論文 - 下田 和哉
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Akizuki K., Matsuoka H., Toyama T., Kamiunten A., Sekine M., Shide K., Kameda T., Kawano N., Maeda K., Takeuchi M., Kawano H., Sato S., Ishizaki J., Tahira Y., Shimoda H., Hidaka T., Yamashita K., Kubuki Y., Shimoda K.
Journal of Clinical Medicine 10 ( 1 ) 1 - 9 2021年1月
記述言語：英語 掲載種別：研究論文（学術雑誌） 出版者・発行元：Journal of Clinical Medicine
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).
DOI： 10.3390/jcm10010105
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Miike T., Kawakami H., Kameda T., Yamamoto S., Tahara Y., Hidaka T., Kubuki Y., Yorita K., Akiyama Y., Arimura Y., Kubota Y., Kataoka H., Shimoda K.
BMC Gastroenterology 20 ( 1 ) 298 2020年9月
記述言語：英語 掲載種別：研究論文（学術雑誌） 出版者・発行元：BMC Gastroenterology
Background: Adult T-cell leukemia/lymphoma (ATLL) is a peripheral T-cell malignancy caused by human T-cell leukemia virus type 1. The clinical course of ATLL is very heterogeneous, and many organs, including the gastrointestinal (GI) tract, can be involved. However, there are few detailed reports on ATLL infiltration in the GI tract. We investigated the clinical characteristics of ATLL infiltration in the GI tract. Methods: This retrospective observational single-center study included 40 consecutive ATLL patients who underwent GI endoscopy. The patients' demographic and clinical characteristics and endoscopic findings were analyzed retrospectively. Patients with ATLL who were diagnosed by histological examination were divided into two groups based on GI tract infiltration. Results: Multivariate analysis revealed that the absence of skin lesions was significantly associated with GI infiltration (P < 0.05). Furthermore, the infiltration group tended to have similar macroscopic lesions in the upper and lower GI tracts, such as diffuse type, tumor-forming type, and giant-fold type. Conclusions: GI endoscopy may be considered for ATLL patients without skin lesions.
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Uterine relapse of Philadelphia chromosome-negative acute lymphoblastic leukemia. 査読あり
Kawano N, Maeda T, Kawano S, Naghiro Y, Takami A, Tochigi T, Nakaike T, Yamashita K, Kodama T, Marutsuka K, Sugimoto Y, Imamura T, Mori Y, Ochiai H, Hidaka T, Shimoda K, Mashiba K, Kikuchi I
Journal of clinical and experimental hematopathology : JCEH 60 ( 3 ) 103 - 107 2020年9月
記述言語：英語 掲載種別：研究論文（学術雑誌） 出版者・発行元：日本リンパ網内系学会
The relapse of acute lymphoblastic leukemia (ALL) usually involves the bone marrow, with the central nervous system being the most frequent extramedullary site. The relapse of ALL in the female genital organs, particularly the uterus, is markedly rare. We report such a patient who developed relapse in the bone marrow and uterus. The uterine lesion, which presented as abnormal uterine bleeding, consisted of a mass on MRI and proliferation of ALL cells on histology. MRI revealed a heterogeneous high-intensity mass (T2-WI/D-WI) with a diameter of 6.8 cm, a notable decrease in the apparent diffusion coefficient (ADC), and mild enhancement by contrast enhancement study. Histological findings of the uterine cervix demonstrated the infiltration of ALL. The patient achieved remission by allogeneic haplo-identical hematopoietic stem-cell transplantation, but died of complications of the transplantation. This case suggested that attention should be paid to the uterus as a site of extramedullary relapse. In addition, abnormal uterine bleeding, which is a common sign of hormonal imbalance and hormone replacement therapy after chemotherapy, may be an initial sign of extramedullary recurrence. To confirm uterine relapse as an intractable disease, the accumulation of more cases is required.
