Anne, Visakorpi, Tapio, Voet, Douglas, Vyas, Paresh, Vázquez-García, Ignacio, Waddell, Nick M, Wadelius, Claes, Wadi, Lina, Wagener, Rabea, Wang, Jian, Wang, Jiayin, Wang, Linghua, Wang, Qi, Wang, Wenyi, Wang, Yumeng, Wang, Zhining, Waring, Paul M, Warnatz, Hans-Jörg, Warrell, Jonathan, Warren, Anne Y, Waszak, Sebastian M, Wedge, David C, Weichenhan, Dieter, Weinberger, Paul, Weinstein, John N, Weisenberger, Daniel J, Welch, Ian, Wendl, Michael C, Werner, Johannes, Whalley, Justin P, Wheeler, David A, Whitaker, Hayley C, Wigle, Dennis, Wilkerson, Matthew D, Williams, Ashley, Wilmott, James S, Wilson, Gavin W, Wilson, Julie M, Wilson, Richard K, Winterhoff, Boris, Wintersinger, Jeffrey A, Wiznerowicz, Maciej, Wolf, Stephan, Wong, Bernice H, Wong, Tina, Wong, Winghing, Woo, Youngchoon, Wood, Scott, Wouters, Bradly G, Wright, Adam J, Wright, Derek W, Wright, Mark H, Wu, Chin-Lee, Wu, Dai-Ying, Wu, Guanming, Wu, Jianmin, Wu, Kui, Wu, Yang, Wu, Zhenggang, Xi, Liu, Xia, Tian, Xiang, Qian, Xiao, Xiao, Xing, Rui, Xiong, Heng, Xu, Qinying, Xu, Yanxun, Xue, Hong, Yachida, Shinichi, Yakneen, Sergei, Yamaguchi, Rui, Yamaguchi, Takafumi N, Yamamoto, Masakazu, Yamamoto, Shogo, Yamaue, Hiroki, Yang, Fan, Yang, Huanming, Yang, Jean Y, Yang, Liming, Yang, Shanlin, Yang, Tsun-Po, Yang, Yang, Yaspo, Marie-Laure, Yates, Lucy, Yau, Christina, Ye, Chen, Ye, Kai, Yellapantula, Venkata D, Yoon, Christopher J, Yousif, Fouad, Yu, Jun, Yu, Kaixian, Yu, Willie, Yu, Yingyan, Yuan, Ke, Yuan, Yuan, Yuen, Denis, Yung, Christina K, Zaikova, Olga, Zapatka, Marc, Zenklusen, Jean C, Zenz, Thorsten, Zeps, Nikolajs, Zhang, Fan, Zhang, Hailei, Zhang, Hongwei, Zhang, Hongxin, Zhang, Jiashan, Zhang, Jing, Zhang, Junjun, Zhang, Xiuqing, Zhang, Xuanping, Zhang, Yan, Zhang, Zemin, Zhao, Zhongming, Zheng, Liangtao, Zheng, Xiuqing, Zhou, Wanding, Zhou, Yong, Zhu, Bin, Zhu, Hongtu, Zhu, Jingchun, Zhu, Shida, Zou, Lihua, Zou, Xueqing, deFazio, Anna, van As, Nicholas, van Deurzen, Carolien HM, van de Vijver, Marc J, Veer, L van’t, and von Mering, Christian
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Human Biology & Physiology ,Ecology,Evolution & Ethology ,Tumour Biology ,Genetics & Genomics ,Structural Biology & Biophysics ,Computational & Systems Biology - Abstract
Cancers require telomere maintenance mechanisms for unlimited replicative potential. They achieve this through TERT activation or alternative telomere lengthening associated with ATRX or DAXX loss. Here, as part of the ICGC/TCGA Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium, we dissect whole-genome sequencing data of over 2500 matched tumor-control samples from 36 different tumor types aggregated within the ICGC/TCGA Pan-Cancer Analysis of Whole Genomes (PCAWG) Consortium to characterize the genomic footprints of these mechanisms. While the telomere content of tumors with ATRX or DAXX mutations (ATRX/DAXXtrunc) is increased, tumors with TERT modifications show a moderate decrease of telomere content. One quarter of all tumor samples contain somatic integrations of telomeric sequences into non-telomeric DNA. This fraction is increased to 80% prevalence in ATRX/DAXXtrunc tumors, which carry an aberrant telomere variant repeat (TVR) distribution as another genomic marker. The latter feature includes enrichment or depletion of the previously undescribed singleton TVRs TTCGGG and TTTGGG, respectively. Our systematic analysis provides new insight into the recurrent genomic alterations associated with telomere maintenance mechanisms in cancer.
