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1. Impaired humoral immunity following COVID-19 vaccination in HTLV-1 carriers

Author

Kameda, Takuro, Utsunomiya, Atae, Otsuka, Nobuaki, Kubuki, Yoko, Uchida, Taisuke, Shide, Kotaro, Kamiunten, Ayako, Nakano, Nobuaki, Tokunaga, Masahito, Miyazono, Takayoshi, Ito, Yoshikiyo, Yonekura, Kentaro, Kawakita, Toshiro, Akizuki, Keiichi, Tahira, Yuki, Karasawa, Masayoshi, Hidaka, Tomonori, Konagata, Ayaka, Taniguchi, Norifumi, Nagatomo, Yuma, Kogo, Fumiko, Shimizu, Koichiro, Ueno, Hiroaki, Ishizaki, Junzo, Takahashi, Naoya, Ikei, Yoshihiko, Hidaka, Michihiro, Yamaguchi, Hideki, and Shimoda, Kazuya

Published
2024
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2. CARD11 mutation and HBZ expression induce lymphoproliferative disease and adult T-cell leukemia/lymphoma

Author

Kameda, Takuro, Shide, Kotaro, Kamiunten, Ayako, Kogure, Yasunori, Morishita, Daisuke, Koya, Junji, Tahira, Yuki, Akizuki, Keiichi, Yokomizo-Nakano, Takako, Kubota, Sho, Marutsuka, Kosuke, Sekine, Masaaki, Hidaka, Tomonori, Kubuki, Yoko, Kitai, Yuichi, Matsuda, Tadashi, Yoda, Akinori, Ohshima, Takayuki, Sugiyama, Midori, Sashida, Goro, Kataoka, Keisuke, Ogawa, Seishi, and Shimoda, Kazuya

Published
2022
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3. Whole-genome landscape of adult T-cell leukemia/lymphoma

Author

Kogure, Yasunori, Kameda, Takuro, Koya, Junji, Yoshimitsu, Makoto, Nosaka, Kisato, Yasunaga, Jun-ichirou, Imaizumi, Yoshitaka, Watanabe, Mizuki, Saito, Yuki, Ito, Yuta, McClure, Marni B., Tabata, Mariko, Shingaki, Sumito, Yoshifuji, Kota, Chiba, Kenichi, Okada, Ai, Kakiuchi, Nobuyuki, Nannya, Yasuhito, Kamiunten, Ayako, Tahira, Yuki, Akizuki, Keiichi, Sekine, Masaaki, Shide, Kotaro, Hidaka, Tomonori, Kubuki, Yoko, Kitanaka, Akira, Hidaka, Michihiro, Nakano, Nobuaki, Utsunomiya, Atae, Sica, R. Alejandro, Acuna-Villaorduna, Ana, Janakiram, Murali, Shah, Urvi, Ramos, Juan Carlos, Shibata, Tatsuhiro, Takeuchi, Kengo, Takaori-Kondo, Akifumi, Miyazaki, Yasushi, Matsuoka, Masao, Ishitsuka, Kenji, Shiraishi, Yuichi, Miyano, Satoru, Ogawa, Seishi, Ye, B. Hilda, Shimoda, Kazuya, and Kataoka, Keisuke

Published
2022
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5. Early/prefibrotic primary myelofibrosis in patients who were initially diagnosed with essential thrombocythemia

Author

Kamiunten, Ayako, Shide, Kotaro, Kameda, Takuro, Ito, Masafumi, Sekine, Masaaki, Kubuki, Yoko, Hidaka, Tomonori, Akizuki, Keiichi, Tahira, Yuki, Toyama, Takanori, Kawano, Noriaki, Marutsuka, Kousuke, Maeda, Kouichi, Takeuchi, Masanori, Kawano, Hiroshi, Sato, Seiichi, Ishizaki, Junzo, Shimoda, Haruko, Yamashita, Kiyoshi, Matsuoka, Hitoshi, and Shimoda, Kazuya

Published
2018
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6. Table S2 from Single-Cell Analysis of the Multicellular Ecosystem in Viral Carcinogenesis by HTLV-1

Author

Koya, Junji, primary, Saito, Yuki, primary, Kameda, Takuro, primary, Kogure, Yasunori, primary, Yuasa, Mitsuhiro, primary, Nagasaki, Joji, primary, McClure, Marni B., primary, Shingaki, Sumito, primary, Tabata, Mariko, primary, Tahira, Yuki, primary, Akizuki, Keiichi, primary, Kamiunten, Ayako, primary, Sekine, Masaaki, primary, Shide, Kotaro, primary, Kubuki, Yoko, primary, Hidaka, Tomonori, primary, Kitanaka, Akira, primary, Nakano, Nobuaki, primary, Utsunomiya, Atae, primary, Togashi, Yosuke, primary, Ogawa, Seishi, primary, Shimoda, Kazuya, primary, and Kataoka, Keisuke, primary

