Research Achievements - Other -

Clinical Practice of Treatment Switch in Transplant-eligible Patients with Multiple Myeloma: An Exploratory Retrospective Analysis

Ikeda Sho, Kobayashi Takahiro, Kitadate Akihiro, Yamashita Takaya, Watanabe Atsushi, Fujishima Naohito, Yoshioka Tomoko, Kume Masaaki, Kameoka Yoshihiro, Kitabayashi Atsushi, Kuroki Jun, Takahashi Naoto

Internal Medicine ( 一般社団法人 日本内科学会 )  advpub ( 0 )   2025

<p><b>Objective </b>In the real-world clinical setting of transplant-eligible patients with multiple myeloma (MM), a certain proportion of patients switch from induction therapy to other regimens because of insufficient response or adverse events. However, the prognostic benefits of these changes remain unclear. This retrospective study investigated the impact of pre-transplant induction therapy switches on the prognosis. </p><p><b>Methods </b>We analyzed the treatment course, patient background, risk classification, and post-transplantation event-free survival (EFS) of 35 patients who achieved partial response (PR) or better with triplet therapy and underwent autologous stem cell transplantation (ASCT) at our institution between January 2017 and July 2023. </p><p><b>Results </b>Induction therapy included VRd therapy in 11 patients and switching therapy in 20 patients (7 due to intolerance and 13 due to insufficient treatment effects). Among the 13 patients who switched treatment due to insufficient treatment effects, 10 showed an improved response, leading to a trend towards a better EFS. Nevertheless, high-risk chromosomal abnormalities, particularly t(4;14), were associated with a significantly poorer EFS, regardless of the treatment received. </p><p><b>Conclusion </b>Even with a response-guided induction treatment switch, maintaining long-term remission after ASCT in high-risk patients remains challenging. A careful risk assessment using fluorescence <i>in situ</i> hybridization or a genomic analysis may improve the prognosis of patients with MM in the future. </p>

DOI CiNii Research

Successful Salvage Therapy with Pomalidomide, Cyclophosphamide, and Dexamethasone for IgM Myeloma with t(11;14) and Dim CD38 Expression Refractory to Daratumumab, Lenalidomide, and Dexamethasone

Fujishima Takashi, Kobayashi Takahiro, Kobayashi Isuzu, Kitadate Akihiro, Kameoka Yoshihiro, Takahashi Naoto

Internal Medicine ( 一般社団法人 日本内科学会 )  advpub ( 0 ) 3020 - 3026   2025

<p>We herein present the case of a 73-year-old man with IgM multiple myeloma (IgM-MM) and t(11;14). The tumor cells showed a small lymphoplasmacytic morphology and dim expression of CD38 and CD138. The MYD 88^L265P mutation was found to be negative. After plasma exchange, bortezomib and dexamethasone treatments were refractory. Subsequent daratumumab, lenalidomide, and dexamethasone therapy failed to respond despite the standard therapy for non-IgM MM. Subsequently, pomalidomide, cyclophosphamide, and dexamethasone therapies demonstrated a good response, and a stringent complete response was therefore achieved. This case highlights the need for different treatment strategies for IgM-MM compared with non-IgM-MM because the biological features of IgM-MM and non-IgM-MM are different. </p>

DOI PubMed CiNii Research

Overexposure to venetoclax is associated with prolonged-duration of neutropenia during venetoclax and azacitidine therapy in Japanese patients with acute myeloid leukemia

Kobayashi Takahiro, Honami Sato, Miura Masatomo, Fukushi Yayoi, Kuroki Wataru, Ito Fumiko, Teshima Kazuaki, Watanabe Atsushi, Fujishima Naohito, Kobayashi Isuzu, Kameoka Yoshihiro, Takahashi Naoto

Cancer Chemotherapy and Pharmacology ( Springer Nature )    2024

CiNii Research

AMLのVEN/AZA治療におけるベネトクラクスの血中濃度と好中球減少症との関連

小林 敬宏, 佐藤 保奈実, 三浦 昌朋, 福司 弥生, 藤田 菜々子, 黒木 航, 伊藤 史子, 手島 和暁, 渡部 敦, 藤島 直仁, 高橋 直人

日本血液学会学術集会 ( (一社)日本血液学会 )  85回   377 - 377   2023.10

髄外病変はヒアルロン酸とCD44バリアントを介した骨髄腫細胞同士の凝集から発症する(Extramedullary diseases originate from hyaluronan-induced homophilic cell-cell interaction of CD44 variant-expressing myeloma cells)

菊池 次郎, 小玉 信之, 竹下 昌孝, 比島 智子, 池田 翔, 小林 敬宏, 黒田 芳明, 内山 倫宏, 長田 直希, ボーゲン・ビヤーネ, 安井 寛, 高橋 直人, 三輪 哲義, 古川 雄祐