DOI： 10.3960/jslrt.20016
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Fagnan A., Bagger F.O., Piqué-Borràs M.R., Ignacimouttou C., Caulier A., Lopez C.K., Robert E., Uzan B., Gelsi-Boyer V., Aid Z., Thirant C., Moll U., Tauchmann S., Kurtovic-Kozaric A., Maciejewski J., Dierks C., Spinelli O., Salmoiraghi S., Pabst T., Shimoda K., Deleuze V., Lapillonne H., Sweeney C., de Mas V., Leite B., Kadri Z., Malinge S., de Botton S., Micol J.B., Kile B., Carmichael C.L., Iacobucci I., Mullighan C.G., Carroll M., Valent P., Bernard O.A., Delabesse E., Vyas P., Birnbaum D., Anguita E., Garçon L., Soler E., Schwaller J., Mercher T.
Blood 136 ( 6 ) 698 - 714 2020年8月
記述言語：英語 掲載種別：研究論文（学術雑誌） 出版者・発行元：Blood
Acute erythroleukemia (AEL or acute myeloid leukemia [AML]-M6) is a rare but aggressive hematologic malignancy. Previous studies showed that AEL leukemic cells often carry complex karyotypes and mutations in known AML-associated oncogenes. To better define the underlying molecular mechanisms driving the erythroid phenotype, we studied a series of 33 AEL samples representing 3 genetic AEL subgroups including TP53-mutated, epigenetic regulator-mutated (eg, DNMT3A, TET2, or IDH2), and undefined cases with low mutational burden. We established an erythroid vs myeloid transcriptome-based space in which, independently of the molecular subgroup, the majority of the AEL samples exhibited a unique mapping different from both non-M6 AML and myelodysplastic syndrome samples. Notably, >25% of AEL patients, including in the genetically undefined subgroup, showed aberrant expression of key transcriptional regulators, including SKI, ERG, and ETO2. Ectopic expression of these factors in murine erythroid progenitors blocked in vitro erythroid differentiation and led to immortalization associated with decreased chromatin accessibility at GATA1-binding sites and functional interference with GATA1 activity. In vivo models showed development of lethal erythroid, mixed erythroid/myeloid, or other malignancies depending on the cell population in which AEL-associated alterations were expressed. Collectively, our data indicate that AEL is a molecularly heterogeneous disease with an erythroid identity that results in part from the aberrant activity of key erythroid transcription factors in hematopoietic stem or progenitor cells.
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Shide K., Kameda T., Kamiunten A., Ozono Y., Tahira Y., Yokomizo-Nakano T., Kubota S., Ono M., Ikeda K., Sekine M., Akizuki K., Nakamura K., Hidaka T., Kubuki Y., Iwakiri H., Hasuike S., Nagata K., Sashida G., Shimoda K.
Blood 136 ( 1 ) 106 - 118 2020年7月
記述言語：英語 掲載種別：研究論文（学術雑誌） 出版者・発行元：Blood
Mutations in JAK2, myeloproliferative leukemia virus (MPL), or calreticulin (CALR) occur in hematopoietic stem cells (HSCs) and are detected in more than 80% of patients with myeloproliferative neoplasms (MPNs). They are thought to play a driver role in MPN pathogenesis via autosomal activation of the JAK-STAT signaling cascade. Mutant CALR binds to MPL, activates downstream MPL signaling cascades, and induces essential thrombocythemia in mice. However, embryonic lethality of Calr-deficient mice precludes determination of a role for CALR in hematopoiesis. To clarify the role of CALR in normal hematopoiesis and MPN pathogenesis, we generated hematopoietic cell-specific Calr-deficient mice. CALR deficiency had little effect on the leukocyte count, hemoglobin levels, or platelet count in peripheral blood. However, Calr-deficient mice showed some hematopoietic properties of MPN, including decreased erythropoiesis and increased myeloid progenitor cells in the bone marrow and extramedullary hematopoiesis in the spleen. Transplantation experiments revealed that Calr haploinsufficiency promoted the self-renewal capacity of HSCs. We generated CALRdel52 mutant transgenic mice with Calr haploinsufficiency as a model that mimics human MPN patients and found that Calr haploinsufficiency restored the self-renewal capacity of HSCs damaged by CALR mutations. Only recipient mice transplanted with Lineage−Sca1+c-kit+ cells harboring both CALR mutation and Calr haploinsufficiency developed MPN in competitive conditions, showing that CALR haploinsufficiency was necessary for the onset of CALR-mutated MPNs. Key Points: • Calr deficiency induces reduction of erythropoiesis in the bone marrow and extramedullary hematopoiesis in the spleen. • CALR haploinsufficiency restores the self-renewal capacity of HSCs damaged by CALR del52 and is required for the development of MPN.