Published
2023
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7. Supplementary Data from Single-Cell Analysis of the Multicellular Ecosystem in Viral Carcinogenesis by HTLV-1

Author

Koya, Junji, primary, Saito, Yuki, primary, Kameda, Takuro, primary, Kogure, Yasunori, primary, Yuasa, Mitsuhiro, primary, Nagasaki, Joji, primary, McClure, Marni B., primary, Shingaki, Sumito, primary, Tabata, Mariko, primary, Tahira, Yuki, primary, Akizuki, Keiichi, primary, Kamiunten, Ayako, primary, Sekine, Masaaki, primary, Shide, Kotaro, primary, Kubuki, Yoko, primary, Hidaka, Tomonori, primary, Kitanaka, Akira, primary, Nakano, Nobuaki, primary, Utsunomiya, Atae, primary, Togashi, Yosuke, primary, Ogawa, Seishi, primary, Shimoda, Kazuya, primary, and Kataoka, Keisuke, primary

Published
2023
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8. Data from Single-Cell Analysis of the Multicellular Ecosystem in Viral Carcinogenesis by HTLV-1

Author

Koya, Junji, primary, Saito, Yuki, primary, Kameda, Takuro, primary, Kogure, Yasunori, primary, Yuasa, Mitsuhiro, primary, Nagasaki, Joji, primary, McClure, Marni B., primary, Shingaki, Sumito, primary, Tabata, Mariko, primary, Tahira, Yuki, primary, Akizuki, Keiichi, primary, Kamiunten, Ayako, primary, Sekine, Masaaki, primary, Shide, Kotaro, primary, Kubuki, Yoko, primary, Hidaka, Tomonori, primary, Kitanaka, Akira, primary, Nakano, Nobuaki, primary, Utsunomiya, Atae, primary, Togashi, Yosuke, primary, Ogawa, Seishi, primary, Shimoda, Kazuya, primary, and Kataoka, Keisuke, primary

Published
2023
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10. Thrombohemorrhagic events, disease progression, and survival in polycythemia vera and essential thrombocythemia: a retrospective survey in Miyazaki prefecture, Japan

Author

Kamiunten, Ayako, Shide, Kotaro, Kameda, Takuro, Sekine, Masaaki, Kubuki, Yoko, Ito, Masafumi, Toyama, Takanori, Kawano, Noriaki, Marutsuka, Kousuke, Maeda, Kouichi, Takeuchi, Masanori, Kawano, Hiroshi, Sato, Seiichi, Ishizaki, Junzo, Akizuki, Keiichi, Tahira, Yuki, Shimoda, Haruko, Hidaka, Tomonori, Yamashita, Kiyoshi, Matsuoka, Hitoshi, and Shimoda, Kazuya

Published
2018
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11. Mice with Calr mutations homologous to human CALR mutations only exhibit mild thrombocytosis

Author

Shide, Kotaro, Kameda, Takuro, Kamiunten, Ayako, Oji, Asami, Ozono, Yoshinori, Sekine, Masaaki, Honda, Arata, Kitanaka, Akira, Akizuki, Keiichi, Tahira, Yuki, Nakamura, Kenichi, Hidaka, Tomonori, Kubuki, Yoko, Abe, Hiroo, Miike, Tadashi, Iwakiri, Hisayoshi, Tahara, Yoshihiro, Sueta, Mitsue, Hasuike, Satoru, Yamamoto, Shojiro, Nagata, Kenji, Ikawa, Masahito, and Shimoda, Kazuya

Published
2019
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12. Prognosis of Indolent Adult T-Cell Leukemia/Lymphoma

Author

Kameda, Takuro, primary, Shide, Kotaro, additional, Tahira, Yuki, additional, Sekine, Masaaki, additional, Sato, Seiichi, additional, Ishizaki, Junzo, additional, Takeuchi, Masanori, additional, Akizuki, Keiichi, additional, Kamiunten, Ayako, additional, Shimoda, Haruko, additional, Toyama, Takanori, additional, Maeda, Kouichi, additional, Yamashita, Kiyoshi, additional, Kawano, Noriaki, additional, Kawano, Hiroshi, additional, Hidaka, Tomonori, additional, Yamaguchi, Hideki, additional, Kubuki, Yoko, additional, Kitanaka, Akira, additional, Matsuoka, Hitoshi, additional, and Shimoda, Kazuya, additional

