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1. Integrated genetic and clinical prognostic factors for aggressive adult T-cell leukemia/lymphoma

Author

70866582, Kameda, Takuro, Kataoka, Keisuke, Kamiunten, Ayako, Hidaka, Michihiro, Miyoshi, Hiroaki, Nakano, Nobuaki, Nosaka, Kisato, Yoshimitsu, Makoto, Yasunaga, Jun-Ichirou, Kogure, Yasunori, Shide, Kotaro, Miyahara, Masaharu, Sakamoto, Takashi, Akizuki, Keiichi, Hidaka, Tomonori, Kubuki, Yoko, Koya, Junji, Kawano, Noriaki, Yamashita, Kiyoshi, Kawano, Hiroshi, Toyama, Takanori, Maeda, Kouichi, Marutsuka, Kosuke, Imaizumi, Yoshitaka, Kato, Koji, Sugio, Takeshi, Tokunaga, Masahito, Tashiro, Yukie, Takaori-Kondo, Akifumi, Miyazaki, Yasushi, Akashi, Koichi, Ishitsuka, Kenji, Matsuoka, Masao, Ohshima, Koichi, Watanabe, Toshiki, Kitanaka, Akira, Utsunomiya, Atae, Ogawa, Seishi, Shimoda, Kazuya, 70866582, Kameda, Takuro, Kataoka, Keisuke, Kamiunten, Ayako, Hidaka, Michihiro, Miyoshi, Hiroaki, Nakano, Nobuaki, Nosaka, Kisato, Yoshimitsu, Makoto, Yasunaga, Jun-Ichirou, Kogure, Yasunori, Shide, Kotaro, Miyahara, Masaharu, Sakamoto, Takashi, Akizuki, Keiichi, Hidaka, Tomonori, Kubuki, Yoko, Koya, Junji, Kawano, Noriaki, Yamashita, Kiyoshi, Kawano, Hiroshi, Toyama, Takanori, Maeda, Kouichi, Marutsuka, Kosuke, Imaizumi, Yoshitaka, Kato, Koji, Sugio, Takeshi, Tokunaga, Masahito, Tashiro, Yukie, Takaori-Kondo, Akifumi, Miyazaki, Yasushi, Akashi, Koichi, Ishitsuka, Kenji, Matsuoka, Masao, Ohshima, Koichi, Watanabe, Toshiki, Kitanaka, Akira, Utsunomiya, Atae, Ogawa, Seishi, and Shimoda, Kazuya

Abstract

The prognosis of aggressive adult T-cell leukemia/lymphoma (ATL) is poor, and allogeneic hematopoietic stem-cell transplantation (allo-HSCT) is a curative treatment. To identify favorable prognostic patients after intensive chemotherapy, and who therefore might not require upfront allo-HSCT, we aimed to improve risk stratification of aggressive ATL patients aged <70 years. The clinical risk factors and genetic mutations were incorporated into risk modeling for overall survival (OS). We generated the m7-ATLPI, a clinicogenetic risk model for OS, that included the ATL prognostic index (PI) (ATL-PI) risk category, and non-silent mutations in seven genes, namely TP53, IRF4, RHOA, PRKCB, CARD11, CCR7, and GATA3. In the training cohort of 99 patients, the m7-ATLPI identified a low-, intermediate-, and high-risk group with 2-year OS of 100%, 43%, and 19%, respectively (hazard ratio [HR] 5.46, p < 0.0001). The m7-ATLPI achieved superior risk stratification compared to the current ATL-PI (C-index 0.92 vs. 0.85, respectively). In the validation cohort of 84 patients, the m7-ATLPI defined low-, intermediate-, and high-risk groups with a 2-year OS of 81%, 30%, and 0%, respectively (HR 2.33, p = 0.0094), and the model again outperformed the ATL-PI (C-index 0.72 vs. 0.70, respectively). The simplified m7-ATLPI, which is easier to use in clinical practice, achieved superior risk stratification compared to the ATL-PI, as did the original m7-ATLPI; the simplified version was calculated by summing the following: high-risk ATL-PI category (+10), low-risk ATL-PI category (−4), and non-silent mutations in TP53 (+4), IRF4 (+3), RHOA (+1), PRKCB (+1), CARD11 (+0.5), CCR7 (−2), and GATA3 (−3).

Published
2023

2. Generation of functional oocytes from male mice in vitro

Author

Murakami, Kenta, Hamazaki, Nobuhiko, Hamada, Norio, Nagamatsu, Go, Okamoto, Ikuhiro, Ohta, Hiroshi, Nosaka, Yoshiaki, Ishikura, Yukiko, Kitajima, S Tomoya, Semba, Yuichiro, Kunisaki, Yuya, Arai, Fumio, Akashi, Koichi, Saitou, Mitinori, Kato, Kiyoko, Hayashi, Katsuhiko, Murakami, Kenta, Hamazaki, Nobuhiko, Hamada, Norio, Nagamatsu, Go, Okamoto, Ikuhiro, Ohta, Hiroshi, Nosaka, Yoshiaki, Ishikura, Yukiko, Kitajima, S Tomoya, Semba, Yuichiro, Kunisaki, Yuya, Arai, Fumio, Akashi, Koichi, Saitou, Mitinori, Kato, Kiyoko, and Hayashi, Katsuhiko

Abstract

type:Article, Sex chromosome disorders severely compromise gametogenesis in both males and females. In oogenesis, the presence of an additional Y chromosome or the loss of an X chromosome disturbs the robust production of oocytes. Here we efficiently converted the XY chromosome set to XX without an additional Y chromosome in mouse pluripotent stem (PS) cells. In addition, this chromosomal alteration successfully eradicated trisomy 16, a model of Down’s syndrome, in PS cells. Artificially produced euploid XX PS cells differentiated into mature oocytes in culture with similar efficiency to native XX PS cells. Using this method, we differentiated induced pluripotent stem cells from the tail of a sexually mature male mouse into fully potent oocytes, which gave rise to offspring after fertilization. This study provides insights that could ameliorate infertility caused by sex chromosome or autosomal disorders, and opens the possibility of bipaternal reproduction.

Published
2023

3. TET2 Clonal Hematopoiesis Is Associated With Anthracycline-Induced Cardiotoxicity in Patients With Lymphoma

Author

Hatakeyama, Kiwamu, Hieda, Michinari, Semba, Yuichiro, Moriyama, Shohei, Wang, Yuqing, Maeda, Takahiro, Kato, Koji, Miyamoto, Toshihiro, Akashi, Koichi, Kikushige, Yoshikane, Hatakeyama, Kiwamu, Hieda, Michinari, Semba, Yuichiro, Moriyama, Shohei, Wang, Yuqing, Maeda, Takahiro, Kato, Koji, Miyamoto, Toshihiro, Akashi, Koichi, and Kikushige, Yoshikane

Abstract

type:RESEARCH LETTER, Clonal hematopoiesis (CH) refers to the disproportionate expansion of hematopoietic stem cell clones and their corresponding progeny following the acquisition of somatic mutations. CH is common at the time of diagnosis in patients with blood cancers, including multiple myeloma (MM) and lymphoma. The presence of CH mutations correlates with IL-6 mediated inflammation and may result in lymphoma or MM modulation through microenvironment effects or by manifestations of the mutations themselves within the founding tumor clone. As might be expected with a variety of mutations and multiple potential mechanisms, CH exerts context-dependent effects, being protective in some settings and harmful in others. Though CH is very common in patients with hematologic malignancies, how it intersects with therapy and the natural disease course of these cancers are active areas of investigation. In lymphomas and MM specifically, patients have high rates of CH at diagnosis and are subsequently exposed to therapies, such as cytotoxic chemotherapy, that can cause CH progression to overt hematologic malignancy. The expanding diversity of treatment modalities for these cancers also increases the opportunities for CH to impact clinical outcome and modulate clinical responses. Here we review the basic biology and known health effects of CH, and we focus on the clinical relevance of CH in lymphoma and MM.

Published
2023

4. TET2 Clonal Hematopoiesis Is Associated With Anthracycline-Induced Cardiotoxicity in Patients With Lymphoma

Author

Hatakeyama, Kiwamu, Hieda, Michinari, Semba, Yuichiro, Moriyama, Shohei, Wang, Yuqing, Maeda, Takahiro, Kato, Koji, Miyamoto, Toshihiro, Akashi, Koichi, Kikushige, Yoshikane, Hatakeyama, Kiwamu, Hieda, Michinari, Semba, Yuichiro, Moriyama, Shohei, Wang, Yuqing, Maeda, Takahiro, Kato, Koji, Miyamoto, Toshihiro, Akashi, Koichi, and Kikushige, Yoshikane

Abstract

type:RESEARCH LETTER, Clonal hematopoiesis (CH) refers to the disproportionate expansion of hematopoietic stem cell clones and their corresponding progeny following the acquisition of somatic mutations. CH is common at the time of diagnosis in patients with blood cancers, including multiple myeloma (MM) and lymphoma. The presence of CH mutations correlates with IL-6 mediated inflammation and may result in lymphoma or MM modulation through microenvironment effects or by manifestations of the mutations themselves within the founding tumor clone. As might be expected with a variety of mutations and multiple potential mechanisms, CH exerts context-dependent effects, being protective in some settings and harmful in others. Though CH is very common in patients with hematologic malignancies, how it intersects with therapy and the natural disease course of these cancers are active areas of investigation. In lymphomas and MM specifically, patients have high rates of CH at diagnosis and are subsequently exposed to therapies, such as cytotoxic chemotherapy, that can cause CH progression to overt hematologic malignancy. The expanding diversity of treatment modalities for these cancers also increases the opportunities for CH to impact clinical outcome and modulate clinical responses. Here we review the basic biology and known health effects of CH, and we focus on the clinical relevance of CH in lymphoma and MM.