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- 2023
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38. Distinct molecular profile of diffuse cerebellar gliomas
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Nomura, Masashi, Mukasa, Akitake, Nagae, Genta, Yamamoto, Shogo, Tatsuno, Kenji, Ueda, Hiroki, Fukuda, Shiro, Umeda, Takayoshi, Suzuki, Tomonari, Otani, Ryohei, Kobayashi, Keiichi, Maruyama, Takashi, Tanaka, Shota, Takayanagi, Shunsaku, Nejo, Takahide, Takahashi, Satoshi, Ichimura, Koichi, Nakamura, Taishi, Muragaki, Yoshihiro, Narita, Yoshitaka, Nagane, Motoo, Ueki, Keisuke, Nishikawa, Ryo, Shibahara, Junji, Aburatani, Hiroyuki, and Saito, Nobuhito
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- 2017
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39. Methionine Metabolism Regulates Maintenance and Differentiation of Human Pluripotent Stem Cells
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Shiraki, Nobuaki, Shiraki, Yasuko, Tsuyama, Tomonori, Obata, Fumiaki, Miura, Masayuki, Nagae, Genta, Aburatani, Hiroyuki, Kume, Kazuhiko, Endo, Fumio, and Kume, Shoen
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- 2014
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40. EPEN-27. Epigenetic dissection of spinal ependymomas (SP-EPN) separates tumors with and withoutNF2 mutation
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Neyazi, Sina, primary, Yamazawa, Erika, additional, Kresbach, Catena, additional, Nagae, Genta, additional, Eckhardt, Alicia, additional, Umeda, Takayoshi, additional, Pohl, Lara, additional, Tatsuno, Kenji, additional, Saygi, Ceren, additional, Hana, Taijun, additional, Alawi, Malik, additional, Kim, Phyo, additional, Dorostkar, Mario M, additional, Higuchi, Fumi, additional, Suwala, Abigail K, additional, Takami, Toshihiro, additional, Wefers, Annika, additional, Nakanishi, Yuta, additional, Schweizer, Leonille, additional, Takai, Keisuke, additional, Engertsberger, Lara, additional, Komori, Takashi, additional, Mohme, Theresa, additional, Takami, Hirokazu, additional, Mynarek, Martin, additional, Nomura, Masashi, additional, Lamszus, Karin, additional, Mukasa, Akitake, additional, Kluwe, Lan, additional, Takayanagi, Shunsaku, additional, von Deimling, Andreas, additional, Ishii, Kazuhiko, additional, Benesch, Martin, additional, Imai, Hideaki, additional, Snuderl, Matija, additional, Frank, Stephan, additional, Ichimura, Koichi, additional, Hagel, Christian, additional, Mautner, Viktor F, additional, Rutkowski, Stefan, additional, Tanaka, Shota, additional, Aburatani, Hiroyuki, additional, Nobuhito, Saito, additional, and Schüller, Ulrich, additional
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- 2022
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41. Identification of the ultrahigh-risk subgroup in neuroblastoma cases through DNA methylation analysis and its treatment exploiting cancer metabolism