Published
2022
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13. The effect of CARD11 mutation and HBZ expression accelerated lymphoproliferative diseases and formed the pathological basis for adult T-cell leukemia/lymphoma

Author

Shimoda, Kazuya, primary, Kameda, Takuro, additional, Shide, Kotaro, additional, Kamiunten, Ayako, additional, Kogure, Yasunori, additional, Morishita, Daisuke, additional, Koya, Junji, additional, Tahira, Yuki, additional, Akizuki, Keiichi, additional, Yokomizo-Nakano, Takako, additional, Kubota, Sho, additional, Marutsuka, Kosuke, additional, Sekine, Masaaki, additional, Hidaka, Tomonori, additional, Kubuki, Yoko, additional, Yoda, Akinori, additional, Ohshima, Takayuki, additional, Sugiyama, Midori, additional, Sashida, Goro, additional, Kataoka, Keisuke, additional, and Ogawa, Seishi, additional

Published
2022
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14. Single-Cell Analysis of the Multicellular Ecosystem in Viral Carcinogenesis by HTLV-1

Author

Koya, Junji, primary, Saito, Yuki, additional, Kameda, Takuro, additional, Kogure, Yasunori, additional, Yuasa, Mitsuhiro, additional, Nagasaki, Joji, additional, McClure, Marni B., additional, Shingaki, Sumito, additional, Tabata, Mariko, additional, Tahira, Yuki, additional, Akizuki, Keiichi, additional, Kamiunten, Ayako, additional, Sekine, Masaaki, additional, Shide, Kotaro, additional, Kubuki, Yoko, additional, Hidaka, Tomonori, additional, Kitanaka, Akira, additional, Nakano, Nobuaki, additional, Utsunomiya, Atae, additional, Togashi, Yosuke, additional, Ogawa, Seishi, additional, Shimoda, Kazuya, additional, and Kataoka, Keisuke, additional

Published
2021
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15. Real-World Data on Clinical Features, Outcomes, and Prognostic Factors in Multiple Myeloma from Miyazaki Prefecture, Japan

Author

Akizuki, Keiichi, primary, Matsuoka, Hitoshi, additional, Toyama, Takanori, additional, Kamiunten, Ayako, additional, Sekine, Masaaki, additional, Shide, Kotaro, additional, Kameda, Takuro, additional, Kawano, Noriaki, additional, Maeda, Kouichi, additional, Takeuchi, Masanori, additional, Kawano, Hiroshi, additional, Sato, Seiichi, additional, Ishizaki, Junzo, additional, Tahira, Yuki, additional, Shimoda, Haruko, additional, Hidaka, Tomonori, additional, Yamashita, Kiyoshi, additional, Kubuki, Yoko, additional, and Shimoda, Kazuya, additional

Published
2020
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16. Higher average chemotherapy dose intensity improves prognosis in patients with aggressive adult T‐cell leukemia/lymphoma

Author

Sekine, Masaaki, primary, Kameda, Takuro, additional, Shide, Kotaro, additional, Maeda, Kouichi, additional, Toyama, Takanori, additional, Kawano, Noriaki, additional, Takeuchi, Masanori, additional, Kawano, Hiroshi, additional, Sato, Seiichi, additional, Ishizaki, Junzo, additional, Kukita, Toshimasa, additional, Kamiunten, Ayako, additional, Akizuki, Keiichi, additional, Tahira, Yuki, additional, Shimoda, Haruko, additional, Hidaka, Tomonori, additional, Yamashita, Kiyoshi, additional, Matsuoka, Hitoshi, additional, Kitanaka, Akira, additional, Kubuki, Yoko, additional, and Shimoda, Kazuya, additional

Published
2020
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17. CARD11 Mutation Induces Oligoclonal Expansion of T-Cells, and Accelerates ATL Development in Combination with HBZ

Author

Midori Sugiyama, Tahira Yuki, Yoko Kubuki, Daisuke Morishita, Kazuya Shimoda, Masaaki Sekine, Kotaro Shide, Tomonori Hidaka, Ayako Kamiunten, Takuro Kameda, and Keiichi Akizuki

Subjects
medicine.medical_specialty, Hematology, CD3, Immunology, Alveolar septum, Spleen, Cell Biology, Gene mutation, Biology, medicine.disease, Biochemistry, Molecular biology, Lymphoma, Leukemia, medicine.anatomical_structure, Internal medicine, medicine, biology.protein, Lymph node
Abstract