Published
2023

5. Platypnea-Orthodeoxia Syndrome in Coronavirus Disease 2019 Pneumonia: A Case Report and Literature Review

Author

Tanimoto,Takahiko, Eriguchi,Yoshihiro, Sato,Tomonori, Yonekawa,Akiko, Miyake,Noriko, Akashi,Koichi, Shimono,Nobuyuki, Tanimoto,Takahiko, Eriguchi,Yoshihiro, Sato,Tomonori, Yonekawa,Akiko, Miyake,Noriko, Akashi,Koichi, and Shimono,Nobuyuki

Abstract

Takahiko Tanimoto,1,2 Yoshihiro Eriguchi,1 Tomonori Sato,1 Akiko Yonekawa,1 Noriko Miyake,1 Koichi Akashi,1 Nobuyuki Shimono3 1Department of Clinical Immunology and Rheumatology / Infectious Disease, Kyushu University Hospital, Fukuoka, Japan; 2Department of Infectious Diseases, Kagoshima Seikyo Hospital, Kagoshima, Japan; 3Center for the Study of Global Infection, Kyushu University Hospital, Fukuoka, JapanCorrespondence: Yoshihiro Eriguchi, Department of Clinical Immunology and Rheumatology / Infectious Disease, Kyushu University Hospital, 3-1-1, Maidashi, Higashi-ku, Fukuoka, 812-8582, Japan, Tel +81 92-801-1011, Fax +81 92-862-8200, Email eriguchi.yoshihiro.145@m.kyushu-u.ac.jpAbstract: Platypnea-orthodeoxia syndrome (POS) is a rare disorder associated with coronavirus disease 2019 (COVID-19) pneumonia. However, POS may be underdiagnosed. We report the case of a 59-year-old female patient with POS complicated by pulmonary embolism in COVID-19. Imaging revealed ground-glass opacities predominantly in the lower lobes and a pulmonary embolus in the right upper lobe. She was diagnosed with POS due to marked postural discrepancies between supine and upright oxygen saturations and blood oxygenation. Intracardiac shunt, one of the etiologies of POS, was not detected by bubble contrast echocardiography, and postural de-saturation gradually improved with methylprednisolone and edoxaban administration. In our literature review, only 3 of the 16 patients with POS associated with COVID-19 had cardiac shunting, suggesting that moderate to severe COVID-19 causes POS without cardiac shunts. COVID-19-associated vasculopathy and lower lung lesion predominance in COVID-19 pneumonia may cause ventilation-perfusion mismatch due to gravitational shunting of blood into the poorly ventilated lower lungs in the upright position, which may ultimately cause POS. Hypoxemia impedes rehabilitation, whereas early initiation of supine positioning in bed, with knowledge of the pathophysiology o

Published
2023

6. Myeloid differentiation factor 88 signaling in donor T cells accelerates graft-versus-host disease

Author

Matsuoka, Satomi, 1000020419576, Hashimoto, Daigo, Kadowaki, Masanori, Ohigashi, Hiroyuki, Hayase, Eiko, Yokoyama, Emi, Hasegawa, Yuta, Tateno, Takahiro, Chen, Xuanzhong, Aoyama, Kazutoshi, Oka, Hideyo, 1000070455632, Onozawa, Masahiro, 1000020309446, Takeda, Kiyoshi, 1000080380385, Akashi, Koichi, 1000040284096, Teshima, Takanori, Matsuoka, Satomi, 1000020419576, Hashimoto, Daigo, Kadowaki, Masanori, Ohigashi, Hiroyuki, Hayase, Eiko, Yokoyama, Emi, Hasegawa, Yuta, Tateno, Takahiro, Chen, Xuanzhong, Aoyama, Kazutoshi, Oka, Hideyo, 1000070455632, Onozawa, Masahiro, 1000020309446, Takeda, Kiyoshi, 1000080380385, Akashi, Koichi, 1000040284096, and Teshima, Takanori

Abstract

Myeloid differentiation factor 88 (MyD88) signaling has a crucial role in activation of both innate and adoptive immunity. MyD88 transduces signals via Toll-like receptor and interleukin-1 receptor superfamily to the NF kappa B pathway and inflammasome by forming a molecular complex with interleukin-1 receptor-associated kinase 4. The MyD88/interleukin-1 receptor-associated kinase 4 pathway plays an important role, not only in innate immunity, but also T-cell immunity; however, its role in donor T cells on the pathophysiology of graft-versus-host disease (GvHD) remains to be elucidated. We addressed this issue by using MyD88-deficient T cells in a mouse model of allogeneic hematopoietic stem cell transplantation (allo-SCT). While MyD88-deficient and wild-type T cells proliferated equivalently after transplantation, MyD88-deficient T cells demonstrated impaired survival and differentiation toward Th1, Tc1, and Th17, and induced less severe GvHD compared to wild-type T cells. Administration of interleukin-1 receptor-associated kinase 4 inhibitor PF-06650833 significantly ameliorated GvHD after allo-SCT. These results thus demonstrate that donor T-cell receptor-associated kinase 4 pathway is a novel therapeutic target against GvHD after allo-SCT.

Published
2020

7. Efficacy and safety of tisagenlecleucel in Japanese adult patients with relapsed/refractory diffuse large B-cell lymphoma

Author

1000070759290, Goto, Hideki, Makita, Shinichi, Kato, Koji, Tokushige, Kota, Fujita, Taizo, 1000080380385, Akashi, Koichi, 1000030361471, Izutsu, Koji, 1000040284096, Teshima, Takanori, 1000070759290, Goto, Hideki, Makita, Shinichi, Kato, Koji, Tokushige, Kota, Fujita, Taizo, 1000080380385, Akashi, Koichi, 1000030361471, Izutsu, Koji, 1000040284096, and Teshima, Takanori

Abstract

Background Tisagenlecleucel demonstrated a high rate of durable response in adult patients with relapsed/refractory (r/r) diffuse large B-cell lymphoma (DLBCL) in the pivotal global phase 2 JULIET study. Here, we report the efficacy and safety of tisagenlecleucel in the Japanese subgroup. Methods JULIET (NCT02445248) is a single-arm, open-label, multicenter, phase 2 study involving adult patients with r/r DLBCL who either relapsed after or were ineligible for autologous stem cell transplant. Primary endpoint was best overall response rate (ORR; complete response [CR] + partial response [PR]) as judged by an independent review committee. Results In Japan, of 17 patients enrolled, 9 were infused with tisagenlecleucel and completed >= 3 months of follow-up. Best ORR was 77.8% (7/9; 95% confidence interval, 40.0-97.2), with 5 patients (55.6%) in CR and 2 (22.2%) in PR. Cytokine release syndrome (CRS) occurred in 6 patients (66.7%), with grade 3 CRS in 2 patients (Penn grading scale). Two patients received tocilizumab. Two deaths (22.2%) occurred more than 30 days after tisagenlecleucel infusion due to disease progression, neither of which were related to tisagenlecleucel. Conclusion Tisagenlecleucel showed a high best ORR with a manageable safety profile, thus offering a new treatment option in selected Japanese patients with r/r DLBCL.

Published
2020

8. Efficacy and safety of tisagenlecleucel in Japanese adult patients with relapsed/refractory diffuse large B-cell lymphoma

Author

Goto, Hideki, Makita, Shinichi, Kato, Koji, Tokushige, Kota, Fujita, Taizo, Akashi, Koichi, Izutsu, Koji, Teshima, Takanori, Goto, Hideki, Makita, Shinichi, Kato, Koji, Tokushige, Kota, Fujita, Taizo, Akashi, Koichi, Izutsu, Koji, and Teshima, Takanori

Abstract

Background Tisagenlecleucel demonstrated a high rate of durable response in adult patients with relapsed/refractory (r/r) diffuse large B-cell lymphoma (DLBCL) in the pivotal global phase 2 JULIET study. Here, we report the efficacy and safety of tisagenlecleucel in the Japanese subgroup. Methods JULIET (NCT02445248) is a single-arm, open-label, multicenter, phase 2 study involving adult patients with r/r DLBCL who either relapsed after or were ineligible for autologous stem cell transplant. Primary endpoint was best overall response rate (ORR; complete response [CR] + partial response [PR]) as judged by an independent review committee. Results In Japan, of 17 patients enrolled, 9 were infused with tisagenlecleucel and completed >= 3 months of follow-up. Best ORR was 77.8% (7/9; 95% confidence interval, 40.0-97.2), with 5 patients (55.6%) in CR and 2 (22.2%) in PR. Cytokine release syndrome (CRS) occurred in 6 patients (66.7%), with grade 3 CRS in 2 patients (Penn grading scale). Two patients received tocilizumab. Two deaths (22.2%) occurred more than 30 days after tisagenlecleucel infusion due to disease progression, neither of which were related to tisagenlecleucel. Conclusion Tisagenlecleucel showed a high best ORR with a manageable safety profile, thus offering a new treatment option in selected Japanese patients with r/r DLBCL.