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Hirashima K., Muromoto R., Minoguchi H., Matsumoto T., Kitai Y., Kashiwakura J.i., Shimoda K., Oritani K., Matsuda T.
Cytokine 130 25 - 34 2020年3月
記述言語：英語 掲載種別：研究論文（学術雑誌） 出版者・発行元：Cytokine
© 2020 Elsevier Ltd Macrophages are highly plastic in their pro-inflammatory/anti-inflammatory roles. Type I and II interferons (IFNs) are known to modulate macrophage activation. Tyrosine kinase 2 (Tyk2) has an intimate relationship with type I and II IFN signaling. Animal studies have shown that Tyk2 knock-out (KO) in mice is associated with reduced inflammatory responses in various mouse models of diseases. To investigate the role of Tyk2 in inflammation in more detail, we intraperitoneally injected heat-killed Propionibacterium acnes (P. acnes) to Tyk2 KO mice. P. acnes–induced acute peritoneal inflammation, assessed by neutrophil infiltration, was reduced in Tyk2 KO mice. The reduction was accompanied with diminished productions of inflammatory cytokines and an enhanced production of anti-inflammatory IL-10. Unexpectedly, pre-treatment of wild-type mice with the neutralizing antibodies for IFNs did not affect P. acnes-induced neutrophil infiltration. A neutralizing antibody for the IL-10 receptor in Tyk2 KO mice restored P. acnes-induced peritoneal inflammation. Enhanced production of IL-10 from Tyk2 KO peritoneal cells was suppressed by either the cyclooxygenase inhibitor diclofenac or protein kinase A inhibitor H-89. The level of prostaglandin E2 (PGE2) in the steady-state peritoneal cavity in Tyk2 KO mice was higher than that in wild-type mice. Tyk2 KO macrophages showed an enhanced CREB phosphorylation induced by P. acnes plus PGE2. Taken together, these results showed that Tyk2 deficiency potentiates the PGE2-protein kinase A-IL-10 pathway in macrophages, and thereby contributes to potentiation of the immunosuppressive phenotype.
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Single Rectal Neuroendocrine Tumor Associated with Multiple Endocrine Cell Micronests 査読あり
Suzuki S., Kawakami H., Miike T., Yamamoto S., Abe H., Shimoda K., Ashizuka S., Inatsu H., Kubota Y., Ban T., Yorita K., Kataoka H.
Internal Medicine 59 ( 5 ) 619 - 623 2020年3月
記述言語：英語 掲載種別：研究論文（学術雑誌） 出版者・発行元：Internal Medicine
© 2020 Japanese Society of Internal Medicine. All rights reserved. Although a few reports of neuroendocrine tumor (NET) in the stomach or appendix with surrounding micronests have been published, cases of rectal NET are rare. We herein report a unique case of a patient with single rectal NET treated endoscopically. A pathological examination revealed multiple endocrine cell micronests (ECMs) in the submucosal layer around the main NET lesion. Neither lymph node metastasis nor distant metastasis in computed tomography was observed six years after the treatment. Because case reports of multiple ECM are very rare, the significance of malignancy is unclear. It therefore appears to be necessary to accumulate similar cases.