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00359621, Watanabe, Kentaro, Kimura, Shunsuke, Seki, Masafumi, Isobe, Tomoya, Kubota, Yasuo, Sekiguchi, Masahiro, Sato-Otsubo, Aiko, Hiwatari, Mitsuteru, Kato, Motohiro, Oka, Akira, Koh, Katsuyoshi, Sato, Yusuke, Tanaka, Hiroko, Miyano, Satoru, Kawai, Tomoko, Hata, Kenichiro, Ueno, Hiroo, Nannya, Yasuhito, Suzuki, Hiromichi, Yoshida, Kenichi, Fujii, Yoichi, Nagae, Genta, Aburatani, Hiroyuki, Ogawa, Seishi, Takita, Junko, 00359621, Watanabe, Kentaro, Kimura, Shunsuke, Seki, Masafumi, Isobe, Tomoya, Kubota, Yasuo, Sekiguchi, Masahiro, Sato-Otsubo, Aiko, Hiwatari, Mitsuteru, Kato, Motohiro, Oka, Akira, Koh, Katsuyoshi, Sato, Yusuke, Tanaka, Hiroko, Miyano, Satoru, Kawai, Tomoko, Hata, Kenichiro, Ueno, Hiroo, Nannya, Yasuhito, Suzuki, Hiromichi, Yoshida, Kenichi, Fujii, Yoichi, Nagae, Genta, Aburatani, Hiroyuki, Ogawa, Seishi, and Takita, Junko
- Abstract
Neuroblastomas require novel therapies that are based on the exploitation of their biological mechanism. To address this need, we analyzed the DNA methylation and expression datasets of neuroblastomas, extracted a candidate gene characterizing the aggressive features, and conducted functional studies. Based on the DNA methylation data, we identified a subgroup of neuroblastoma cases with 11q loss of heterozygosity with extremely poor prognosis. PHGDH, a serine metabolism-related gene, was extracted as a candidate with strong expression and characteristic methylation in this subgroup as well as in cases with MYCN amplification. PHGDH inhibition suppressed neuroblastoma cell proliferation in vitro and in vivo, indicating that the inhibition of serine metabolism by PHGDH inhibitors is a therapeutic alternative for neuroblastoma. Inhibiting the arginine metabolism, which is closely related to serine metabolism using arginine deiminase, had a combination effect both in vitro and in vivo, especially on extracellular arginine-dependent neuroblastoma cells with ASS1 deficiency. Expression and metabolome analyses of post-dose cells confirmed the synergistic effects of treatments targeting serine and arginine indicated that xCT inhibitors that inhibit cystine uptake could be candidates for further combinatorial treatment. Our results highlight the rational therapeutic strategy of targeting serine/arginine metabolism for intractable neuroblastoma.
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- 2022
42. Multi-omics analysis defines highly refractory RAS burdened immature subgroup of infant acute lymphoblastic leukemia