Published
2020

9. Myeloid differentiation factor 88 signaling in donor T cells accelerates graft-versus-host disease

Author

Matsuoka, Satomi, Hashimoto, Daigo, Kadowaki, Masanori, Ohigashi, Hiroyuki, Hayase, Eiko, Yokoyama, Emi, Hasegawa, Yuta, Tateno, Takahiro, Chen, Xuanzhong, Aoyama, Kazutoshi, Oka, Hideyo, Onozawa, Masahiro, Takeda, Kiyoshi, Akashi, Koichi, Teshima, Takanori, Matsuoka, Satomi, Hashimoto, Daigo, Kadowaki, Masanori, Ohigashi, Hiroyuki, Hayase, Eiko, Yokoyama, Emi, Hasegawa, Yuta, Tateno, Takahiro, Chen, Xuanzhong, Aoyama, Kazutoshi, Oka, Hideyo, Onozawa, Masahiro, Takeda, Kiyoshi, Akashi, Koichi, and Teshima, Takanori

Abstract

Myeloid differentiation factor 88 (MyD88) signaling has a crucial role in activation of both innate and adoptive immunity. MyD88 transduces signals via Toll-like receptor and interleukin-1 receptor superfamily to the NF kappa B pathway and inflammasome by forming a molecular complex with interleukin-1 receptor-associated kinase 4. The MyD88/interleukin-1 receptor-associated kinase 4 pathway plays an important role, not only in innate immunity, but also T-cell immunity; however, its role in donor T cells on the pathophysiology of graft-versus-host disease (GvHD) remains to be elucidated. We addressed this issue by using MyD88-deficient T cells in a mouse model of allogeneic hematopoietic stem cell transplantation (allo-SCT). While MyD88-deficient and wild-type T cells proliferated equivalently after transplantation, MyD88-deficient T cells demonstrated impaired survival and differentiation toward Th1, Tc1, and Th17, and induced less severe GvHD compared to wild-type T cells. Administration of interleukin-1 receptor-associated kinase 4 inhibitor PF-06650833 significantly ameliorated GvHD after allo-SCT. These results thus demonstrate that donor T-cell receptor-associated kinase 4 pathway is a novel therapeutic target against GvHD after allo-SCT.

Published
2020

10. Oral ixazomib maintenance following autologous stem cell transplantation (TOURMALINE-MM3): a double-blind, randomised, placebo-controlled phase 3 trial

Author

Dimopoulos, Meletios A., Gay, Francesca, Schjesvold, Fredrik, Beksac, Meral, Hajek, Roman, Weisel, Katja Christina, Goldschmidt, Hartmut, Maisnar, Vladimir, Moreau, Philippe, Min, Chang Ki, Pluta, Agnieszka, Chng, Wee-Joo, Kaiser, Martin, Zweegman, Sonja, Mateos, Maria Victoria, Spencer, Andrew, Iida, Shinsuke, Morgan, Gareth, Suryanarayan, Kaveri, Teng, Zhaoyang, Skacel, Tomas, Palumbo, Antonio, Dash, Ajeeta B., Gupta, Neeraj, Labotka, Richard, Rajkumar, S. Vincent, Bar, Daniel, Basso, Alfredo, Fantl, Dorotea, He, Simon, Horvath, Neomi, Lee, Cindy, Rowlings, Phillip, Taylor, Kerry, Cochrane, Tara, Kwok, Fiona, Ramanathan, Sundreswran, Agis, Hermine, Zojer, Niklas, Kentos, Alain, Offner, Fritz, Van Droogenbroeck, Jan, Wu, Ka Lung, Maiolino, Angelo, Martinez, Gracia, Zanella, Karla, Capra, Marcelo, Araujo, Sergio, Gregora, Evzen, Pour, Ludek, Scudla, Vlastimil, Spicka, Ivan, Abildgaard, Niels, Andersen, Niels, Jensen, Bo Amdi, Helleberg, Carsten, Plesner, Torben, Salomo, Morten, Svirskaite, Asta, Delarue, Richard, Blau, Igor, Schieferdecker, Aneta, Teleanu, Veronica, Munder, Markus, Rollig, Christoph, Salwender, Han-Juergen, Fuhrmann, Stephan, Weisel, Katja, Duerig, Jan, Zeis, Matthias, Klein, Stefan, Reimer, Peter, Schmidt, Christian, Scheid, Christof, Mayer, Karin, Hoffmann, Martin, Sosada, Markus, Dimopoulos, Athanasios, Delimpasi, Sosana, Kyrtsonis, Mary-Christine, Anagnostopoulos, Achilleas, Nagy, Zsolt, Illes, Arpad, Egyed, Miklos, Borbenyi, Zita, Mikala, Gabor, Dally, Najib, Horowitz, Netanel, Gutwein, Odit, Nemets, Anatoly, Vaxman, Iuliana, Shvetz, Olga, Trestman, Svetlana, Ruchlemer, Rosa, Nagler, Arnon, Tadmor, Tamar, Rouvio, Ory, Preis, Meir, Cavo, Michele, De Rosa, Luca, Musto, Pellegrino, Cafro, Anna, Tosi, Patrizia, Offidani, Massimo, Corso, Alessandro, Rossi, Giuseppe, Liberati, Anna Marina, Bosi, Alberto, Suzuki, Kenshi, Nakaseko, Chiaki, Ishikawa, Takayuki, Matsumoto, Morio, Nagai, Hirokazu, Sunami, Kazutaka, Chou, Takaaki, Akashi, Koichi, Takezako, Naoki, Hagiwara, Shotaro, Eom, Hyeon Seok, Jo, Deog-Yeon, Kim, Jin Seok, Lee, Jae Hoon, Yoon, Sung Soo, Yoon, Dok Hyun, Kim, Kihyun, Levin, Mark-David, Vellenga, Edo, Minnema, Monique, Waage, Anders, Haukas, Einar, Grosicki, Sebastian, Pluta, Andrzej, Robak, Tadeusz, Marques, Herlander, Bergantim, Rui, Campilho, Fernando, Chng, Wee Joo, Goh, Yeow Tee, McDonald, Andrew, Rapoport, Bernado, Rivas, Miguel Angel Alvarez, de La Fuente, Felipe De Arriba, Montes, Yolanda Gonzalez, Sanchez, Jesus Martin, Rocafiguera, Albert Oriol, Rosinol, Laura, San Miguel, Jesus, de Oteyza, Jaime Perez, Encinas, Cristina, Alegre-Amor, Adrian, Lopez-Guia, Ana, Axelsson, Per, Carlson, Kristina, Stromberg, Olga, Hansson, Markus, Blimark, Cecile Hveding, Mueller, Rouven, Chen, Chih-Cheng, Liu, Ta-Chih, Huang, Shang-Yi, Wang, Po-Nan, Nakorn, Thanyaphong Na, Prayongratana, Kannadit, Unal, Ali, Goker, Hakan, Sonmez, Mehmet, Korenkova, Sybiryna, Chaidos, Aristeidis, Oakervee, Heather, Sati, Hamdi, Benjamin, Reuben, Wechalekar, Ashutosh, Garg, Mamta, Ramasamy, Karthik, Cook, Gordon, Chantry, Andrew, Jenner, Matthew, Buadi, Francis, Berryman, Robert, Janakiram, Murali, Dimopoulos, Meletios A., Gay, Francesca, Schjesvold, Fredrik, Beksac, Meral, Hajek, Roman, Weisel, Katja Christina, Goldschmidt, Hartmut, Maisnar, Vladimir, Moreau, Philippe, Min, Chang Ki, Pluta, Agnieszka, Chng, Wee-Joo, Kaiser, Martin, Zweegman, Sonja, Mateos, Maria Victoria, Spencer, Andrew, Iida, Shinsuke, Morgan, Gareth, Suryanarayan, Kaveri, Teng, Zhaoyang, Skacel, Tomas, Palumbo, Antonio, Dash, Ajeeta B., Gupta, Neeraj, Labotka, Richard, Rajkumar, S. Vincent, Bar, Daniel, Basso, Alfredo, Fantl, Dorotea, He, Simon, Horvath, Neomi, Lee, Cindy, Rowlings, Phillip, Taylor, Kerry, Cochrane, Tara, Kwok, Fiona, Ramanathan, Sundreswran, Agis, Hermine, Zojer, Niklas, Kentos, Alain, Offner, Fritz, Van Droogenbroeck, Jan, Wu, Ka Lung, Maiolino, Angelo, Martinez, Gracia, Zanella, Karla, Capra, Marcelo, Araujo, Sergio, Gregora, Evzen, Pour, Ludek, Scudla, Vlastimil, Spicka, Ivan, Abildgaard, Niels, Andersen, Niels, Jensen, Bo Amdi, Helleberg, Carsten, Plesner, Torben, Salomo, Morten, Svirskaite, Asta, Delarue, Richard, Blau, Igor, Schieferdecker, Aneta, Teleanu, Veronica, Munder, Markus, Rollig, Christoph, Salwender, Han-Juergen, Fuhrmann, Stephan, Weisel, Katja, Duerig, Jan, Zeis, Matthias, Klein, Stefan, Reimer, Peter, Schmidt, Christian, Scheid, Christof, Mayer, Karin, Hoffmann, Martin, Sosada, Markus, Dimopoulos, Athanasios, Delimpasi, Sosana, Kyrtsonis, Mary-Christine, Anagnostopoulos, Achilleas, Nagy, Zsolt, Illes, Arpad, Egyed, Miklos, Borbenyi, Zita, Mikala, Gabor, Dally, Najib, Horowitz, Netanel, Gutwein, Odit, Nemets, Anatoly, Vaxman, Iuliana, Shvetz, Olga, Trestman, Svetlana, Ruchlemer, Rosa, Nagler, Arnon, Tadmor, Tamar, Rouvio, Ory, Preis, Meir, Cavo, Michele, De Rosa, Luca, Musto, Pellegrino, Cafro, Anna, Tosi, Patrizia, Offidani, Massimo, Corso, Alessandro, Rossi, Giuseppe, Liberati, Anna Marina, Bosi, Alberto, Suzuki, Kenshi, Nakaseko, Chiaki, Ishikawa, Takayuki, Matsumoto, Morio, Nagai, Hirokazu, Sunami, Kazutaka, Chou, Takaaki, Akashi, Koichi, Takezako, Naoki, Hagiwara, Shotaro, Eom, Hyeon Seok, Jo, Deog-Yeon, Kim, Jin Seok, Lee, Jae Hoon, Yoon, Sung Soo, Yoon, Dok Hyun, Kim, Kihyun, Levin, Mark-David, Vellenga, Edo, Minnema, Monique, Waage, Anders, Haukas, Einar, Grosicki, Sebastian, Pluta, Andrzej, Robak, Tadeusz, Marques, Herlander, Bergantim, Rui, Campilho, Fernando, Chng, Wee Joo, Goh, Yeow Tee, McDonald, Andrew, Rapoport, Bernado, Rivas, Miguel Angel Alvarez, de La Fuente, Felipe De Arriba, Montes, Yolanda Gonzalez, Sanchez, Jesus Martin, Rocafiguera, Albert Oriol, Rosinol, Laura, San Miguel, Jesus, de Oteyza, Jaime Perez, Encinas, Cristina, Alegre-Amor, Adrian, Lopez-Guia, Ana, Axelsson, Per, Carlson, Kristina, Stromberg, Olga, Hansson, Markus, Blimark, Cecile Hveding, Mueller, Rouven, Chen, Chih-Cheng, Liu, Ta-Chih, Huang, Shang-Yi, Wang, Po-Nan, Nakorn, Thanyaphong Na, Prayongratana, Kannadit, Unal, Ali, Goker, Hakan, Sonmez, Mehmet, Korenkova, Sybiryna, Chaidos, Aristeidis, Oakervee, Heather, Sati, Hamdi, Benjamin, Reuben, Wechalekar, Ashutosh, Garg, Mamta, Ramasamy, Karthik, Cook, Gordon, Chantry, Andrew, Jenner, Matthew, Buadi, Francis, Berryman, Robert, and Janakiram, Murali

