Tomomitsu Miyagaki

The University of Tokyo, Tōkyō, Japan

Are you Tomomitsu Miyagaki?

Claim your profile

Publications (72)323.22 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: Interleukin (IL)-21 is regarded as a potent antitumor agent, which increases the cytotoxicity of both natural killer (NK) and CD8+ T cells. In this study, we investigated the role of IL-21 in mycosis fungoides (MF). IL-21 mRNA expression levels in patch and plaque MF were significantly higher than those in normal skin. IL-21 mRNA expression levels in tumor MF were significantly decreased compared with those in patch and plaque MF. Interestingly, mRNA expression levels of IL-21 in MF lesional skin significantly correlated with those of T-helper type-1 cytokines/chemokines such as CXCL10, CXCL11 and γ-interferon. Immunohistochemistry showed that IL-21 was expressed by keratinocytes in patch and plaque MF. Furthermore, serum IL-21 levels in patients with tumor MF were significantly lower than those of healthy controls and plaque MF. Thus, IL-21 expression was significantly downregulated in skin and blood of patients with tumor MF, which may contribute to progression of MF. Our study suggests that recombinant IL-21 would be a promising therapy for MF.
    No preview · Article · Jan 2016 · The Journal of Dermatology
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: We recently demonstrated that upregulation of a chemokine receptor CCR6 and its ligand CCL20 led to metastasis of advanced cutaneous T-cell lymphoma (CTCL) cells, suggesting the involvement of CCL20-CCR6 interaction in initiating CTCL cell metastasis. In this study, we determined whether this interaction is functional in metastatic CTCL cells. We first demonstrated increased STAT3 expression during the progression of primary CTCL. STAT3 was spontaneously activated and mediated the transcription of CCL20 in CTCL cell lines. Next, to determine whether the transient knockdown of STAT3, CCL20, or CCR6 or treatment with newtralizing antibody against CCL20 (neutralizing CCL20 antibody) could reduce the migration ability of CTCL cells, we conducted an in vitro migration assay. All treatments reduced the nutrition-dependent migration activity of CTCL cells. Notably, treatment with neutralizing CCL20 antibody reduced the migration ability of the cells without decreasing the expression of CCL20 and CCR6. This demonstrated that the CCL20-CCR6 interaction is actually functional in metastatic CTCL cells. Finally, to examine the in vivo effect of neutralizing CCL20 antibody, we used NOD/Shi-scid IL-2γnul mice inoculated with CTCL cells. These mice were expected to die due to metastasis of CTCL cells into multiple organs. However, administration of neutralizing CCL20 antibody significantly prolonged the survival of the xenografted mice. These findings suggested that automatic activation of the STAT3/CCL20/CCR6 cascade was involved in CTCL lymphomagenesis and that disruption of CCL20-CCR6 interaction could be a key therapeutic strategy against advanced CTCL.
    Full-text · Article · Jan 2016 · Oncotarget
  • [Show abstract] [Hide abstract]
    ABSTRACT: Systemic sclerosis (SSc) is a chronic autoimmune inflammatory disease characterized by extensive tissue fibrosis and various vascular complications. A wealth of evidence suggests the substantial contribution of pro-inflammatory cytokines to the development of SSc, but the role of interleukin (IL)-18 signaling in this disease still remains elusive. To address this issue, we herein determined serum levels of IL-18-binding protein isoform a (IL-18BPa), a soluble decoy receptor for IL-18, by enzyme-linked immunosorbent assay in 57 SSc patients and 20 healthy controls and evaluated their clinical correlation. Serum IL-18BPa levels were higher in SSc patients than in healthy controls, while comparable between diffuse cutaneous SSc and limited cutaneous SSc patients. Although serum IL-18BPa levels were not associated with dermal and pulmonary fibrotic parameters in SSc patients, there was a significant positive correlation between serum IL-18BPa levels and right ventricular systolic pressure estimated by echocardiography. Furthermore, in 24 SSc patients who underwent right heart catheterization, serum IL-18BPa levels positively correlated with mean pulmonary arterial pressure. As for systemic inflammatory markers, significant positive correlations of circulating IL-18BPa levels with erythrocyte sedimentation rate and C-reactive protein were noted. These results suggest that the inhibition of IL-18 signaling by IL-18BPa may be involved in the development of pulmonary vascular involvement leading to pulmonary hypertension and modulate the systemic inflammation in SSc.