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Clinical significance of soluble CADM1 as a novel marker for adult T-cell leukemia/lymphoma. 査読あり
Nakahata S, Syahrul C, Nakatake A, Sakamoto K, Yoshihama M, Nishikata I, Ukai Y, Matsuura T, Kameda T, Shide K, Kubuki Y, Hidaka T, Kitanaka A, Ito A, Takemoto S, Nakano N, Saito M, Iwanaga M, Sagara Y, Mochida K, Amano M, Maeda K, Sueoka E, Okayama A, Utsunomiya A, Shimoda K, Watanabe T, Morishita K
Haematologica 106 ( 2 ) 532 - 542 2020年2月
記述言語：英語 掲載種別：研究論文（学術雑誌） 出版者・発行元：Haematologica
Adult T-cell leukemia/leukemia (ATLL) is an aggressive peripheral T-cell malignancy, caused by infection with the human T-cell leukemia virus type 1 (HTLV-1). We recently showed that the cell adhesion molecule 1 (CADM1), a member of the immunoglobulin superfamily, is specifically and consistently overexpressed in ATLL cells, and functions as a novel cell surface marker. In this study, we first show that a soluble form of CADM1 (sCADM1) is secreted from ATLL cells by mainly alternative splicing. After developing the Alpha linked immunosorbent assay (AlphaLISA) for sCADM1, we show that plasma sCADM1 concentrations gradually increased during disease progression from indolent to aggressive ATLL. Although other known biomarkers of tumor burden such as soluble interleukin-2 receptor α (sIL-2Rα) also increased with sCADM1 during ATLL progression, multivariate statistical analysis of biomarkers revealed that only plasma sCADM1 was selected as a specific biomarker for aggressive ATLL, suggesting that plasma sCADM1 may be a potential risk factor for aggressive ATLL. In addition, plasma sCADM1 is a useful marker for monitoring response to chemotherapy as well as for predicting relapse of ATLL. Furthermore, the change in sCADM1 concentration between indolent and aggressive type ATLL was more prominent than the change in the percentage of CD4+CADM1+ ATLL cells. As plasma sCADM1 values fell within normal ranges in HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP) patients with higher levels of serum sIL-2Rα, the measurement of sCADM1 may become a useful tool to discriminate between ATLL and other inflammatory diseases, including HAM/TSP.
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Ichikawa T., Shanab O., Nakahata S., Shimosaki S., Manachai N., Ono M., Iha H., Shimoda K., Morishita K.
Biochimica et Biophysica Acta - Molecular Cell Research 1867 ( 2 ) 118615 2020年2月
記述言語：英語 掲載種別：研究論文（学術雑誌） 出版者・発行元：Biochimica et Biophysica Acta - Molecular Cell Research
N-myc downstream-regulated gene 2 (NDRG2) as a tumor suppressor is frequently downregulated in human T-lymphotropic retrovirus (HTLV-1)-infected adult T-cell leukemia (ATL) and variety of cancers, and negatively regulates PI3K signaling pathways through dephosphorylation of PTEN with protein phosphatase 2A (PP2A). We recently identified that protein arginine methyltransferase 5 (PRMT5) is one of novel NDRG2 binding proteins and the knockdown of PRMT5 induces cell apoptosis with degradation of several signaling molecules. To investigate how the apoptosis is induced by the knockdown PRMT5 expression, heat shock protein 90 alpha (HSP90A) was identified as a binding protein for NDRG2 or PRMT5 by immunoprecipitation-mass analysis. NDRG2/PP2A complex inhibited arginine methyltransferase activity of PRMT5 through dephosphorylation at Serine 335 (S335); however, in NDRG2low ATL-related cells, highly phosphorylated PRMT5 at S335 was mainly localized in cytoplasm with binding to HSP90A, resulting in enhancing arginine-methylation at the middle domain (R345 and R386). Since knockdown of PRMT5 expression or forced expression of HSP90A with alanine replacement of R345 or R386 induced apoptosis with the degradation of client proteins in NDRG2low ATL-related and other cancer cells, we here identified that the novel arginine methylations of HSP90A are essential for maintenance of its function in NDRG2low ATL and other cancer cells.