Published
2019

11. Oral ixazomib maintenance following autologous stem cell transplantation (TOURMALINE-MM3): a double-blind, randomised, placebo-controlled phase 3 trial

Author

Dimopoulos, Meletios A., Gay, Francesca, Schjesvold, Fredrik, Beksac, Meral, Hajek, Roman, Weisel, Katja Christina, Goldschmidt, Hartmut, Maisnar, Vladimir, Moreau, Philippe, Min, Chang Ki, Pluta, Agnieszka, Chng, Wee-Joo, Kaiser, Martin, Zweegman, Sonja, Mateos, Maria Victoria, Spencer, Andrew, Iida, Shinsuke, Morgan, Gareth, Suryanarayan, Kaveri, Teng, Zhaoyang, Skacel, Tomas, Palumbo, Antonio, Dash, Ajeeta B., Gupta, Neeraj, Labotka, Richard, Rajkumar, S. Vincent, Bar, Daniel, Basso, Alfredo, Fantl, Dorotea, He, Simon, Horvath, Neomi, Lee, Cindy, Rowlings, Phillip, Taylor, Kerry, Cochrane, Tara, Kwok, Fiona, Ramanathan, Sundreswran, Agis, Hermine, Zojer, Niklas, Kentos, Alain, Offner, Fritz, Van Droogenbroeck, Jan, Wu, Ka Lung, Maiolino, Angelo, Martinez, Gracia, Zanella, Karla, Capra, Marcelo, Araujo, Sergio, Gregora, Evzen, Pour, Ludek, Scudla, Vlastimil, Spicka, Ivan, Abildgaard, Niels, Andersen, Niels, Jensen, Bo Amdi, Helleberg, Carsten, Plesner, Torben, Salomo, Morten, Svirskaite, Asta, Delarue, Richard, Blau, Igor, Schieferdecker, Aneta, Teleanu, Veronica, Munder, Markus, Rollig, Christoph, Salwender, Han-Juergen, Fuhrmann, Stephan, Weisel, Katja, Duerig, Jan, Zeis, Matthias, Klein, Stefan, Reimer, Peter, Schmidt, Christian, Scheid, Christof, Mayer, Karin, Hoffmann, Martin, Sosada, Markus, Dimopoulos, Athanasios, Delimpasi, Sosana, Kyrtsonis, Mary-Christine, Anagnostopoulos, Achilleas, Nagy, Zsolt, Illes, Arpad, Egyed, Miklos, Borbenyi, Zita, Mikala, Gabor, Dally, Najib, Horowitz, Netanel, Gutwein, Odit, Nemets, Anatoly, Vaxman, Iuliana, Shvetz, Olga, Trestman, Svetlana, Ruchlemer, Rosa, Nagler, Arnon, Tadmor, Tamar, Rouvio, Ory, Preis, Meir, Cavo, Michele, De Rosa, Luca, Musto, Pellegrino, Cafro, Anna, Tosi, Patrizia, Offidani, Massimo, Corso, Alessandro, Rossi, Giuseppe, Liberati, Anna Marina, Bosi, Alberto, Suzuki, Kenshi, Nakaseko, Chiaki, Ishikawa, Takayuki, Matsumoto, Morio, Nagai, Hirokazu, Sunami, Kazutaka, Chou, Takaaki, Akashi, Koichi, Takezako, Naoki, Hagiwara, Shotaro, Eom, Hyeon Seok, Jo, Deog-Yeon, Kim, Jin Seok, Lee, Jae Hoon, Yoon, Sung Soo, Yoon, Dok Hyun, Kim, Kihyun, Levin, Mark-David, Vellenga, Edo, Minnema, Monique, Waage, Anders, Haukas, Einar, Grosicki, Sebastian, Pluta, Andrzej, Robak, Tadeusz, Marques, Herlander, Bergantim, Rui, Campilho, Fernando, Chng, Wee Joo, Goh, Yeow Tee, McDonald, Andrew, Rapoport, Bernado, Rivas, Miguel Angel Alvarez, de La Fuente, Felipe De Arriba, Montes, Yolanda Gonzalez, Sanchez, Jesus Martin, Rocafiguera, Albert Oriol, Rosinol, Laura, San Miguel, Jesus, de Oteyza, Jaime Perez, Encinas, Cristina, Alegre-Amor, Adrian, Lopez-Guia, Ana, Axelsson, Per, Carlson, Kristina, Stromberg, Olga, Hansson, Markus, Blimark, Cecile Hveding, Mueller, Rouven, Chen, Chih-Cheng, Liu, Ta-Chih, Huang, Shang-Yi, Wang, Po-Nan, Nakorn, Thanyaphong Na, Prayongratana, Kannadit, Unal, Ali, Goker, Hakan, Sonmez, Mehmet, Korenkova, Sybiryna, Chaidos, Aristeidis, Oakervee, Heather, Sati, Hamdi, Benjamin, Reuben, Wechalekar, Ashutosh, Garg, Mamta, Ramasamy, Karthik, Cook, Gordon, Chantry, Andrew, Jenner, Matthew, Buadi, Francis, Berryman, Robert, Janakiram, Murali, Dimopoulos, Meletios A., Gay, Francesca, Schjesvold, Fredrik, Beksac, Meral, Hajek, Roman, Weisel, Katja Christina, Goldschmidt, Hartmut, Maisnar, Vladimir, Moreau, Philippe, Min, Chang Ki, Pluta, Agnieszka, Chng, Wee-Joo, Kaiser, Martin, Zweegman, Sonja, Mateos, Maria Victoria, Spencer, Andrew, Iida, Shinsuke, Morgan, Gareth, Suryanarayan, Kaveri, Teng, Zhaoyang, Skacel, Tomas, Palumbo, Antonio, Dash, Ajeeta B., Gupta, Neeraj, Labotka, Richard, Rajkumar, S. Vincent, Bar, Daniel, Basso, Alfredo, Fantl, Dorotea, He, Simon, Horvath, Neomi, Lee, Cindy, Rowlings, Phillip, Taylor, Kerry, Cochrane, Tara, Kwok, Fiona, Ramanathan, Sundreswran, Agis, Hermine, Zojer, Niklas, Kentos, Alain, Offner, Fritz, Van Droogenbroeck, Jan, Wu, Ka Lung, Maiolino, Angelo, Martinez, Gracia, Zanella, Karla, Capra, Marcelo, Araujo, Sergio, Gregora, Evzen, Pour, Ludek, Scudla, Vlastimil, Spicka, Ivan, Abildgaard, Niels, Andersen, Niels, Jensen, Bo Amdi, Helleberg, Carsten, Plesner, Torben, Salomo, Morten, Svirskaite, Asta, Delarue, Richard, Blau, Igor, Schieferdecker, Aneta, Teleanu, Veronica, Munder, Markus, Rollig, Christoph, Salwender, Han-Juergen, Fuhrmann, Stephan, Weisel, Katja, Duerig, Jan, Zeis, Matthias, Klein, Stefan, Reimer, Peter, Schmidt, Christian, Scheid, Christof, Mayer, Karin, Hoffmann, Martin, Sosada, Markus, Dimopoulos, Athanasios, Delimpasi, Sosana, Kyrtsonis, Mary-Christine, Anagnostopoulos, Achilleas, Nagy, Zsolt, Illes, Arpad, Egyed, Miklos, Borbenyi, Zita, Mikala, Gabor, Dally, Najib, Horowitz, Netanel, Gutwein, Odit, Nemets, Anatoly, Vaxman, Iuliana, Shvetz, Olga, Trestman, Svetlana, Ruchlemer, Rosa, Nagler, Arnon, Tadmor, Tamar, Rouvio, Ory, Preis, Meir, Cavo, Michele, De Rosa, Luca, Musto, Pellegrino, Cafro, Anna, Tosi, Patrizia, Offidani, Massimo, Corso, Alessandro, Rossi, Giuseppe, Liberati, Anna Marina, Bosi, Alberto, Suzuki, Kenshi, Nakaseko, Chiaki, Ishikawa, Takayuki, Matsumoto, Morio, Nagai, Hirokazu, Sunami, Kazutaka, Chou, Takaaki, Akashi, Koichi, Takezako, Naoki, Hagiwara, Shotaro, Eom, Hyeon Seok, Jo, Deog-Yeon, Kim, Jin Seok, Lee, Jae Hoon, Yoon, Sung Soo, Yoon, Dok Hyun, Kim, Kihyun, Levin, Mark-David, Vellenga, Edo, Minnema, Monique, Waage, Anders, Haukas, Einar, Grosicki, Sebastian, Pluta, Andrzej, Robak, Tadeusz, Marques, Herlander, Bergantim, Rui, Campilho, Fernando, Chng, Wee Joo, Goh, Yeow Tee, McDonald, Andrew, Rapoport, Bernado, Rivas, Miguel Angel Alvarez, de La Fuente, Felipe De Arriba, Montes, Yolanda Gonzalez, Sanchez, Jesus Martin, Rocafiguera, Albert Oriol, Rosinol, Laura, San Miguel, Jesus, de Oteyza, Jaime Perez, Encinas, Cristina, Alegre-Amor, Adrian, Lopez-Guia, Ana, Axelsson, Per, Carlson, Kristina, Stromberg, Olga, Hansson, Markus, Blimark, Cecile Hveding, Mueller, Rouven, Chen, Chih-Cheng, Liu, Ta-Chih, Huang, Shang-Yi, Wang, Po-Nan, Nakorn, Thanyaphong Na, Prayongratana, Kannadit, Unal, Ali, Goker, Hakan, Sonmez, Mehmet, Korenkova, Sybiryna, Chaidos, Aristeidis, Oakervee, Heather, Sati, Hamdi, Benjamin, Reuben, Wechalekar, Ashutosh, Garg, Mamta, Ramasamy, Karthik, Cook, Gordon, Chantry, Andrew, Jenner, Matthew, Buadi, Francis, Berryman, Robert, and Janakiram, Murali