Adult T-cell leukemia/lymphoma (ATL) is an aggressive peripheral T-cell lymphoma that develops in about 5% of human T-cell leukemia/lymphoma virus 1 (HTLV-1) carriers. In addition to viral oncogenes, namely tax and HTLV-1 bZIP factor (HBZ), gene mutations, highly enriched for T-cell receptor (TCR)-NF-kB signaling, should be involved in the development of ATL. Among gene mutations, mutation in CARD11, a cytoplasmic scaffolding protein required for TCR-induced NF-kB activation, was detected in 24% of ATL patients. Here we generated a mouse model for conditional expression of a human ATL-derived CARD11(E626K) gain-of-function mutant, and demonstrated CARD11 activation induced oligoclonal expansion of T-cell and infiltration to many organs. We also showed that expression of HBZ accelerated mutant CARD11-induced lymphoproliferative diseases. We introduced a human Card11(E626K) into the mouse genome at the ROSA26 locus. After crossing with CD4-Cre Tg, CARD11(E626K)CD4-Cre mice was obtained. In CD4+ cells from CARD11(E626K)CD4-Cre, the amount of cleaved BCL-10 and NF-kBp65 increased compared with those in WT CD4+cells, confirming the activation of NF-kB. About half of CARD11(E626K)CD4-Cre mice died on or after 6 months after birth. At 6 months, leukocytosis was observed in CARD11(E626K)CD4-Cre, and accordingly the number of CD4+ cells cells was about 1.43 times greater than those in WT mice. The most affected organ in CARD11(E626K)CD4-Cre mice was lung. Alveolar septum was thickened by infiltrated cells at 6 months, and worsened subsequently. CD3+ T-cell accumulated around capillary blood vessels, and had high proliferation indices (>50%), as assayed by Ki-67 staining. CARD11(E626K)CD4-Cre mice developed lymphadenopathy (4/8 mice (50%) at 6M and 4/6 mice (66.7%) at 12M). Normal lymph node (LN) architecture was barely preserved, and medullary sinus was expanded with CD3+ T-cell. Some of them were positive for FoxP3, and had moderate proliferation indices (25%-50%). Among CD4+ T-cell, the proportion of naive T-cell (Tn) decreased, and that of effector/memory T-cell (Tem) and regulatory T-cell (Treg) increased compared to WT LNs. The proportion of Treg in CD4+ T-cell from LN of 6M- and 12M-old CARD11(E626K)CD4-Cre mice was 25% and 40%, respectively, which values were much larger than the normal range as 10-15%. We next examined the clonality of CD4+ cells in spleen and swollen LNs from CARD11(E626K)CD4-Cre mice. The clonality of the TCR repertoires of 20 individual Vb gene famines from Vb1-20 was assessed by a PCR. The clonality assay using the TCR repertoires exhibited an oligoclonal pattern in 4 of 5 splenic CD4+ cells, and 1 of 2 LN CD4+ cells from CARD11(E626K)CD4-Cre mice. To assess the effect of HBZ constant expression on CARD11(E626K)CD4-Cre mice, we generated HBZ Tg, in which HBZ cDNA was expressed under the CD4 promoter. Similar to the previous report (by Satou et al.), our HBZ Tg showed increased number of Tem, destroyed architecture of lung such as thickened alveolar septum by infiltrated cells and decreased alveolar space by edema, and the lymphadenopathy after 12M (66.7%). We then crossed CARD11(E626K)CD4-Creand HBZ Tg, and obtained the compound mice. The compound mice caused more aggressive lymphoproliferative diseases compared with CARD11(E626K)CD4-Cre mice. Most of compound mice died within 8M. At 6M, architecture of lung, kidney, spleen, and LN was destroyed. In lung, alveolar space of lung was scarcely observed caused of T-cell invasion. Alveolar septum was thickened with infiltrated cells, and CD3+ cells accumulated around capillary blood vessel. Some of them were positive for FoxP3, and indicated moderate proliferation indices (25-50%). T-cell invasion was also observed in kidney. Lymphadenopathy was detected in 6 of 9 (66.7%) with completely destroyed architecture, increment of the proportion of Fox3+ cells, and moderate proliferation indices (25-50%). The clonality assay using the TCR repertoires exhibited an oligoclonal pattern in 4 of 4 splenic CD4+ cells, and 2 of 2 LNs CD4+ cells from compound mice. These results suggest that CARD11 mutant-induced NFkB activation and constant HBZ expression may have similar effects, such as T-cell infiltration into organs and LN adenopathy, and that the simultaneous occurrence of both may have additive effects. Disclosures Sugiyama: Chordia Therapeutics, Japan.: Current Employment. Morishita:Chordia Therapeutics Inc.: Current Employment, Current equity holder in private company. Shimoda:Perseus Proteomics: Research Funding; PharmaEssentia Japan: Research Funding; AbbVie Inc.: Research Funding; Astellas Pharma: Research Funding; Merck & Co.: Research Funding; CHUGAI PHARMACEUTICAL CO., LTD.: Research Funding; Kyowa Hakko Kirin Co., Ltd.: Research Funding; Pfizer Inc.: Research Funding; Otsuka Pharmaceutical: Research Funding; Asahi Kasei Medical: Research Funding; Japanese Society of Hematology: Research Funding; The Shinnihon Foundation of Advanced Medical Treatment Research: Research Funding; Celgene: Honoraria; Shire plc: Honoraria; Novartis: Honoraria, Research Funding; Takeda Pharmaceutical Company: Honoraria; Bristol-Myers Squibb: Honoraria.