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Akizuki K., Sekine M., Kogure Y., Kameda T., Shide K., Koya J., Kamiunten A., Kubuki Y., Tahira Y., Hidaka T., Kiwaki T., Tanaka H., Sato Y., Kataoka H., Kataoka K., Shimoda K.
BMC Cancer 20 ( 1 ) 5 2020年1月
記述言語：英語 掲載種別：研究論文（学術雑誌） 出版者・発行元：BMC Cancer
© 2019 The Author(s). Background: The occurrence of a mediastinal germ cell tumor (GCT) and hematological malignancy in the same patient is very rare. Due to its rarity, there have been only two reports of the concurrent cases undergoing detailed genetic analysis with whole-exome sequencing (WES), and the possible clonal relationship between the both tumors remained not fully elucidated. Methods: We performed whole-exome sequencing analysis of mediastinal GCT and acute myeloid leukemia (AML) samples obtained from one young Japanese male adult patient with concurrent both tumors, and investigated the possible clonal relationship between them. Results: Sixteen somatic mutations were detected in the mediastinal GCT sample and 18 somatic mutations in the AML sample. Mutations in nine genes, including TP53 and PTEN both known as tumor suppressor genes, were shared in both tumors. Conclusions: All in our case and in the previous two cases with concurrent mediastinal GCT and AML undergoing with whole-exome sequencing analysis, TP53 and PTEN mutations were commonly shared in both tumors. These data not only suggest that these tumors share a common founding clone, but also indicate that associated mediastinal GCT and AML harboring TP53 and PTEN mutations represent a unique biological entity.
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Ogasawara T., Kawauchi K., Ono T., Marshall S., Shide K., Shimoda K., Mori N., Sakura H.
Leukemia Research Reports 13 100194 2020年
記述言語：英語 掲載種別：研究論文（学術雑誌） 出版者・発行元：Leukemia Research Reports
© 2019 The Author(s) Essential thrombocythemia (ET) is an indolent myeloproliferative neoplasm (MPN) with a transformation to acute myeloid leukemia in <5% of patients. A 79-year-old man with JAK2V617F-positive ET exhibited leukocytosis with an increase in monoblastic cells, leading to a diagnosis of acute monoblastic and monocytic leukemia. Leukemic cells carried a TET2 mutation but not JAK2V617F mutation. We concluded that the TET2 mutation occurred in MPN-initiating cells and overcame JAK2-mutated cells. The absence of a JAK2 mutation in the leukemic cells in this case suggests the leukemia emerged from a JAK2-negative MPN cell clone carrying the TET2 mutation.
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Kai K., Hamada T., Hiyoshi M., Imamura N., Yano K., Nagano M., Kai M., Hidaka T., Shimoda K., Haruyama Y., Kataoka H., Nanashima A.
International Journal of Surgery Case Reports 76 19 - 24 2020年
記述言語：英語 掲載種別：研究論文（学術雑誌） 出版者・発行元：International Journal of Surgery Case Reports
Introduction: Gallbladder involvement in lymphoma is extremely rare, and only 68 cases have been reported in the English literature so far. We experienced a case of diffuse large B-cell lymphoma (DLBCL) of the gallbladder arising 8 years after DLBCL of the right testis. Presentation of case: A 68-year-old man underwent orchiectomy for malignant lymphoma of the right testis pathologically diagnosed as DLBCL 8 years ago. Systemic surveillance incidentally revealed a gallbladder tumour, and elective resection of the gallbladder bed of the liver was performed under a preoperative diagnosis of gallbladder cancer. The histopathological examination revealed DLBCL. At re-evaluation 3 months after surgery, he was diagnosed as having DLBCL involving the stomach. There had been no recurrence for 39 months after chemotherapy and radiation, but he suffered from a poor general condition due to protein-losing enteropathy and died of infection. Discussion: We compiled and analysed reported cases of malignant lymphomas involving the gallbladder in terms of background, symptoms, imaging findings, and prognosis. Compared to MALT lymphoma, DLBCL was significantly more involved in other organs simultaneously or heterochronously (p = 0.004). Conclusion: Gallbladder lymphoma should be added to the differential diagnosis of gallbladder tumours, especially when clinical findings are not consistent with the typical course of gallbladder carcinoma and cholecystitis.