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60451811, 00359621, Isobe, Tomoya, Takagi, Masatoshi, Sato-Otsubo, Aiko, Nishimura, Akira, Nagae, Genta, Yamagishi, Chika, Tamura, Moe, Tanaka, Yosuke, Asada, Shuhei, Takeda, Reina, Tsuchiya, Akiho, Wang, Xiaonan, Yoshida, Kenichi, Nannya, Yasuhito, Ueno, Hiroo, Akazawa, Ryo, Kato, Itaru, Mikami, Takashi, Watanabe, Kentaro, Sekiguchi, Masahiro, Seki, Masafumi, Kimura, Shunsuke, Hiwatari, Mitsuteru, Kato, Motohiro, Fukuda, Shiro, Tatsuno, Kenji, Tsutsumi, Shuichi, Kanai, Akinori, Inaba, Toshiya, Shiozawa, Yusuke, Shiraishi, Yuichi, Chiba, Kenichi, Tanaka, Hiroko, Kotecha, Rishi S., Cruickshank, Mark N., Ishikawa, Fumihiko, Morio, Tomohiro, Eguchi, Mariko, Deguchi, Takao, Kiyokawa, Nobutaka, Arakawa, Yuki, Koh, Katsuyoshi, Aoki, Yuki, Ishihara, Takashi, Tomizawa, Daisuke, Miyamura, Takako, Ishii, Eiichi, Mizutani, Shuki, Wilson, Nicola K., Göttgens, Berthold, Miyano, Satoru, Kitamura, Toshio, Goyama, Susumu, Yokoyama, Akihiko, Aburatani, Hiroyuki, Ogawa, Seishi, Takita, Junko, 60451811, 00359621, Isobe, Tomoya, Takagi, Masatoshi, Sato-Otsubo, Aiko, Nishimura, Akira, Nagae, Genta, Yamagishi, Chika, Tamura, Moe, Tanaka, Yosuke, Asada, Shuhei, Takeda, Reina, Tsuchiya, Akiho, Wang, Xiaonan, Yoshida, Kenichi, Nannya, Yasuhito, Ueno, Hiroo, Akazawa, Ryo, Kato, Itaru, Mikami, Takashi, Watanabe, Kentaro, Sekiguchi, Masahiro, Seki, Masafumi, Kimura, Shunsuke, Hiwatari, Mitsuteru, Kato, Motohiro, Fukuda, Shiro, Tatsuno, Kenji, Tsutsumi, Shuichi, Kanai, Akinori, Inaba, Toshiya, Shiozawa, Yusuke, Shiraishi, Yuichi, Chiba, Kenichi, Tanaka, Hiroko, Kotecha, Rishi S., Cruickshank, Mark N., Ishikawa, Fumihiko, Morio, Tomohiro, Eguchi, Mariko, Deguchi, Takao, Kiyokawa, Nobutaka, Arakawa, Yuki, Koh, Katsuyoshi, Aoki, Yuki, Ishihara, Takashi, Tomizawa, Daisuke, Miyamura, Takako, Ishii, Eiichi, Mizutani, Shuki, Wilson, Nicola K., Göttgens, Berthold, Miyano, Satoru, Kitamura, Toshio, Goyama, Susumu, Yokoyama, Akihiko, Aburatani, Hiroyuki, Ogawa, Seishi, and Takita, Junko
- Abstract
KMT2A-rearranged infant acute lymphoblastic leukemia (ALL) represents the most refractory type of childhood leukemia. To uncover the molecular heterogeneity of this disease, we perform RNA sequencing, methylation array analysis, whole exome and targeted deep sequencing on 84 infants with KMT2A-rearranged leukemia. Our multi-omics clustering followed by single-sample and single-cell inference of hematopoietic differentiation establishes five robust integrative clusters (ICs) with different master transcription factors, fusion partners and corresponding stages of B-lymphopoietic and early hemato-endothelial development: IRX-type differentiated (IC1), IRX-type undifferentiated (IC2), HOXA-type MLLT1 (IC3), HOXA-type MLLT3 (IC4), and HOXA-type AFF1 (IC5). Importantly, our deep mutational analysis reveals that the number of RAS pathway mutations predicts prognosis and that the most refractory subgroup of IC2 possesses 100% frequency and the heaviest burden of RAS pathway mutations. Our findings highlight the previously under-appreciated intra- and inter-patient heterogeneity of KMT2A-rearranged infant ALL and provide a rationale for the future development of genomics-guided risk stratification and individualized therapy.