Published
2019

12. Oral ixazomib maintenance following autologous stem cell transplantation (TOURMALINE-MM3): a double-blind, randomised, placebo-controlled phase 3 trial

Author

Dimopoulos, Meletios A., Gay, Francesca, Schjesvold, Fredrik, Beksac, Meral, Hajek, Roman, Weisel, Katja Christina, Goldschmidt, Hartmut, Maisnar, Vladimir, Moreau, Philippe, Min, Chang Ki, Pluta, Agnieszka, Chng, Wee-Joo, Kaiser, Martin, Zweegman, Sonja, Mateos, Maria Victoria, Spencer, Andrew, Iida, Shinsuke, Morgan, Gareth, Suryanarayan, Kaveri, Teng, Zhaoyang, Skacel, Tomas, Palumbo, Antonio, Dash, Ajeeta B., Gupta, Neeraj, Labotka, Richard, Rajkumar, S. Vincent, Bar, Daniel, Basso, Alfredo, Fantl, Dorotea, He, Simon, Horvath, Neomi, Lee, Cindy, Rowlings, Phillip, Taylor, Kerry, Cochrane, Tara, Kwok, Fiona, Ramanathan, Sundreswran, Agis, Hermine, Zojer, Niklas, Kentos, Alain, Offner, Fritz, Van Droogenbroeck, Jan, Wu, Ka Lung, Maiolino, Angelo, Martinez, Gracia, Zanella, Karla, Capra, Marcelo, Araujo, Sergio, Gregora, Evzen, Pour, Ludek, Scudla, Vlastimil, Spicka, Ivan, Abildgaard, Niels, Andersen, Niels, Jensen, Bo Amdi, Helleberg, Carsten, Plesner, Torben, Salomo, Morten, Svirskaite, Asta, Delarue, Richard, Blau, Igor, Schieferdecker, Aneta, Teleanu, Veronica, Munder, Markus, Rollig, Christoph, Salwender, Han-Juergen, Fuhrmann, Stephan, Weisel, Katja, Duerig, Jan, Zeis, Matthias, Klein, Stefan, Reimer, Peter, Schmidt, Christian, Scheid, Christof, Mayer, Karin, Hoffmann, Martin, Sosada, Markus, Dimopoulos, Athanasios, Delimpasi, Sosana, Kyrtsonis, Mary-Christine, Anagnostopoulos, Achilleas, Nagy, Zsolt, Illes, Arpad, Egyed, Miklos, Borbenyi, Zita, Mikala, Gabor, Dally, Najib, Horowitz, Netanel, Gutwein, Odit, Nemets, Anatoly, Vaxman, Iuliana, Shvetz, Olga, Trestman, Svetlana, Ruchlemer, Rosa, Nagler, Arnon, Tadmor, Tamar, Rouvio, Ory, Preis, Meir, Cavo, Michele, De Rosa, Luca, Musto, Pellegrino, Cafro, Anna, Tosi, Patrizia, Offidani, Massimo, Corso, Alessandro, Rossi, Giuseppe, Liberati, Anna Marina, Bosi, Alberto, Suzuki, Kenshi, Nakaseko, Chiaki, Ishikawa, Takayuki, Matsumoto, Morio, Nagai, Hirokazu, Sunami, Kazutaka, Chou, Takaaki, Akashi, Koichi, Takezako, Naoki, Hagiwara, Shotaro, Eom, Hyeon Seok, Jo, Deog-Yeon, Kim, Jin Seok, Lee, Jae Hoon, Yoon, Sung Soo, Yoon, Dok Hyun, Kim, Kihyun, Levin, Mark-David, Vellenga, Edo, Minnema, Monique, Waage, Anders, Haukas, Einar, Grosicki, Sebastian, Pluta, Andrzej, Robak, Tadeusz, Marques, Herlander, Bergantim, Rui, Campilho, Fernando, Chng, Wee Joo, Goh, Yeow Tee, McDonald, Andrew, Rapoport, Bernado, Rivas, Miguel Angel Alvarez, de La Fuente, Felipe De Arriba, Montes, Yolanda Gonzalez, Sanchez, Jesus Martin, Rocafiguera, Albert Oriol, Rosinol, Laura, San Miguel, Jesus, de Oteyza, Jaime Perez, Encinas, Cristina, Alegre-Amor, Adrian, Lopez-Guia, Ana, Axelsson, Per, Carlson, Kristina, Stromberg, Olga, Hansson, Markus, Blimark, Cecile Hveding, Mueller, Rouven, Chen, Chih-Cheng, Liu, Ta-Chih, Huang, Shang-Yi, Wang, Po-Nan, Nakorn, Thanyaphong Na, Prayongratana, Kannadit, Unal, Ali, Goker, Hakan, Sonmez, Mehmet, Korenkova, Sybiryna, Chaidos, Aristeidis, Oakervee, Heather, Sati, Hamdi, Benjamin, Reuben, Wechalekar, Ashutosh, Garg, Mamta, Ramasamy, Karthik, Cook, Gordon, Chantry, Andrew, Jenner, Matthew, Buadi, Francis, Berryman, Robert, Janakiram, Murali, Dimopoulos, Meletios A., Gay, Francesca, Schjesvold, Fredrik, Beksac, Meral, Hajek, Roman, Weisel, Katja Christina, Goldschmidt, Hartmut, Maisnar, Vladimir, Moreau, Philippe, Min, Chang Ki, Pluta, Agnieszka, Chng, Wee-Joo, Kaiser, Martin, Zweegman, Sonja, Mateos, Maria Victoria, Spencer, Andrew, Iida, Shinsuke, Morgan, Gareth, Suryanarayan, Kaveri, Teng, Zhaoyang, Skacel, Tomas, Palumbo, Antonio, Dash, Ajeeta B., Gupta, Neeraj, Labotka, Richard, Rajkumar, S. Vincent, Bar, Daniel, Basso, Alfredo, Fantl, Dorotea, He, Simon, Horvath, Neomi, Lee, Cindy, Rowlings, Phillip, Taylor, Kerry, Cochrane, Tara, Kwok, Fiona, Ramanathan, Sundreswran, Agis, Hermine, Zojer, Niklas, Kentos, Alain, Offner, Fritz, Van Droogenbroeck, Jan, Wu, Ka Lung, Maiolino, Angelo, Martinez, Gracia, Zanella, Karla, Capra, Marcelo, Araujo, Sergio, Gregora, Evzen, Pour, Ludek, Scudla, Vlastimil, Spicka, Ivan, Abildgaard, Niels, Andersen, Niels, Jensen, Bo Amdi, Helleberg, Carsten, Plesner, Torben, Salomo, Morten, Svirskaite, Asta, Delarue, Richard, Blau, Igor, Schieferdecker, Aneta, Teleanu, Veronica, Munder, Markus, Rollig, Christoph, Salwender, Han-Juergen, Fuhrmann, Stephan, Weisel, Katja, Duerig, Jan, Zeis, Matthias, Klein, Stefan, Reimer, Peter, Schmidt, Christian, Scheid, Christof, Mayer, Karin, Hoffmann, Martin, Sosada, Markus, Dimopoulos, Athanasios, Delimpasi, Sosana, Kyrtsonis, Mary-Christine, Anagnostopoulos, Achilleas, Nagy, Zsolt, Illes, Arpad, Egyed, Miklos, Borbenyi, Zita, Mikala, Gabor, Dally, Najib, Horowitz, Netanel, Gutwein, Odit, Nemets, Anatoly, Vaxman, Iuliana, Shvetz, Olga, Trestman, Svetlana, Ruchlemer, Rosa, Nagler, Arnon, Tadmor, Tamar, Rouvio, Ory, Preis, Meir, Cavo, Michele, De Rosa, Luca, Musto, Pellegrino, Cafro, Anna, Tosi, Patrizia, Offidani, Massimo, Corso, Alessandro, Rossi, Giuseppe, Liberati, Anna Marina, Bosi, Alberto, Suzuki, Kenshi, Nakaseko, Chiaki, Ishikawa, Takayuki, Matsumoto, Morio, Nagai, Hirokazu, Sunami, Kazutaka, Chou, Takaaki, Akashi, Koichi, Takezako, Naoki, Hagiwara, Shotaro, Eom, Hyeon Seok, Jo, Deog-Yeon, Kim, Jin Seok, Lee, Jae Hoon, Yoon, Sung Soo, Yoon, Dok Hyun, Kim, Kihyun, Levin, Mark-David, Vellenga, Edo, Minnema, Monique, Waage, Anders, Haukas, Einar, Grosicki, Sebastian, Pluta, Andrzej, Robak, Tadeusz, Marques, Herlander, Bergantim, Rui, Campilho, Fernando, Chng, Wee Joo, Goh, Yeow Tee, McDonald, Andrew, Rapoport, Bernado, Rivas, Miguel Angel Alvarez, de La Fuente, Felipe De Arriba, Montes, Yolanda Gonzalez, Sanchez, Jesus Martin, Rocafiguera, Albert Oriol, Rosinol, Laura, San Miguel, Jesus, de Oteyza, Jaime Perez, Encinas, Cristina, Alegre-Amor, Adrian, Lopez-Guia, Ana, Axelsson, Per, Carlson, Kristina, Stromberg, Olga, Hansson, Markus, Blimark, Cecile Hveding, Mueller, Rouven, Chen, Chih-Cheng, Liu, Ta-Chih, Huang, Shang-Yi, Wang, Po-Nan, Nakorn, Thanyaphong Na, Prayongratana, Kannadit, Unal, Ali, Goker, Hakan, Sonmez, Mehmet, Korenkova, Sybiryna, Chaidos, Aristeidis, Oakervee, Heather, Sati, Hamdi, Benjamin, Reuben, Wechalekar, Ashutosh, Garg, Mamta, Ramasamy, Karthik, Cook, Gordon, Chantry, Andrew, Jenner, Matthew, Buadi, Francis, Berryman, Robert, and Janakiram, Murali