Published
2020

18. Neoplastic fibrocytes play an essential role in bone marrow fibrosis in Jak2V617F-induced primary myelofibrosis mice

Author

Ozono, Yoshinori, primary, Shide, Kotaro, additional, Kameda, Takuro, additional, Kamiunten, Ayako, additional, Tahira, Yuki, additional, Sekine, Masaaki, additional, Akizuki, Keiichi, additional, Nakamura, Kenichi, additional, Iwakiri, Hisayoshi, additional, Sueta, Mitsue, additional, Hidaka, Tomonori, additional, Kubuki, Yoko, additional, Yamamoto, Shojiro, additional, Hasuike, Satoru, additional, Sawaguchi, Akira, additional, Nagata, Kenji, additional, and Shimoda, Kazuya, additional

Published
2020
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19. Calreticulin haploinsufficiency augments stem cell activity and is required for onset of myeloproliferative neoplasms

Author

Shide, Kotaro, primary, Kameda, Takuro, primary, Kamiunten, Ayako, primary, Ozono, Yoshinori, primary, Tahira, Yuki, primary, Yokomizo-Nakano, Takako, primary, Kubota, Sho, primary, Ono, Masaya, primary, Ikeda, Kazuhiko, primary, Sekine, Masaaki, primary, Akizuki, Keiichi, primary, Nakamura, Kenichi, primary, Hidaka, Tomonori, primary, Kubuki, Yoko, primary, Iwakiri, Hisayoshi, primary, Hasuike, Satoru, primary, Nagata, Kenji, primary, Sashida, Goro, primary, and Shimoda, Kazuya, primary

Published
2020
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20. TP53 and PTEN Mutations Were Shared in Concurrent Germ Cell Tumor and Acute Megakaryoblastic Leukemia

Author

Akizuki, Keiichi, primary, Sekine, Masaaki, additional, Kogure, Yasunori, additional, Kameda, Takuro, additional, Shide, Kotaro, additional, Koya, Junji, additional, Kamiunten, Ayako, additional, Kubuki, Yoko, additional, Tahira, Yuki, additional, Hidara, Tomonori, additional, Kiwaki, Takumi, additional, Tanaka, Hiroyuki, additional, Sato, Yuichiro, additional, Kataoka, Hiroaki, additional, Kataoka, Keisuke, additional, and Shimoda, Kazuya, additional

Published
2019
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21. Depletion of Neoplastic CD11b Positive Cells in Jak2V617F Mutant Mice Reduced Fibrocytes in Bone Marrow and Improved Myelofibrosis

Author

Ozono, Yoshinori, primary, Shide, Kotaro, primary, Kameda, Takuro, primary, Kamiunten, Ayako, primary, Tahira, Yuki, primary, Sekine, Masaaki, primary, Akizuki, Keiichi, primary, Nakamura, Kenichi, primary, Iwakiri, Hisayoshi, primary, Hidaka, Tomonori, primary, Kubuki, Yoko, primary, Hasuike, Satoru, primary, Toyoshima, Fumiyo, primary, Sawaguchi, Akira, primary, Nagata, Kenji, primary, and Shimoda, Kazuya, primary

Published
2019
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22. The Role of Calreticulin in Normal Hematopoiesis and Neoplastic Hematopoiesis of Myeloproliferative Neoplasms