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- 2022
43. Generation of induced pluripotent stem cells from primary chronic myelogenous leukemia patient samples
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Kumano, Keiki, Arai, Shunya, Hosoi, Masataka, Taoka, Kazuki, Takayama, Naoya, Otsu, Makoto, Nagae, Genta, Ueda, Koki, Nakazaki, Kumi, Kamikubo, Yasuhiko, Eto, Koji, Aburatani, Hiroyuki, Nakauchi, Hiromitsu, and Kurokawa, Mineo
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- 2012
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44. EPCO-01. MOLECULAR PROFILING OF SPINAL CORD EPENDYMOMA
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Yamazawa, Erika, primary, Tanaka, Shota, additional, Nagae, Genta, additional, Umeda, Takayoshi, additional, Hana, Taijun, additional, Kim, Phyo, additional, Higuchi, Fumi, additional, Takami, Toshihiro, additional, Nakanishi, Yuta, additional, Takai, Keisuke, additional, Komori, Takashi, additional, Takami, Hirokazu, additional, Nomura, Masashi, additional, Mukasa, Akitake, additional, Takayanagi, Shunsaku, additional, Ishii, Kazuhiko, additional, Imai, Hideaki, additional, Matsuura, Reiko, additional, Koike, Tsukasa, additional, Kushihara, Yoshihiro, additional, Nambu, Shohei, additional, Kugasawa, Kazuha, additional, Aburatani, Hiroyuki, additional, and Saito, Nobuhito, additional
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- 2021
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45. Genome‐wide analysis of DNA methylation identifies the apoptosis‐related geneUQCRHas a tumor suppressor in renal cancer
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Miyakuni, Kosuke, primary, Nishida, Jun, additional, Koinuma, Daizo, additional, Nagae, Genta, additional, Aburatani, Hiroyuki, additional, Miyazono, Kohei, additional, and Ehata, Shogo, additional
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- 2021
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46. Molecular classification and diagnostics of upper urinary tract urothelial carcinoma
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Fujii, Yoichi, primary, Sato, Yusuke, additional, Suzuki, Hiromichi, additional, Kakiuchi, Nobuyuki, additional, Yoshizato, Tetsuichi, additional, Lenis, Andrew T., additional, Maekawa, Shigekatsu, additional, Yokoyama, Akira, additional, Takeuchi, Yasuhide, additional, Inoue, Yoshikage, additional, Ochi, Yotaro, additional, Shiozawa, Yusuke, additional, Aoki, Kosuke, additional, Yoshida, Kenichi, additional, Kataoka, Keisuke, additional, Nakagawa, Masahiro M., additional, Nannya, Yasuhito, additional, Makishima, Hideki, additional, Miyakawa, Jimpei, additional, Kawai, Taketo, additional, Morikawa, Teppei, additional, Shiraishi, Yuichi, additional, Chiba, Kenichi, additional, Tanaka, Hiroko, additional, Nagae, Genta, additional, Sanada, Masashi, additional, Sugihara, Eiji, additional, Sato, Taka-Aki, additional, Nakagawa, Tohru, additional, Fukayama, Masashi, additional, Ushiku, Tetsuo, additional, Aburatani, Hiroyuki, additional, Miyano, Satoru, additional, Coleman, Jonathan A., additional, Homma, Yukio, additional, Solit, David B., additional, Kume, Haruki, additional, and Ogawa, Seishi, additional
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- 2021
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47. Molecular classification and diagnostics of upper urinary tract urothelial carcinoma