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Clinical features and treatment outcomes of opportunistic infections among human T-lymphotrophic virus type 1 (HTLV-1) carriers and patients with adult T-cell leukemia-lymphoma (ATL) at a single institution from 2006 to 2016
NoriakiKawano,YuriNagahiro,_ShuroYoshida,_YoshihiroTahara,_DaisukeHimeji,_TakuroKuriyama,_TaroTochigi,_TakashiNakaike,_TomonoriShimokawa,_KiyoshiYamashita,_HidenobuOchiai,_KouskeMarutsuka,_KoichiMashiba,_KazuyaShimoda,_TakanoriTeshima,_Ikuo Kikuchi
Journal of clinical and experimental hematopathology 59 ( 4 ) 156 - 167 2019年12月
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Essential thrombocytosis attributed to JAK2-T875N germline mutation.
Makoto Yoshimitsu, Miho Hachiman, Yuichiro Uchida, Naosuke Arima, Akihiko Arai, Yuhei Kamada, Kotaro Shide, Masafumi Ito, Kazuya Shimoda, Kenji Ishitsuka
International journal of hematology. 110 ( 5 ) 584 - 590 2019年11月
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The regulation of NDRG2 expression during ATLL development after HTLV-1 infection. 査読あり
Ichikawa T., Nakahata S., Fujii M., Iha H., Shimoda K., Morishita K.
Biochimica et Biophysica Acta - Molecular Basis of Disease 1865 ( 10 ) 2633 - 2646 2019年10月
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Monocyte-derived fibrocytes elimination had little contribution on liver fibrosis 査読あり
Ozono Y., Shide K., Toyoshima F., Takaishi Y., Tsuchimochi M., Kamiunten A., Kameda T., Nakamura K., Miike T., Kusumoto K., Iwakiri H., Hasuike S., Nagata K., Sawaguchi A., Shimoda K.
Hepatobiliary and Pancreatic Diseases International 18 ( 4 ) 348 - 353 2019年8月
記述言語：英語 掲載種別：研究論文（学術雑誌） 出版者・発行元：Hepatobiliary and Pancreatic Diseases International
© 2019 First Affiliated Hospital, Zhejiang University School of Medicine in China Background: Monocyte-derived fibrocytes play an important role in the progression of fibrosis in the skin, lungs, heart and kidney. However, the contribution of fibrocytes to liver fibrosis is unclear. The aim of this study was to investigate whether fibrocytes contributed to fibrosis progression in the livers of carbon tetrachloride (CCl4)-treated mice. Methods: C57BL/6J mice were divided into 4 groups: normal control group, CCl4-treated group, CCl4 + control liposome-treated group, and CCl4 + clodronate liposome-treated group. For the elimination of systemic monocyte and monocyte-derived fibrocyte, one group was treated with clodronate liposome, and another group with control liposome as a control. After 4 weeks of treatment, hepatic mononuclear cells were subjected to immunofluorescent (IF) staining and fluorescence-activated cell sorter (FACS) analysis to detect fibrocytes. Measurement of collagen-positive Sirius red stained area and collagen-I mRNA expression in the liver were performed to evaluate the degree of liver fibrosis quantitatively. Results: In the liver of the CCl4-treated and CCl4 + control liposome-treated groups, the number of fibrocytes, the area positive for Sirius red staining and collagen-I mRNA expression significantly increased compared with those in the normal control group. In the liver of the CCl4 + clodronate liposome-treated group, few fibrocytes was observed as in the normal control group, but Sirius red staining positive area and collagen-I mRNA expression were increased and equivalent to the CCl4-treated and CCl4 + control liposome-treated groups. Conclusion: Monocyte-derived fibrocytes play a minimal role in CCl4-induced liver fibrosis. Cells other than fibrocytes such as hepatic stellate cells play a central role in liver fibrosis.