Author

Shide, Kotaro, primary, Kameda, Takuro, primary, Kamiunten, Ayako, primary, Ozono, Yoshinori, primary, Tahira, Yuki, primary, Sekine, Masaaki, primary, Ono, Masaya, primary, Yokomizo, Takako, primary, Kubota, Sho, primary, Akizuki, Keiichi, primary, Kubuki, Yoko, primary, Hidaka, Tomonori, primary, Sashida, Goro, primary, and Shimoda, Kazuya, primary

Published
2019
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23. Haploinsufficiency of CALR Confers Hematopoietic Stem Cells (HSCs) with a Clonal Advantage over Wild-Type Cells, and, in Setting of Myeloproliferative Neoplasms, Compensates for the Functions of HSCs Impaired By the Calr Mutation

Author

Shide, Kotaro, primary, Kameda, Takuro, additional, Kamiunten, Ayako, additional, Sekine, Masaaki, additional, Ozono, Yoshinori, additional, Yokomizo, Takako, additional, Akizuki, Keiichi, additional, Tahira, Yuki, additional, Kubuki, Yoko, additional, Hidaka, Tomonori, additional, Sashida, Goro, additional, and Shimoda, Kazuya, additional

Published
2018
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24. TET2 Mutation Associated with Organ Infiltrations in ATLL

Author

Kameda, Takuro, primary, Shide, Kotaro, additional, Kamiunten, Ayako, additional, Tahira, Yuki, additional, Akizuki, Keiichi, additional, Sekine, Masaaki, additional, Hidaka, Tomonori, additional, Kubuki, Yoko, additional, Hidaka, Michihiro, additional, Utsunomiya, Atae, additional, Ohshima, Takayuki, additional, Kataoka, Keisuke, additional, Ogawa, Seishi, additional, and Shimoda, Kazuya, additional

Published
2018
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25. Higher average chemotherapy dose intensity improves prognosis in patients with aggressive adult T‐cell leukemia/lymphoma.

Author

Sekine, Masaaki, Kameda, Takuro, Shide, Kotaro, Maeda, Kouichi, Toyama, Takanori, Kawano, Noriaki, Takeuchi, Masanori, Kawano, Hiroshi, Sato, Seiichi, Ishizaki, Junzo, Kukita, Toshimasa, Kamiunten, Ayako, Akizuki, Keiichi, Tahira, Yuki, Shimoda, Haruko, Hidaka, Tomonori, Yamashita, Kiyoshi, Matsuoka, Hitoshi, Kitanaka, Akira, and Kubuki, Yoko

Subjects
ADULT T-cell leukemia, CANCER chemotherapy, T-cell lymphoma, LYMPHOMAS, PROGNOSIS
Abstract

Objective and Method: Adult T‐cell leukemia/lymphoma (ATL) is an aggressive peripheral T‐cell lymphoma with poor prognosis. We retrospectively reviewed the medical records of 312 patients with aggressive ATL and analyzed the effect of chemotherapy dose intensity on prognosis in clinical practice. Result: As first‐line therapy, 62 patients underwent best supportive care (BSC) or single‐agent chemotherapy, and 235 underwent intensive chemotherapy. The median survival time (MST) was 0.58 years in the 312 total patients, and 0.13 years and 0.75 years in the BSC/single‐agent chemotherapy group and intensive chemotherapy group, respectively. The median average relative dose intensity (ARDI) of patients who received intensive chemotherapy was 60%. We divided patients into 3 groups according to ARDI. Those in the top tertile of ARDI (ARDI ≥ 75%, n = 82) had better overall survival compared with those in the intermediate tertile (45% ≤ ARDI < 75%, n = 79) (P <.0001), with MSTs of 4.69 and 0.75 years, respectively. The occurrence of organ dysfunction and infectious complications was comparable between the two ARDI groups. Conclusion: Higher ARDI improves prognosis in patients with aggressive ATL in clinical practice. [ABSTRACT FROM AUTHOR]

Published
2021
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27. Effects of mogamulizumab in adult T-cell leukemia/lymphoma in clinical practice

Author

Sekine, Masaaki, primary, Kubuki, Yoko, additional, Kameda, Takuro, additional, Takeuchi, Masanori, additional, Toyama, Takanori, additional, Kawano, Noriaki, additional, Maeda, Kouichi, additional, Sato, Seiichi, additional, Ishizaki, Junzo, additional, Kawano, Hiroshi, additional, Kamiunten, Ayako, additional, Akizuki, Keiichi, additional, Tahira, Yuki, additional, Shimoda, Haruko, additional, Shide, Kotaro, additional, Hidaka, Tomonori, additional, Kitanaka, Akira, additional, Yamashita, Kiyoshi, additional, Matsuoka, Hitoshi, additional, and Shimoda, Kazuya, additional