International Journal of Myeloma ( (一社)日本骨髄腫学会 )  12 ( 3 ) 111 - 111   2022.05

Postmortem diagnosis of intravascular large B-cell lymphoma after atraumatic splenic rupture due to splenic infiltration

KUROKI Wataru, KOBAYASHI Takahiro, UMAKOSHI Michinobu, KITADATE Akihiro, IMAIZUMI Chihiro, SAITO Masaya, KOBAYASHI Isuzu, FUJISHIMA Masumi, FUJISHIMA Naohito, YOSHIOKA Tomoko, GOTO Akiteru, TAKAHASHI Naoto

Rinsho Ketsueki ( The Japanese Society of Hematology )  63 ( 6 ) 523 - 529   2022

<p>Atraumatic splenic rupture (ASR) is a rare but fatal complication of malignant lymphoma. However, only one case of intravascular large B-cell lymphoma (IVLBCL)-related ASR (IVLBCL-ASR) has previously been reported, and the mechanism of IVLBCL-ASR is unknown. We present the case of a 78-year-old man who died unexpectedly and was diagnosed with IVLBCL-ASR pathologically by autopsy. A massive intraperitoneal hemorrhage and four lacerations on the splenic surface were discovered during the autopsy. CD20-positive lymphoma cells that infiltrated into small vessels were highly concentrated in the center of the spleen and were only slightly distributed in the lacerations on the splenic surface. Therefore, increased intrasplenic pressure due to lymphoma cell proliferation was identified as the cause of ASR. The patient had undergone ¹⁸F-fluorodeoxyglucose positron emission tomography/computed tomography (¹⁸F-FDG PET/CT) for tongue cancer evaluation 3 months earlier, and positive uptake was found in the right adrenal gland, where lymphoma cell infiltration was confirmed by the autopsy. Our findings suggest that clinicians should be aware that the advanced stage of IVLBCL can cause fatal ASR via increased intrasplenic pressure. Therefore, early diagnosis and early treatment intervention are desirable to prevent the onset of IVLBCL-ASR, and ¹⁸F-FDG PET/CT is useful for the early diagnosis of IVLBCL.</p>

DOI PubMed CiNii Research

髄外疾患はヒアルロナン誘導同種親和性骨髄腫細胞-細胞相互作用に由来する【JST・京大機械翻訳】|||

菊池次郎, 小玉信之, 小玉信之, 竹下昌孝, 竹下昌孝, 比島智子, 比島智子, 池田翔, 小林敬宏, 黒田芳明, 内山倫宏, 長田直希, 小山大輔, BOGEN Bjarne, 安井寛, 高橋直人, 三輪哲義, 三輪哲義

日本血液学会学術集会抄録(Web) ( (一社)日本血液学会 )  83rd ( 2 ) OS2 - 1   2021

J-GLOBAL

Durable remission attained with rituximab therapy in a patient with acquired von Willebrand syndrome associated with CD20-positive lymphoproliferative disorder

KURAHASHI Honami, KAWABATA Yoshinari, MICHISHITA Yoshihiro, KITABAYASHI Atsushi, KOBAYASHI Takahiro, KITADATE Akihiro, TAKAHASHI Naoto

Rinsho Ketsueki ( The Japanese Society of Hematology )  59 ( 4 ) 420 - 425   2018

<p>A 61-year-old female with no history of bleeding was admitted to our hospital owing to persistent bleeding after the left knee joint injection and activated partial thromboplastin time prolongation. Subsequent coagulation tests revealed a critically declined level of the von Willebrand factor (VWF) antigen (<10%) and activity (<10%) measurement besides a significantly declined factor VIII activity (4%). Despite diagnosing her with acquired von Willebrand syndrome (AvWS) and managing her bleeding with desmopressin acetate hydrate (DDAVP), we could not precisely make a definitive diagnosis the underlying disorder. More than 15 months after the onset of AvWS, CD20-positive atypical lymphocytes appeared in the peripheral blood and bone marrow without systemic lymphadenopathy. We initiated rituximab monotherapy eight times a week for CD20-positive lymphoproliferative disorders. The treatment not only caused the disappearance of the clonal expansion of CD20-positive atypical lymphocytes in both peripheral blood and bone marrow but also exhibited the clinical remission of AvWS. In addition, the maintenance therapy with rituximab every 3 months resulted in the durable remission of over 5 years. AvWS is a rare bleeding disorder, similar to von Willebrand disease, which arises from various underlying diseases. Our experience with this case highlights that rituximab proved to be one of the effective and well-tolerated treatment options for AvWS associated with CD20-positive B-cell lymphoproliferative disorders.</p>

DOI CiNii Research