Published
2019

13. Oral ixazomib maintenance following autologous stem cell transplantation (TOURMALINE-MM3): a double-blind, randomised, placebo-controlled phase 3 trial

Author

MS Hematologie, Infection & Immunity, Regenerative Medicine and Stem Cells, Dimopoulos, Meletios A., Gay, Francesca, Schjesvold, Fredrik, Beksac, Meral, Hajek, Roman, Weisel, Katja Christina, Goldschmidt, Hartmut, Maisnar, Vladimir, Moreau, Philippe, Min, Chang Ki, Pluta, Agnieszka, Chng, Wee-Joo, Kaiser, Martin, Zweegman, Sonja, Mateos, Maria Victoria, Spencer, Andrew, Iida, Shinsuke, Morgan, Gareth, Suryanarayan, Kaveri, Teng, Zhaoyang, Skacel, Tomas, Palumbo, Antonio, Dash, Ajeeta B., Gupta, Neeraj, Labotka, Richard, Rajkumar, S. Vincent, Bar, Daniel, Basso, Alfredo, Fantl, Dorotea, He, Simon, Horvath, Neomi, Lee, Cindy, Rowlings, Phillip, Taylor, Kerry, Cochrane, Tara, Kwok, Fiona, Ramanathan, Sundreswran, Agis, Hermine, Zojer, Niklas, Kentos, Alain, Offner, Fritz, Van Droogenbroeck, Jan, Wu, Ka Lung, Maiolino, Angelo, Martinez, Gracia, Zanella, Karla, Capra, Marcelo, Araujo, Sergio, Gregora, Evzen, Pour, Ludek, Scudla, Vlastimil, Spicka, Ivan, Abildgaard, Niels, Andersen, Niels, Jensen, Bo Amdi, Helleberg, Carsten, Plesner, Torben, Salomo, Morten, Svirskaite, Asta, Delarue, Richard, Blau, Igor, Schieferdecker, Aneta, Teleanu, Veronica, Munder, Markus, Rollig, Christoph, Salwender, Han-Juergen, Fuhrmann, Stephan, Weisel, Katja, Duerig, Jan, Zeis, Matthias, Klein, Stefan, Reimer, Peter, Schmidt, Christian, Scheid, Christof, Mayer, Karin, Hoffmann, Martin, Sosada, Markus, Dimopoulos, Athanasios, Delimpasi, Sosana, Kyrtsonis, Mary-Christine, Anagnostopoulos, Achilleas, Nagy, Zsolt, Illes, Arpad, Egyed, Miklos, Borbenyi, Zita, Mikala, Gabor, Dally, Najib, Horowitz, Netanel, Gutwein, Odit, Nemets, Anatoly, Vaxman, Iuliana, Shvetz, Olga, Trestman, Svetlana, Ruchlemer, Rosa, Nagler, Arnon, Tadmor, Tamar, Rouvio, Ory, Preis, Meir, Cavo, Michele, De Rosa, Luca, Musto, Pellegrino, Cafro, Anna, Tosi, Patrizia, Offidani, Massimo, Corso, Alessandro, Rossi, Giuseppe, Liberati, Anna Marina, Bosi, Alberto, Suzuki, Kenshi, Nakaseko, Chiaki, Ishikawa, Takayuki, Matsumoto, Morio, Nagai, Hirokazu, Sunami, Kazutaka, Chou, Takaaki, Akashi, Koichi, Takezako, Naoki, Hagiwara, Shotaro, Eom, Hyeon Seok, Jo, Deog-Yeon, Kim, Jin Seok, Lee, Jae Hoon, Yoon, Sung Soo, Yoon, Dok Hyun, Kim, Kihyun, Levin, Mark-David, Vellenga, Edo, Minnema, Monique, Waage, Anders, Haukas, Einar, Grosicki, Sebastian, Pluta, Andrzej, Robak, Tadeusz, Marques, Herlander, Bergantim, Rui, Campilho, Fernando, Chng, Wee Joo, Goh, Yeow Tee, McDonald, Andrew, Rapoport, Bernado, Rivas, Miguel Angel Alvarez, de La Fuente, Felipe De Arriba, Montes, Yolanda Gonzalez, Sanchez, Jesus Martin, Rocafiguera, Albert Oriol, Rosinol, Laura, San Miguel, Jesus, de Oteyza, Jaime Perez, Encinas, Cristina, Alegre-Amor, Adrian, Lopez-Guia, Ana, Axelsson, Per, Carlson, Kristina, Stromberg, Olga, Hansson, Markus, Blimark, Cecile Hveding, Mueller, Rouven, Chen, Chih-Cheng, Liu, Ta-Chih, Huang, Shang-Yi, Wang, Po-Nan, Nakorn, Thanyaphong Na, Prayongratana, Kannadit, Unal, Ali, Goker, Hakan, Sonmez, Mehmet, Korenkova, Sybiryna, Chaidos, Aristeidis, Oakervee, Heather, Sati, Hamdi, Benjamin, Reuben, Wechalekar, Ashutosh, Garg, Mamta, Ramasamy, Karthik, Cook, Gordon, Chantry, Andrew, Jenner, Matthew, Buadi, Francis, Berryman, Robert, Janakiram, Murali, MS Hematologie, Infection & Immunity, Regenerative Medicine and Stem Cells, Dimopoulos, Meletios A., Gay, Francesca, Schjesvold, Fredrik, Beksac, Meral, Hajek, Roman, Weisel, Katja Christina, Goldschmidt, Hartmut, Maisnar, Vladimir, Moreau, Philippe, Min, Chang Ki, Pluta, Agnieszka, Chng, Wee-Joo, Kaiser, Martin, Zweegman, Sonja, Mateos, Maria Victoria, Spencer, Andrew, Iida, Shinsuke, Morgan, Gareth, Suryanarayan, Kaveri, Teng, Zhaoyang, Skacel, Tomas, Palumbo, Antonio, Dash, Ajeeta B., Gupta, Neeraj, Labotka, Richard, Rajkumar, S. Vincent, Bar, Daniel, Basso, Alfredo, Fantl, Dorotea, He, Simon, Horvath, Neomi, Lee, Cindy, Rowlings, Phillip, Taylor, Kerry, Cochrane, Tara, Kwok, Fiona, Ramanathan, Sundreswran, Agis, Hermine, Zojer, Niklas, Kentos, Alain, Offner, Fritz, Van Droogenbroeck, Jan, Wu, Ka Lung, Maiolino, Angelo, Martinez, Gracia, Zanella, Karla, Capra, Marcelo, Araujo, Sergio, Gregora, Evzen, Pour, Ludek, Scudla, Vlastimil, Spicka, Ivan, Abildgaard, Niels, Andersen, Niels, Jensen, Bo Amdi, Helleberg, Carsten, Plesner, Torben, Salomo, Morten, Svirskaite, Asta, Delarue, Richard, Blau, Igor, Schieferdecker, Aneta, Teleanu, Veronica, Munder, Markus, Rollig, Christoph, Salwender, Han-Juergen, Fuhrmann, Stephan, Weisel, Katja, Duerig, Jan, Zeis, Matthias, Klein, Stefan, Reimer, Peter, Schmidt, Christian, Scheid, Christof, Mayer, Karin, Hoffmann, Martin, Sosada, Markus, Dimopoulos, Athanasios, Delimpasi, Sosana, Kyrtsonis, Mary-Christine, Anagnostopoulos, Achilleas, Nagy, Zsolt, Illes, Arpad, Egyed, Miklos, Borbenyi, Zita, Mikala, Gabor, Dally, Najib, Horowitz, Netanel, Gutwein, Odit, Nemets, Anatoly, Vaxman, Iuliana, Shvetz, Olga, Trestman, Svetlana, Ruchlemer, Rosa, Nagler, Arnon, Tadmor, Tamar, Rouvio, Ory, Preis, Meir, Cavo, Michele, De Rosa, Luca, Musto, Pellegrino, Cafro, Anna, Tosi, Patrizia, Offidani, Massimo, Corso, Alessandro, Rossi, Giuseppe, Liberati, Anna Marina, Bosi, Alberto, Suzuki, Kenshi, Nakaseko, Chiaki, Ishikawa, Takayuki, Matsumoto, Morio, Nagai, Hirokazu, Sunami, Kazutaka, Chou, Takaaki, Akashi, Koichi, Takezako, Naoki, Hagiwara, Shotaro, Eom, Hyeon Seok, Jo, Deog-Yeon, Kim, Jin Seok, Lee, Jae Hoon, Yoon, Sung Soo, Yoon, Dok Hyun, Kim, Kihyun, Levin, Mark-David, Vellenga, Edo, Minnema, Monique, Waage, Anders, Haukas, Einar, Grosicki, Sebastian, Pluta, Andrzej, Robak, Tadeusz, Marques, Herlander, Bergantim, Rui, Campilho, Fernando, Chng, Wee Joo, Goh, Yeow Tee, McDonald, Andrew, Rapoport, Bernado, Rivas, Miguel Angel Alvarez, de La Fuente, Felipe De Arriba, Montes, Yolanda Gonzalez, Sanchez, Jesus Martin, Rocafiguera, Albert Oriol, Rosinol, Laura, San Miguel, Jesus, de Oteyza, Jaime Perez, Encinas, Cristina, Alegre-Amor, Adrian, Lopez-Guia, Ana, Axelsson, Per, Carlson, Kristina, Stromberg, Olga, Hansson, Markus, Blimark, Cecile Hveding, Mueller, Rouven, Chen, Chih-Cheng, Liu, Ta-Chih, Huang, Shang-Yi, Wang, Po-Nan, Nakorn, Thanyaphong Na, Prayongratana, Kannadit, Unal, Ali, Goker, Hakan, Sonmez, Mehmet, Korenkova, Sybiryna, Chaidos, Aristeidis, Oakervee, Heather, Sati, Hamdi, Benjamin, Reuben, Wechalekar, Ashutosh, Garg, Mamta, Ramasamy, Karthik, Cook, Gordon, Chantry, Andrew, Jenner, Matthew, Buadi, Francis, Berryman, Robert, and Janakiram, Murali