    No preview · Article · Jan 2016 · The Journal of Dermatology
  • [Show abstract] [Hide abstract]
    ABSTRACT: Cathepsin L (CTSL) is a lysosomal proteolytic enzyme involved in inflammation and vascular and extracellular matrix remodeling, which are the three cardinal pathological events associated with systemic sclerosis (SSc). To elucidate the potential role of CTSL in the development of SSc, we here investigated CTSL expression in the lesional skin of SSc patients and SSc animal models and the clinical correlation of serum CTSL levels. CTSL expression was elevated in dermal small vessels of SSc patients compared with those of healthy controls. Consistently, CTSL mRNA levels were increased in SSc lesional skin samples, but not in cultivated SSc dermal fibroblasts, compared with corresponding control samples from healthy individuals. Serum CTSL levels were significantly higher in SSc patients than in healthy controls and inversely correlated with skin score. Furthermore, the elevation of serum CTSL levels was linked to SSc vasculopathy. Supporting these results, Ctsl mRNA levels were decreased in the skin of bleomycin-treated mice, an SSc animal model recapitulating its fibrotic aspect, and CTSL expression was enhanced in dermal small vessels of endothelial cell-specific Fli1 knockout mice, reminiscent of SSc vasculopathy. Importantly, gene silencing of FLI1 induced CTSL mRNA expression and Fli1 occupied the CTSL promoter in human dermal microvascular endothelial cells. Collectively, these results suggest that endothelial CTSL up-regulation partially due to Fli1 deficiency may contribute to the development of vasculopathy, while the decrease in dermal CTSL expression is likely associated with dermal fibrosis in SSc. This article is protected by copyright. All rights reserved.
    No preview · Article · Dec 2015 · Experimental Dermatology
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Multiple sequential genetic and epigenetic alterations underlie cancer development and progression. Overcoming cellular senescence is an early step in cancer pathogenesis. Here, we demonstrate that a noncoding regulatory RNA, microRNA-16 (miR-16), has the potential to induce cellular senescence. First, we examined the expression of miR-16 in primary cutaneous T-cell lymphoma (CTCL) and other non-Hodgkin T/natural killer (NK)-cell lymphomas and found that miR-16 was downregulated than that in the corresponding normal cells. Notably, miR-16 expression was reduced as the primary CTCL progressed from the early stage to the advanced stage. Next, we transduced CTCL cells with miR-16 to examine whether this miRNA exhibited tumor-suppressive effects in CTCL cells. In CTCL cells expressing wild-type p53, forced expression of miR-16 enhanced p21 expression via downregulation of the polycomb group protein Bmi1, thereby inducing cellular senescence. Alternatively, in CTCL cells lacking functional p53, miR-16 induced compensatory apoptosis. The miR-16 transfection significantly decreased senescent cells and increased apoptotic cells in p21-knockdown CTCL cells expressing wild-type p53, suggesting that the presence or absence of p21 may be the most important condition in the senescence-apoptosis switch in CTCL lymphomagenesis. Furthermore, we found that the histone deacetylase inhibitor suberoylanilide hydroxamic acid (SAHA) restored the expression of miR-16 and its essential targets, induced senescence in CTCL cells expressing wild-type p53 and promoted apoptosis in cells with nonfunctional p53. Moreover, we found that other T/NK-cell lymphoma cell lines showed similar tumor-suppressive effects in response to miR-16 and SAHA and that these effects were dependent on p53 status. These results suggested that epigenetic silencing of miR-16 may be a key step during lymphoma development. Elucidation of the essential targets of miR-16 and SAHA provides a basis for the clinical application of SAHA in the treatment of CTCL and other non-Hodgkin T/NK-cell lymphomas.Oncogene advance online publication, 7 December 2015; doi:10.1038/onc.2015.435.