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90839721, 20515514, 80646373, 40883707, 60451811, 40402127, Fujii, Yoichi, Sato, Yusuke, Suzuki, Hiromichi, Kakiuchi, Nobuyuki, Yoshizato, Tetsuichi, Lenis, Andrew T., Maekawa, Shigekatsu, Yokoyama, Akira, Takeuchi, Yasuhide, Inoue, Yoshikage, Ochi, Yotaro, Shiozawa, Yusuke, Aoki, Kosuke, Yoshida, Kenichi, Kataoka, Keisuke, Nakagawa, Masahiro M., Nannya, Yasuhito, Makishima, Hideki, Miyakawa, Jimpei, Kawai, Taketo, Morikawa, Teppei, Shiraishi, Yuichi, Chiba, Kenichi, Tanaka, Hiroko, Nagae, Genta, Sanada, Masashi, Sugihara, Eiji, Sato, Taka-Aki, Nakagawa, Tohru, Fukayama, Masashi, Ushiku, Tetsuo, Aburatani, Hiroyuki, Miyano, Satoru, Coleman, Jonathan A., Homma, Yukio, Solit, David B., Kume, Haruki, Ogawa, Seishi, 90839721, 20515514, 80646373, 40883707, 60451811, 40402127, Fujii, Yoichi, Sato, Yusuke, Suzuki, Hiromichi, Kakiuchi, Nobuyuki, Yoshizato, Tetsuichi, Lenis, Andrew T., Maekawa, Shigekatsu, Yokoyama, Akira, Takeuchi, Yasuhide, Inoue, Yoshikage, Ochi, Yotaro, Shiozawa, Yusuke, Aoki, Kosuke, Yoshida, Kenichi, Kataoka, Keisuke, Nakagawa, Masahiro M., Nannya, Yasuhito, Makishima, Hideki, Miyakawa, Jimpei, Kawai, Taketo, Morikawa, Teppei, Shiraishi, Yuichi, Chiba, Kenichi, Tanaka, Hiroko, Nagae, Genta, Sanada, Masashi, Sugihara, Eiji, Sato, Taka-Aki, Nakagawa, Tohru, Fukayama, Masashi, Ushiku, Tetsuo, Aburatani, Hiroyuki, Miyano, Satoru, Coleman, Jonathan A., Homma, Yukio, Solit, David B., Kume, Haruki, and Ogawa, Seishi
- Abstract
Upper urinary tract urothelial carcinoma (UTUC) is one of the common urothelial cancers. Its molecular pathogenesis, however, is poorly understood, with no useful biomarkers available for accurate diagnosis and molecular classification. Through an integrated genetic study involving 199 UTUC samples, we delineate the landscape of genetic alterations in UTUC enabling genetic/molecular classification. According to the mutational status of TP53, MDM2, RAS, and FGFR3, UTUC is classified into five subtypes having discrete profiles of gene expression, tumor location/histology, and clinical outcome, which is largely recapitulated in an independent UTUC cohort. Sequencing of urine sediment-derived DNA has a high diagnostic value for UTUC with 82.2% sensitivity and 100% specificity. These results provide a solid basis for better diagnosis and management of UTUC.
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- 2021
48. TET1 upregulation drives cancer cell growth through aberrant enhancer hydroxymethylation of HMGA2 in hepatocellular carcinoma
- Author
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Shirai, Kiyokazu, primary, Nagae, Genta, additional, Seki, Motoaki, additional, Kudo, Yotaro, additional, Kamio, Asuka, additional, Hayashi, Akimasa, additional, Okabe, Atsushi, additional, Ota, Satoshi, additional, Tsutsumi, Shuichi, additional, Fujita, Takanori, additional, Yamamoto, Shogo, additional, Nakaki, Ryo, additional, Kanki, Yasuharu, additional, Osawa, Tsuyoshi, additional, Midorikawa, Yutaka, additional, Tateishi, Keisuke, additional, Ichinose, Masao, additional, and Aburatani, Hiroyuki, additional
- Published
- 2021
- Full Text
- View/download PDF
49. Cohesin mediates transcriptional insulation by CCCTC-binding factor
- Author
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Wendt, Kerstin S., Yoshida, Keisuke, Itoh, Takehiko, Bando, Masashige, Koch, Birgit, Schirghuber, Erika, Tsutsumi, Shuichi, Nagae, Genta, Ishihara, Ko, Mishiro, Tsuyoshi, Yahata, Kazuhide, Imamoto, Fumio, Aburatani, Hiroyuki, Nakao, Mitsuyoshi, Imamoto, Naoko, Maeshima, Kazuhiro, Shirahige, Katsuhiko, and Peters, Jan-Michael
- Subjects
Environmental issues ,Science and technology ,Zoology and wildlife conservation - Abstract
Cohesin complexes mediate sister-chromatid cohesion in dividing cells but may also contribute to gene regulation in postmitotic cells. How cohesin regulates gene expression is not known. Here we describe cohesin-binding [...]
- Published
- 2008
50. High-resolution mapping of DNA methylation in human genome using oligonucleotide tiling array
- Author
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Hayashi, Hiroshi, Nagae, Genta, Tsutsumi, Shuichi, Kaneshiro, Kiyofumi, Kozaki, Takazumi, Kaneda, Atsushi, Sugisaki, Hajime, and Aburatani, Hiroyuki
- Published
- 2007
- Full Text
- View/download PDF
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