Published
2019

14. Genome-wide Association Study of Idiopathic Osteonecrosis of the Femoral Head

Author

40294938, Sakamoto, Yuma, Yamamoto, Takuaki, Sugano, Nobuhiko, Takahashi, Daisuke, Watanabe, Toshiyuki, Atsumi, Takashi, Nakamura, Junichi, Hasegawa, Yukiharu, Akashi, Koichi, Narita, Ichiei, Miyamoto, Takeshi, Takeuchi, Tsutomu, Ikari, Katsunori, Amano, Koichi, Fujie, Atsuhiro, Kubo, Toshikazu, Tada, Yoshifumi, Kaneuji, Ayumi, Nakamura, Hiroaki, Miyamura, Tomoya, Kabata, Tamon, Yamaji, Ken, Okawa, Takahiro, Sudo, Akihiro, Ohzono, Kenji, Tanaka, Yoshiya, Yasunaga, Yuji, Matsuda, Shuichi, Imai, Yuuki, Akiyama, Masato, Kubo, Michiaki, Kamatani, Yoichiro, Iwamoto, Yukihide, Ikegawa, Shiro, 40294938, Sakamoto, Yuma, Yamamoto, Takuaki, Sugano, Nobuhiko, Takahashi, Daisuke, Watanabe, Toshiyuki, Atsumi, Takashi, Nakamura, Junichi, Hasegawa, Yukiharu, Akashi, Koichi, Narita, Ichiei, Miyamoto, Takeshi, Takeuchi, Tsutomu, Ikari, Katsunori, Amano, Koichi, Fujie, Atsuhiro, Kubo, Toshikazu, Tada, Yoshifumi, Kaneuji, Ayumi, Nakamura, Hiroaki, Miyamura, Tomoya, Kabata, Tamon, Yamaji, Ken, Okawa, Takahiro, Sudo, Akihiro, Ohzono, Kenji, Tanaka, Yoshiya, Yasunaga, Yuji, Matsuda, Shuichi, Imai, Yuuki, Akiyama, Masato, Kubo, Michiaki, Kamatani, Yoichiro, Iwamoto, Yukihide, and Ikegawa, Shiro

Abstract

Idiopathic osteonecrosis of the femoral head (IONFH) is an ischemic disorder that causes bone necrosis of the femoral head, resulting in hip joint dysfunction. IONFH is a polygenic disease and steroid and alcohol have already known to increase its risk; however, the mechanism of IONFH remains to be elucidated. We performed a genome-wide association study using ~60, 000 subjects and found two novel loci on chromosome 20q12 and 12q24. Big data analyses identified LINC01370 as a candidate susceptibility gene in the 20q12 locus. Stratified analysis by IONFH risk factors suggested that the 12q24 locus was associated with IONFH through drinking capacity. Our findings would shed new light on pathophysiology of IONFH.

Published
2017

15. The EGF Receptor Promotes the Malignant Potential of Glioma by Regulating Amino Acid Transport System xc(-).

Author

Tsuchihashi, Kenji, Tsuchihashi, Kenji, Okazaki, Shogo, Ohmura, Mitsuyo, Ishikawa, Miyuki, Sampetrean, Oltea, Onishi, Nobuyuki, Wakimoto, Hiroaki, Yoshikawa, Momoko, Seishima, Ryo, Iwasaki, Yoshimi, Morikawa, Takayuki, Abe, Shinya, Takao, Ayumi, Shimizu, Misato, Masuko, Takashi, Nagane, Motoo, Furnari, Frank B, Akiyama, Tetsu, Suematsu, Makoto, Baba, Eishi, Akashi, Koichi, Saya, Hideyuki, Nagano, Osamu, Tsuchihashi, Kenji, Tsuchihashi, Kenji, Okazaki, Shogo, Ohmura, Mitsuyo, Ishikawa, Miyuki, Sampetrean, Oltea, Onishi, Nobuyuki, Wakimoto, Hiroaki, Yoshikawa, Momoko, Seishima, Ryo, Iwasaki, Yoshimi, Morikawa, Takayuki, Abe, Shinya, Takao, Ayumi, Shimizu, Misato, Masuko, Takashi, Nagane, Motoo, Furnari, Frank B, Akiyama, Tetsu, Suematsu, Makoto, Baba, Eishi, Akashi, Koichi, Saya, Hideyuki, and Nagano, Osamu

Abstract

Extracellular free amino acids contribute to the interaction between a tumor and its microenvironment through effects on cellular metabolism and malignant behavior. System xc(-) is composed of xCT and CD98hc subunits and functions as a plasma membrane antiporter for the uptake of extracellular cystine in exchange for intracellular glutamate. Here, we show that the EGFR interacts with xCT and thereby promotes its cell surface expression and function in human glioma cells. EGFR-expressing glioma cells manifested both enhanced antioxidant capacity as a result of increased cystine uptake, as well as increased glutamate, which promotes matrix invasion. Imaging mass spectrometry also revealed that brain tumors formed in mice by human glioma cells stably overexpressing EGFR contained higher levels of reduced glutathione compared with those formed by parental cells. Targeted inhibition of xCT suppressed the EGFR-dependent enhancement of antioxidant capacity in glioma cells, as well as tumor growth and invasiveness. Our findings establish a new functional role for EGFR in promoting the malignant potential of glioma cells through interaction with xCT at the cell surface. Cancer Res; 76(10); 2954-63. ©2016 AACR.