    Full-text · Article · Dec 2015 · Oncogene
  • [Show abstract] [Hide abstract]
    ABSTRACT: Some patients with cutaneous T-cell lymphoma (CTCL) show a miserable clinical course and the only option that can induce long-term remission for advanced CTCL may be hematopoietic stem cell transplantation (HSCT). So far, studies on HSCT for CTCL patients have been limited. In this study, we summarized 11 cases with CTCL treated with HSCT, including nine cases in Japan and two cases in Brazil. The patients were five cases with mycosis fungoides (MF), two cases with Sézary syndrome (SS), three cases with anaplastic large cell lymphoma, and one case with primary cutaneous peripheral T-cell lymphoma, not otherwise specified (PTL-NOS). Currently, seven out of 11 cases are alive (at 13-108 months after transplantation) and four died at 15 days to 14 months after transplantation. When focusing on the eight patients who received allogeneic HSCT for MF/SS and PTL-NOS, all four patients at 45 years old or under are alive at present. One case showed relapse in the skin. On the other hand, one out of the other four patients at over 45 years old survived. Engraftment failure was seen in one case and all the other three cases experienced relapse. Although this is only a case series with a small number, our study has suggested that we should be careful about age when treating patients with MF/SS by allogeneic HSCT.
    No preview · Article · Nov 2015 · The Journal of Dermatology
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Purpose: Advanced-stage mycosis fungoides (MF; stage IIB to IV) and Sézary syndrome (SS) are aggressive lymphomas with a median survival of 1 to 5 years. Clinical management is stage based; however, there is wide range of outcome within stages. Published prognostic studies in MF/SS have been single-center trials. Because of the rarity of MF/SS, only a large collaboration would power a study to identify independent prognostic markers. Patients and methods: Literature review identified the following 10 candidate markers: stage, age, sex, cutaneous histologic features of folliculotropism, CD30 positivity, proliferation index, large-cell transformation, WBC/lymphocyte count, serum lactate dehydrogenase, and identical T-cell clone in blood and skin. Data were collected at specialist centers on patients diagnosed with advanced-stage MF/SS from 2007. Each parameter recorded at diagnosis was tested against overall survival (OS). Results: Staging data on 1,275 patients with advanced MF/SS from 29 international sites were included for survival analysis. The median OS was 63 months, with 2- and 5-year survival rates of 77% and 52%, respectively. The median OS for patients with stage IIB disease was 68 months, but patients diagnosed with stage III disease had slightly improved survival compared with patients with stage IIB, although patients diagnosed with stage IV disease had significantly worse survival (48 months for stage IVA and 33 months for stage IVB). Of the 10 variables tested, four (stage IV, age > 60 years, large-cell transformation, and increased lactate dehydrogenase) were independent prognostic markers for a worse survival. Combining these four factors in a prognostic index model identified the following three risk groups across stages with significantly different 5-year survival rates: low risk (68%), intermediate risk (44%), and high risk (28%). Conclusion: To our knowledge, this study includes the largest cohort of patients with advanced-stage MF/SS and identifies markers with independent prognostic value, which, used together in a prognostic index, may be useful to stratify advanced-stage patients.
    Full-text · Article · Oct 2015 · Journal of Clinical Oncology
  • [Show abstract] [Hide abstract]
    ABSTRACT: Background Endothelial protein C receptor (EPCR) predominantly expressed on endothelial cells plays a critical role in the regulation of coagulation system and also mediates various cytoprotective effects by binding and activating protein C. So far, the role of EPCR has not been studied in systemic sclerosis (SSc).Objectives To investigate the potential contribution of EPCR to the development of SSc.MethodsEPCR expression was examined in skin samples and cultivated dermal microvascular endothelial cells by immunostaining, immunoblotting, and/or quantitative reverse transcription PCR. Fli1 binding to the EPCR promoter was assessed by chromatin immunoprecipitation. Serum EPCR levels were determined by enzyme-linked immunosorbent assay in 65 SSc and 20 healthy subjects.ResultsEPCR expression was decreased in dermal small vessels of SSc lesional skin compared with those of healthy control skin. Transcription factor Fli1, whose deficiency is implicated in SSc vasculopathy, occupied the EPCR promoter and EPCR expression was suppressed in Fli1 siRNA-treated endothelial cells and dermal small vessels of Fli1+/- mice. In SSc patients, decreased serum EPCR levels were associated with diffuse skin involvement, interstitial lung disease and digital ulcers. Furthermore, serum EPCR levels inversely correlated with plasma levels of plasmin-α2-plasmin inhibitor complex (PIC). Importantly, bosentan significantly reversed circulating EPCR and PIC levels in SSc patients and the expression of Fli1 and EPCR in dermal small vessels was elevated in patients treated with bosentan compared to untreated patients.Conclusions Endothelial EPCR down-regulation due to Fli1 deficiency may contribute to hyper-coagulation status leading to tissue fibrosis and impaired peripheral circulation in SSc.This article is protected by copyright. All rights reserved.