Published
2017
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28. Differences in Hematological and Clinical Features Between Essential Thrombocythemia Cases With JAK2- or CALR-Mutations

Author

Kubuki, Yoko, primary, Shide, Kotaro, additional, Kameda, Takuro, additional, Yamaji, Takumi, additional, Sekine, Masaaki, additional, Kamiunten, Ayako, additional, Akizuki, Keiichi, additional, Shimoda, Haruko, additional, Tahira, Yuki, additional, Nakamura, Kenichi, additional, Abe, Hiroo, additional, Miike, Tadashi, additional, Iwakiri, Hisayoshi, additional, Tahara, Yoshihiro, additional, Sueta, Mitsue, additional, Hashimoto, Kanna, additional, Yamamoto, Shojiro, additional, Hasuike, Satoru, additional, Hidaka, Tomonori, additional, Nagata, Kenji, additional, Kitanaka, Akira, additional, and Shimoda, Kazuya, additional

Published
2017
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29. Physiological Expression of Calr Mutant Increases Cell Growth and Cytokine Independency in Human Cell Lines Expressing Mpl, and Develops Essential Thrombocythemia in Mice

Author

Shide, Kotaro, primary, Kameda, Takuro, additional, Sekine, Masaaki, additional, Kamiunten, Ayako, additional, Akizuki, Keiichi, additional, Tahira, Yuki, additional, Hidaka, Tomonori, additional, Kubuki, Yoko, additional, Honda, Arata, additional, Sawaguchi, Akira, additional, Kitanaka, Akira, additional, and Shimoda, Kazuya, additional

Published
2016
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30. TYK2 Is Essential for IFNα-Induced Resolution of MPN Features in a Murine Jak2V617F PMF Model

Author

Tahira, Yuki, Shide, Kotaro, Kameda, Takuro, Kamiunten, Ayako, Akizuki, Keiichi, Karasawa, Masayoshi, Ikeda, Ryoma, Matsumoto, Kengo, Kubuki, Yoko, and Shimoda, Kazuya

Abstract

Interferon (IFN)-α exhibits antiviral and antiproliferative effects on normal and neoplastic cells. It is an effective treatment option for myeloproliferative neoplasms (MPNs). The intracellular signaling of IFN-α is triggered by binding of IFN-α to its specific receptors on the cell surface, followed by the activation of tyrosine kinase-2 (TYK2) and Janus kinase-1 (JAK1), both of which are receptor-associated Janus kinases (JAKs). Activated JAKs activate many signaling molecules, including signal transducers and activators of transcription (STATs). Antiviral activity of IFN-α was abrogated in Stat1deficient-embryonic fibroblasts, however, Tyk2deficient-cells were resistant to viral infection in the presence of IFN-α, indicating the essential role of STAT1 for the antiviral activity of IFN-α, and TYK2 is not required for that. The antiproliferative effect is another major activity of IFN-α, however, the precise antiproliferative mechanism of IFN-α is not completely understood. We assessed the effect of ropeginterferon-α-2b, a monopegylated IFN-α-2b, on MPN model mice ( Jak2V617F mice), and investigated the role of TYK2 in the antiproliferative effect of IFN-α.

Published
2023
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31. Crystalglobulinemia with Fulminant Course with Cylinder-like Bodies on Peripheral Blood Smear

Author

Kawaguchi, Takeshi, primary, Kariya, Yumi, additional, Matsuda, Motohiro, additional, Kubo, Kazuyoshi, additional, Miyauchi, Syunichi, additional, Kusumoto, Norio, additional, Ueno, Shiro, additional, Takajo, Ichiro, additional, Nagatomo, Yasuhiro, additional, Tahira, Yuki, additional, Yamamoto, Syoko, additional, Yorita, Kenji, additional, Kataoka, Hiroaki, additional, and Okayama, Akihiko, additional

Published
2014
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32. Real-World Data on Clinical Features, Outcomes, and Prognostic Factors in Multiple Myeloma from Miyazaki Prefecture, Japan.