Published
2016

16. Expansion of donor-reactive host T cells in primary graft failure after allogeneic hematopoietic SCT following reduced-intensity conditioning

Author

Koyama, Motoko, Hashimoto, Daigo, Nagafuji, Koji, Eto, Tetsuya, Ohno, Yuju, Aoyama, Kazutoshi, Iwasaki, Hiromi, Miyamoto, Toshihiro, Hill, Geoffrey R., Akashi, Koichi, 1000040284096, Teshima, Takanori, Koyama, Motoko, Hashimoto, Daigo, Nagafuji, Koji, Eto, Tetsuya, Ohno, Yuju, Aoyama, Kazutoshi, Iwasaki, Hiromi, Miyamoto, Toshihiro, Hill, Geoffrey R., Akashi, Koichi, 1000040284096, and Teshima, Takanori

Abstract

Graft rejection remains a major obstacle in allogeneic hematopoietic SCT following reduced-intensity conditioning (RIC-SCT), particularly after cord blood transplantation (CBT). In a murine MHC-mismatched model of RIC-SCT, primary graft rejection was associated with activation and expansion of donor-reactive host T cells in peripheral blood and BM early after SCT. Donor-derived dendritic cells are at least partly involved in host T-cell activation. We then evaluated if such an expansion of host T cells could be associated with graft rejection after RIC-CBT. Expansion of residual host lymphocytes was observed in 4/7 patients with graft rejection at 3 weeks after CBT, but in none of the 17 patients who achieved engraftment. These results suggest the crucial role of residual host T cells after RIC-SCT in graft rejection and expansion of host T cells could be a marker of graft rejection. Development of more efficient T cell-suppressive conditioning regimens may be necessary in the context of RIC-SCT.

Published
2014

17. Expansion of donor-reactive host T cells in primary graft failure after allogeneic hematopoietic SCT following reduced-intensity conditioning

Author

Koyama, Motoko, Hashimoto, Daigo, Nagafuji, Koji, Eto, Tetsuya, Ohno, Yuju, Aoyama, Kazutoshi, Iwasaki, Hiromi, Miyamoto, Toshihiro, Hill, Geoffrey R., Akashi, Koichi, Teshima, Takanori, Koyama, Motoko, Hashimoto, Daigo, Nagafuji, Koji, Eto, Tetsuya, Ohno, Yuju, Aoyama, Kazutoshi, Iwasaki, Hiromi, Miyamoto, Toshihiro, Hill, Geoffrey R., Akashi, Koichi, and Teshima, Takanori

Abstract

Graft rejection remains a major obstacle in allogeneic hematopoietic SCT following reduced-intensity conditioning (RIC-SCT), particularly after cord blood transplantation (CBT). In a murine MHC-mismatched model of RIC-SCT, primary graft rejection was associated with activation and expansion of donor-reactive host T cells in peripheral blood and BM early after SCT. Donor-derived dendritic cells are at least partly involved in host T-cell activation. We then evaluated if such an expansion of host T cells could be associated with graft rejection after RIC-CBT. Expansion of residual host lymphocytes was observed in 4/7 patients with graft rejection at 3 weeks after CBT, but in none of the 17 patients who achieved engraftment. These results suggest the crucial role of residual host T cells after RIC-SCT in graft rejection and expansion of host T cells could be a marker of graft rejection. Development of more efficient T cell-suppressive conditioning regimens may be necessary in the context of RIC-SCT.

Published
2014

18. Reciprocal Expression of Enteric Antimicrobial Proteins in Intestinal Graft-Versus-Host Disease

Author

Eriguchi, Yoshihiro, Uryu, Hidetaka, Nakamura, Kiminori, Shimoji, Sonoko, Takashima, Shuichiro, Iwasaki, Hiromi, Miyamoto, Toshihiro, Shimono, Nobuyuki, Hashimoto, Daigo, Akashi, Koichi, Ayabe, Tokiyoshi, 1000040284096, Teshima, Takanori, Eriguchi, Yoshihiro, Uryu, Hidetaka, Nakamura, Kiminori, Shimoji, Sonoko, Takashima, Shuichiro, Iwasaki, Hiromi, Miyamoto, Toshihiro, Shimono, Nobuyuki, Hashimoto, Daigo, Akashi, Koichi, Ayabe, Tokiyoshi, 1000040284096, and Teshima, Takanori

Abstract

We recently demonstrated that expression of alpha-defensins, the major antimicrobial peptides produced by Paneth cells, was severely suppressed in mice with graft-versus-host disease (GVHD). In this study, we found that antibacterial lectin, regenerating islet-derived III gamma (RegIII gamma) was upregulated in villous enterocytes, thus demonstrating the reciprocal control of enteric antimicrobial proteins in GVHD. Upregulation of RegIII gamma was mediated by a mechanism independent upon radiation-induced intestinal tract damage. MyD88-mediated signaling in intestinal epithelium was required for RegIII gamma upregulation in GVHD and antibiotic therapy downregulated RegIII gamma expression. These results suggest that MyD88-mediated sensing of the intestinal microbes disregulated in GVHD induces RegIII gamma upregulation in GVHD and argue a role for RegIII gamma in the pathogenesis of GVHD. (C) 2013 American Society for Blood and Marrow Transplantation.

Published
2013

19. Reciprocal Expression of Enteric Antimicrobial Proteins in Intestinal Graft-Versus-Host Disease

Author

Eriguchi, Yoshihiro, Uryu, Hidetaka, Nakamura, Kiminori, Shimoji, Sonoko, Takashima, Shuichiro, Iwasaki, Hiromi, Miyamoto, Toshihiro, Shimono, Nobuyuki, Hashimoto, Daigo, Akashi, Koichi, Ayabe, Tokiyoshi, Teshima, Takanori, Eriguchi, Yoshihiro, Uryu, Hidetaka, Nakamura, Kiminori, Shimoji, Sonoko, Takashima, Shuichiro, Iwasaki, Hiromi, Miyamoto, Toshihiro, Shimono, Nobuyuki, Hashimoto, Daigo, Akashi, Koichi, Ayabe, Tokiyoshi, and Teshima, Takanori

Abstract

We recently demonstrated that expression of alpha-defensins, the major antimicrobial peptides produced by Paneth cells, was severely suppressed in mice with graft-versus-host disease (GVHD). In this study, we found that antibacterial lectin, regenerating islet-derived III gamma (RegIII gamma) was upregulated in villous enterocytes, thus demonstrating the reciprocal control of enteric antimicrobial proteins in GVHD. Upregulation of RegIII gamma was mediated by a mechanism independent upon radiation-induced intestinal tract damage. MyD88-mediated signaling in intestinal epithelium was required for RegIII gamma upregulation in GVHD and antibiotic therapy downregulated RegIII gamma expression. These results suggest that MyD88-mediated sensing of the intestinal microbes disregulated in GVHD induces RegIII gamma upregulation in GVHD and argue a role for RegIII gamma in the pathogenesis of GVHD. (C) 2013 American Society for Blood and Marrow Transplantation.

Published
2013

20. Dendritic cell expression of the transcription factor T-bet regulates mast cell progenitor homing to mucosal tissue

Author

Alcaide, Pilar, Jones, Tatiana G, Lord, Graham M, Glimcher, Laurie H, Hallgren, Jenny, Arinobu, Yojiro, Akashi, Koichi, Paterson, Alison M, Gurish, Michael A, Luscinskas, Francis W, Alcaide, Pilar, Jones, Tatiana G, Lord, Graham M, Glimcher, Laurie H, Hallgren, Jenny, Arinobu, Yojiro, Akashi, Koichi, Paterson, Alison M, Gurish, Michael A, and Luscinskas, Francis W

Abstract

The transcription factor T-bet was identified in CD4(+) T cells, and it controls interferon gamma production and T helper type 1 cell differentiation. T-bet is expressed in certain other leukocytes, and we recently showed (Lord, G.M., R.M. Rao, H. Choe, B.M. Sullivan, A.H. Lichtman, F.W. Luscinskas, and L.H. Glimcher. 2005. Blood. 106:3432-3439) that it regulates T cell trafficking. We examined whether T-bet influences homing of mast cell progenitors (MCp) to peripheral tissues. Surprisingly, we found that MCp homing to the lung or small intestine in T-bet(-/-) mice is reduced. This is reproduced in adhesion studies using bone marrow-derived MCs (BMMCs) from T-bet(-/-) mice, which showed diminished adhesion to mucosal addresin cellular adhesion molecule-1 (MAdCAM-1) and vascular cell adhesion molecule-1 (VCAM-1), endothelial ligands required for MCp intestinal homing. MCp, their precursors, and BMMCs do not express T-bet, suggesting that T-bet plays an indirect role in homing. However, adoptive transfer experiments revealed that T-bet expression by BM cells is required for MCp homing to the intestine. Furthermore, transfer of WT BM-derived dendritic cells (DCs) to T-bet(-/-) mice restores normal MCp intestinal homing in vivo and MCp adhesion to MAdCAM-1 and VCAM-1 in vitro. Nonetheless, T-bet(-/-) mice respond vigorously to intestinal infection with Trichinella spiralis, eliminating a role for T-bet in MC recruitment to sites of infection and their activation and function. Therefore, remarkably, T-bet expression by DCs indirectly controls MCp homing to mucosal tissues.

Published
2007
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