    No preview · Article · Sep 2015 · British Journal of Dermatology
  • [Show abstract] [Hide abstract]
    ABSTRACT: We report a 39-year-old man referred to our facility with linear sclerotic lesions along the several Blaschko's lines of the scalp. A year before the referral, he had had an episode of brain hemorrhage, although there was no evidence of vascular malformation or any other risk factors of brain hemorrhage for his young age. On the diagnosis of scleroderma en coup de sabre, prednisolone intake was initiated, and the skin lesions were well controlled. However, in the course of our follow up, he had another episode of brain hemorrhage, again without any evidence of cerebral vascular abnormalities. Organic intracranial abnormalities in this disease are well-documented, but there have been few reports on comorbid recurrent brain hemorrhages. We herein discuss the possible relationship of the skin lesions with the brain hemorrhages in our case, taking notice of the implication of developmental abnormalities behind these apparently independent phenomena inside and outside the cranium. © 2015 Japanese Dermatological Association.
    No preview · Article · Jul 2015 · The Journal of Dermatology
  • [Show abstract] [Hide abstract]
    ABSTRACT: Interleukin (IL)-33 is a recently identified cytokine, which is a member of the IL-1 family and binds to a heterodimeric receptor comprising ST2 (suppression of tumorigenicity 2) and IL-1 receptor accessory protein. Serum levels of IL-33 have been reported to be upregulated in various T helper (Th)1/Th17-mediated diseases, such as rheumatoid arthritis and inflammatory bowel disease. IL-33 expression is increased in lesional skin in patients with psoriasis, but serum levels in patients with psoriasis have not yet been studied. To study serum IL-33 levels in patients with psoriasis, a Th1/Th17-mediated skin disease, before and after anti-tumour necrosis factor (TNF)-α therapy. Serum IL-33 levels were measured in patients with psoriasis vulgaris (PV), psoriatic arthritis (PsA) or pustular psoriasis (PP), and compared with those of healthy controls. Associations between serum IL-33 levels and serum TNF-α, IL-6, vascular endothelial growth factor and C-reactive protein levels were also studied. In addition, the effect of IL-33 stimulation on IL-6, IL-8, TNF-α and VEGF secretion by human keratinocyte was analysed. Serum IL-33 levels in patients with PV, PsA and PP were significantly higher than those in healthy controls. Serum IL-33 levels correlated with serum TNF-α levels in patients with psoriasis, and decreased after anti-TNF-α therapy. IL-33 stimulated IL-6 and IL-8 secretion by human keratinocytes. These results suggest that serum IL-33 levels generally reflect increased inflammation in patients with psoriasis. © 2015 British Association of Dermatologists.
    No preview · Article · May 2015 · Clinical and Experimental Dermatology
  • [Show abstract] [Hide abstract]
    ABSTRACT: Cutaneous apocrine carcinoma (CAC) is a rare malignancy. It develops predominantly in the regions where apocrine glands are distributed. Some cases of CAC have been reported in the axilla and the inguinal regions, but only a few in the scrotum. We herein report a case of CAC which widely spread over both sides of the whole scrotum with plate-like hard induration, and such a manifestation has never been reported before. CAC is known to have high rates of local recurrence or metastasis, and the efficacy of radiotherapy or chemotherapy has not been established. As therapeutic options for CAC are limited, it is critical to reach the diagnosis and treat at an early stage. © 2015 Japanese Dermatological Association.
    No preview · Article · May 2015 · The Journal of Dermatology
  • Source
    Tomomitsu Miyagaki · Manabu Fujimoto · Shinichi Sato
    [Show abstract] [Hide abstract]
    ABSTRACT: B cells have been generally considered to be positive regulators of immune responses because of their ability to produce antigen-specific antibodies and to activate T cells through antigen presentation. Impairment of B cell development and function may cause inflammatory and autoimmune diseases. Recently, specific B cell subsets that can negatively regulate immune responses have been described in mouse models of a wide variety of inflammatory and autoimmune diseases. The concept of those B cells, termed regulatory B cells, is now recognized as important in the murine immune system. Among several regulatory B cell subsets, IL-10-producing regulatory B cells are the most widely investigated. On the basis of discoveries from studies of such mice, human regulatory B cells that produce IL-10 in most cases are becoming an active area of research. There have been emerging data suggesting the importance of human regulatory B cells in various diseases. Revealing the immune regulation mechanisms of human regulatory B cells in human inflammatory and autoimmune diseases could lead to the development of novel B cell targeted therapies. This review highlights the current knowledge on regulatory B cells, mainly IL-10-producing regulatory B cells, in animal models of inflammatory and autoimmune diseases and in clinical research using human samples. © The Japanese Society for Immunology. 2015. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.