Author

Akizuki, Keiichi, Matsuoka, Hitoshi, Toyama, Takanori, Kamiunten, Ayako, Sekine, Masaaki, Shide, Kotaro, Kameda, Takuro, Kawano, Noriaki, Maeda, Kouichi, Takeuchi, Masanori, Kawano, Hiroshi, Sato, Seiichi, Ishizaki, Junzo, Tahira, Yuki, Shimoda, Haruko, Hidaka, Tomonori, Yamashita, Kiyoshi, Kubuki, Yoko, and Shimoda, Kazuya

Subjects
MULTIPLE myeloma, PROGNOSIS, STEM cell transplantation, DIAGNOSIS, MULTIVARIATE analysis, PLASMACYTOMA
Abstract

The prognosis of multiple myeloma (MM) has improved with the introduction of novel agents. These data are largely derived from clinical trials and might not reflect real-world patient outcomes accurately. We surveyed real-world data from 284 patients newly diagnosed with MM between 2010 and 2018 in Miyazaki Prefecture. The median follow-up period was 32.8 months. The median age at diagnosis was 71 years, with 68% of patients aged >65 years. The International Staging System (ISS) stage at diagnosis was I in 18.4% of patients, II in 34.1%, and III in 47.5%. Bortezomib-containing regimens were preferred as initial treatment; they were used in 147 patients (51.8%). In total, 80% of patients were treated with one or more novel agents (thalidomide, lenalidomide, or bortezomib). Among 228 patients who were treated with novel agents as an initial treatment, the overall response rate (partial response (PR) or better) to initial treatment was 78.4%, and the median time to next treatment (TTNT) was 11.6 months. In the multivariate analysis, PR or better responses to initial treatment were independently favorable prognostic factors for TTNT. The median survival time after initial therapy for patients with novel agents was 56.4 months and 3-year overall survival (OS) was 70.4%. In multivariate analysis, ISS stage I/II disease and PR or better response to initial treatment, and autologous stem cell transplantation (ASCT) were identified as independent prognostic factors for overall survival (OS). [ABSTRACT FROM AUTHOR]

Published
2021
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33. TET2Mutation Associated with Organ Infiltrations in ATLL

Author

Kameda, Takuro, Shide, Kotaro, Kamiunten, Ayako, Tahira, Yuki, Akizuki, Keiichi, Sekine, Masaaki, Hidaka, Tomonori, Kubuki, Yoko, Hidaka, Michihiro, Utsunomiya, Atae, Ohshima, Takayuki, Kataoka, Keisuke, Ogawa, Seishi, and Shimoda, Kazuya

Abstract

Introduction: Adult T-cell leukemia/lymphoma (ATLL) is a peripheral T-cell lymphoma that is caused by HTLV-1. The prognosis of acute and lymphomatous variants of ATLL is poor, ranging from 2 weeks to >1 year. Compared to other types of malignant lymphomas, the organ infiltration is frequently observed in ATLL (Yamada et al. Leuk Lymphoma 1997). We previously reported the landscape of genetic mutations in ATLL, and showed that various mutations occurred in the TCR-NFκB pathway in more than 90% of ATLL cases (Kataoka et al. Nat Genet 2015). These somatic mutations are thought to develop ATLL in combination with viral genes such as HTLV-1 bZIP factor (HBZ). Among them, mutations in TET2, an epigenetic regulator, was observed in about 10% of ATLL cases. Higher frequencies inTET2mutation was reported in other types of peripheral T-cell lymphoma (PTCL); it was observed in about 80% of angioimmunoblastic T-cell lymphoma (AITL) and in about 50% of PTCL, not otherwise specified. In PTCL, it has been reported that additional mutations in lymphoid progenitors derived from TET2mutated hematopoietic stem cells cause increased cell proliferation and anti-apoptosis, leading to the disease progression. In ATLL, the role of TET2mutation in disease progression is still unknown. In this study, we investigated the role of TET2mutation in ATLL using mouse model and acute and lymphomatous variant ATLL cohort.

Published
2018
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34. Haploinsufficiency of CALRConfers Hematopoietic Stem Cells (HSCs) with a Clonal Advantage over Wild-Type Cells, and, in Setting of Myeloproliferative Neoplasms, Compensates for the Functions of HSCs Impaired By the CalrMutation

Author

Shide, Kotaro, Kameda, Takuro, Kamiunten, Ayako, Sekine, Masaaki, Ozono, Yoshinori, Yokomizo, Takako, Akizuki, Keiichi, Tahira, Yuki, Kubuki, Yoko, Hidaka, Tomonori, Sashida, Goro, and Shimoda, Kazuya

Abstract

CALRexon9 frameshift mutations function as driver mutations in essential thrombocythemia (ET) and primary myelofibrosis patients with non-mutated JAK2or MPL. The mutations augment signal transducer and activator of transcription activity in the presence of MPL, induce increased cell proliferation and growth factor independence in cell lines, and cause ET-like myeloproliferative neoplasms (MPN) in mice.

Published
2018
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