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A Case of Acute Liver Failure due to Severe Hepatic Metastasis of Small-cell Lung Cancer Producing Adrenocorticotropic Hormone Complicating Ectopic Cushing Syndrome. 査読あり
Sonoko Kamijo, Satoru Hasuike, Kenichi Nakamura, Yuuka Takaishi, Yuri Yamada, Yoshinori Ozono, Mai Tsuchimochi, Mitsue Sueta, Kazunori Kusumoto, Hisayoshi Iwakiri, Mayumi Akaki, Hiroyuki Tanaka, Hiroaki Kataoka, Kazuya Shimoda, Kenji Nagata:
International journal of hematology. 58 ( 20 ) 2977 - 2982 2019年6月
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Mice with Calr mutations homologous to human CALR mutations only exhibit mild thrombocytosis. 査読あり
Kotaro Shide, Takuro Kameda, Ayako Kamiunten, Asami Oji, Yoshinori Ozono, Masaaki Sekine, Arata Honda, Akira Kitanaka, Keiichi Akizuki, Yuki Tahira, Kenichi Nakamura, Tomonori Hidaka, Yoko Kubuki, Hiroo Abe, Tadashi Miike, Hisayoshi Iwakiri, Yoshihiro Tahara, Mitsue Sueta, Satoru Hasuike, Shojiro Yamamoto, Kenji Nagata, Masahito Ikawa & Kazuya Shimoda
Blood cancer journal 9 ( 4 ) 42 2019年5月
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Molecular heterogeneity in peripheral T-cell lymphoma, not otherwise specified revealed by comprehensive genetic profiling.
Yosaku Watatani, Yasuharu Sato, Hiroaki Miyoshi, Kana Sakamoto, Kenji Nishida, Yuka Gion, Yasunobu Nagata, Yuichi Shiraishi, Kenichi Chiba, Hiroko Tanaka, Lanying Zhao, Yotaro Ochi, Yasuhide Takeuchi, June Takeda, Hiroo Ueno, Yasunori Kogure, Yusuke Shiozawa, Nobuyuki Kakiuchi, Tetsuichi Yoshizato, Masahiro M. Nakagawa, Yasuhito Nanya, Kenichi Yoshida, Hideki Makishima, Masashi Sanada, Mamiko Sakata-Yanagimoto, Shigeru Chiba, Ryota Matsuoka, Masayuki Noguchi, Nobuhiro Hiramoto, Takayuki Ishikawa, Junichi Kitagawa, Nobuhiko Nakamura, Hisashi Tsurumi, Tatsuhiko Miyazaki, Yusuke Kito, Satoru Miyano, Kazuya Shimoda, Kengo Takeuchi, Koichi Ohshima, Tadashi Yoshino, Seishi Ogawa, Keisuke Kataoka:
Leukemia 33 ( 12 ) 2867 - 2883 2019年5月
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IκB-ζ Expression Requires Both TYK2/STAT3 Activity and IL-17–Regulated mRNA Stabilization.
Ryuta Muromoto, Keisuke Tawa, Yui Ohgakiuchi, Ami Sato, Yuka Saino, Koki Hirashima, Hiroya Minoguchi, Yuichi Kitai, Jun-ichi Kashiwakura, Kazuya Shimoda, Kenji Oritani and Tadashi Matsuda:
ImmunoHorizons. 3 ( 5 ) 172 - 185 2019年5月