    Preview · Article · May 2015 · International Immunology

  • No preview · Conference Paper · May 2015
  • [Show abstract] [Hide abstract]
    ABSTRACT: Galectin-9 is a member of the galectin family that has a wide spectrum of biological functions. Among them, galectin-9 has been known mainly as a potent chemoattractant for eosinophils. In addition, galectin-9 alters the T-cell balance by negatively regulating T-helper (Th)1 and Th17 cells, resulting in Th2 polarization. Atopic dermatitis (AD) is a skin allergic disease characterized by peripheral eosinophilia, mast cell activation and predominance of Th2 cells. To investigate possible roles of galectin-9 in AD, we measured serum galectin-9 levels in AD patients and investigated galectin-9 expression in lesional skin by immunohistochemistry. Serum galectin-9 levels in patients with AD were significantly higher than those in healthy controls and correlated with the Eczema Area and Severity Index. Serum galectin-9 levels were decreased after treatment, accompanied by improvement of skin lesions. Immunohistochemical study revealed that galectin-9 was expressed on epidermal keratinocytes and mast cells in lesional skin of AD. Our results suggest that elevated galectin-9 expression is associated with progression of AD and that galectin-9 could be a therapeutic target in AD. © 2015 Japanese Dermatological Association.
    No preview · Article · Apr 2015 · The Journal of Dermatology
  • [Show abstract] [Hide abstract]
    ABSTRACT: CCR4 is expressed on tumor cells of mycosis fungoides (MF) and Sézary syndrome (SS). In MF, most infiltrating cells in patches and plaques express CXCR3, while tumor cells express CCR4 in advanced stages. Poteligeo Test IHC (CCR4 staining kit) is a newly developed staining kit that can examine the presence of CCR4 expressed on tumor cells of adult T-cell leukemia/lymphoma, peripheral T-cell lymphoma and cutaneous T-cell lymphoma before treatment of anti-CCR4 antibody using paraffin-embedded samples. In this study, we analyzed CCR4 expression in lesional skin of MF, SS, atopic dermatitis (AD) and psoriasis with this new kit. CCR4 was expressed on infiltrating cells in lesional skin of patch, plaque, tumor MF and SS, and the number of positive cells increased as the disease progressed. Immunohistochemistry with frozen sections also showed some positive cells scattered in the dermis, although the quality was not high enough to quantify positive cells. There were significant positive correlations between CCR4(+) cells and serum lactate dehydrogenase levels. Interestingly, CCR4(+) cells were also detected in AD skin, whose number was larger than that in psoriatic skin. Previous studies showed only scattered CCR4(+) cells in skin samples by standard immunohistochemical staining. The new, sensitive CCR4 staining kit has revealed that CCR4 is expressed on infiltrating cells in lesional skin of early MF and AD as well as advanced MF and SS. These cells can be therapeutic targets for patients who are resistant to standard treatments. © 2015 Japanese Dermatological Association.
    No preview · Article · Mar 2015 · The Journal of Dermatology
  • Tomomitsu Miyagaki · Makoto Sugaya
    [Show abstract] [Hide abstract]
    ABSTRACT: Atopic dermatitis (AD) and psoriasis are common inflammatory skin diseases. Although clinical pictures of these two diseases are quite different, they share some common pathological backgrounds such as barrier dysfunction and enhanced IL-22 expression. To explain the clinical differences of the diseases, it has been proposed that Th2/Th22-polarized immune status together with an attenuated Th17 axis may cause insufficient induction of antimicrobial peptides and more severe barrier dysfunction in AD. While skin barrier dysfunction is commonly seen in AD and psoriasis, a Th2-dominant cytokine milieu down-regulates immunity against infections, which are commonly seen in lesional skin of AD. In the era of biologics, increase in the understanding or new discoveries of molecules involved in the development of various diseases will instantly lead to a new therapeutic strategy. In this review, we give an overview of recent advances in AD and psoriasis, especially on genetic background, barrier function, and therapeutic targets. Copyright © 2015 Japanese Society for Investigative Dermatology. Published by Elsevier Ireland Ltd. All rights reserved.
    No preview · Article · Feb 2015 · Journal of Dermatological Science
  • T Miyagaki · M Sugaya · T Oka · H Fujita · S Sato
    [Show abstract] [Hide abstract]
    ABSTRACT: Vorinostat is the first histone deacetylase inhibitor approved for cutaneous T cell lymphoma (CTCL).(1) Although in vitro effects of this drug on various types of cells have been studied,(2-5) little is known about how this drug has clinical effects on CTCL patients. As many chemokines are reported to reflect disease activity of CTCL, suggesting their important roles in disease progression,(6) we investigated variation of serum chemokine levels during oral vorinostat therapy in a Sézary syndrome (SS) patient. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    No preview · Article · Feb 2015 · British Journal of Dermatology

  • No preview · Article · Nov 2014 · The Journal of Dermatology
  • [Show abstract] [Hide abstract]
    ABSTRACT: Early cutaneous T cell lymphoma clinically and histologically resembles benign inflammatory skin diseases, which sometimes makes it difficult to reach a correct diagnosis. It is recently reported that thymocyte selection-associated high mobility group box factor (TOX) serves as a molecular marker for histological diagnosis of early-stage mycosis fungoides (MF). To examine whether TOX could be a marker of tumour cells in different types of cutaneous lymphoma, we investigated immunohistochemical staining for TOX with the lesional skin of patch, plaque, and tumour MF, Sézary syndrome (SS), lymphomatoid papulosis (LyP), primary cutaneous anaplastic large cell lymphoma (PCALCL), adult T cell leukemia/lymphoma (ATLL), peripheral T-cell lymphoma, not otherwise specified (PTCL, NOS), atopic dermatitis (AD), and normal skin. TOX and CCR4 messenger RNA (mRNA) levels in lesional skin of MF/SS were also examined. Immunohistological staining showed that a high specific nuclear staining of TOX was observed at a high frequency in MF, SS, and PTCL, NOS. Tumour cells in LyP, PCALCL, and ATLL showed a slightly dim nuclear staining of TOX. TOX(+) cells in MF and LyP expressed surface molecules characteristics of tumour cells in these diseases. Lesional skin of SS expressed higher levels of TOX mRNA, compared to normal skin or MF lesional skin. Moreover, TOX expression significantly correlated with CCR4 expression. TOX may be a specific marker for tumour cells in some types of cutaneous lymphoma.
    No preview · Article · Sep 2014 · Archives for Dermatological Research
  • [Show abstract] [Hide abstract]
    ABSTRACT: Dear Editor,Paraneoplastic pemphigus (PNP) is a rare autoimmune mucocutaneous disorder which is predominantly associated with lymphoproliferative disorders including non-Hodgkin lymphoma, B-chronic lymphocytic leukemia, Castleman disease, and Waldenström macroglobulinemia [1]. PNP is characterized by painful mucosal erosion with frequent skin eruption, histological changes of acantholysis or lichenoid/interface dermatitis, and serum autoantibodies against plakin family proteins [2, 3]. Although the cause of PNP is not identified in most cases, previous literatures have indicated that PNP may be triggered by specific treatment modalities for lymphoid neoplasms. Patients with lymphoid malignancies were recurrently affected by PNP within several cycles of fludarabine-containing therapy [4–7] or after local radiotherapy [8–10]. Here, we describe the first case of PNP occurring after bendamustine and rituximab therapy for follicular lymphoma.A 77-year-old Japanese woman was diagnosed with f ...
    No preview · Article · Sep 2014 · Annals of Hematology

Publication Stats

526 Citations
323.22 Total Impact Points

Institutions

  • 2008-2015
    • The University of Tokyo
      • Department of Surgical Sciences
      Tōkyō, Japan
  • 2012
    • Duke University
      Durham, North Carolina, United States
  • 2011
    • National Center for Global Health and Medicine in Japan
      Edo, Tōkyō, Japan
  • 2010
    • Tokyo University and Graduate School of Social Welfare
      Edo, Tōkyō, Japan