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[Rinsho ketsueki] The Japanese journal of clinical hematology最新文献

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[Veno-venous extracorporeal membrane oxygenation for capillary leak syndrome during induction chemotherapy in acute myeloid leukemia]. [静脉-静脉体外膜氧合治疗急性髓性白血病诱导化疗期间的毛细血管渗漏综合征]。
[Rinsho ketsueki] The Japanese journal of clinical hematology Pub Date : 2024-01-01 DOI: 10.11406/rinketsu.65.169
Tadashi Okamura, Shogo Murata, Kyohei Miyamoto, Misato Tane, Yuka Okabe, Satomi Takeda, Shotaro Tabata, Hideki Kosako, Yoshikazu Hori, Yusuke Yamashita, Toshiki Mushino, Hiroki Hosoi, Takashi Sonoki
{"title":"[Veno-venous extracorporeal membrane oxygenation for capillary leak syndrome during induction chemotherapy in acute myeloid leukemia].","authors":"Tadashi Okamura, Shogo Murata, Kyohei Miyamoto, Misato Tane, Yuka Okabe, Satomi Takeda, Shotaro Tabata, Hideki Kosako, Yoshikazu Hori, Yusuke Yamashita, Toshiki Mushino, Hiroki Hosoi, Takashi Sonoki","doi":"10.11406/rinketsu.65.169","DOIUrl":"https://doi.org/10.11406/rinketsu.65.169","url":null,"abstract":"<p><p>A 44-year-old woman was diagnosed with acute myeloid leukemia (RUNX1::RUNX1T1 translocation) and received induction chemotherapy with idarubicin hydrochloride and cytosine arabinoside. The pneumonia that had been present since admission worsened, and a drug-induced skin rash appeared. On day 17, she presented with respiratory failure and shock, complicated by hemoconcentration and hypoalbuminemia. This was considered capillary leak syndrome due to pneumonia and drug allergy, so she was started on pulse steroid therapy and IVIG, and was intubated on the same day. On day 18, venovenous-extracorporeal membrane oxygenation (VV-ECMO) was started due to worsening blood gas parameters despite ventilatory management. Bronchoalveolar lavage fluid was serous, and both blood and sputum cultures yielded negative. The patient was weaned from VV-ECMO on day 26 as the pneumonia improved with recovery of hematopoiesis. She was disoriented, and a CT scan on day 28 revealed cerebral hemorrhage. Her strength recovered with rehabilitation. After induction chemotherapy, RUNX1::RUNX1T1 mRNA was not detected in bone marrow. The patient received consolidation chemotherapy, and has maintained complete remission. Severe respiratory failure during induction chemotherapy for acute leukemia can be fatal, but VV-ECMO may be lifesaving.</p>","PeriodicalId":93844,"journal":{"name":"[Rinsho ketsueki] The Japanese journal of clinical hematology","volume":"65 3","pages":"169-174"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140864717","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
[Molecular profiling of myeloid/natural killer (NK) cell precursor acute leukemia]. [髓系/自然杀伤（NK）细胞前体急性白血病的分子特征]。
[Rinsho ketsueki] The Japanese journal of clinical hematology Pub Date : 2024-01-01 DOI: 10.11406/rinketsu.65.1179
Masatoshi Takagi, Akira Nishimura
{"title":"[Molecular profiling of myeloid/natural killer (NK) cell precursor acute leukemia].","authors":"Masatoshi Takagi, Akira Nishimura","doi":"10.11406/rinketsu.65.1179","DOIUrl":"https://doi.org/10.11406/rinketsu.65.1179","url":null,"abstract":"<p><p>Myeloid/natural killer (NK) cell precursor acute leukemia (MNKPL) has been described based on its clinical phenotype and immunophenotype, and proposed as a unique leukemia entity. However, due to its rarity and lack of defined distinctive molecular characteristics, there is currently no international consensus on this disease concept. We performed multi-omics analysis and revealed that MNKPL is distinct from acute myeloid leukemia, T-cell acute lymphoblastic leukemia, and mixed-phenotype acute leukemia. NOTCH1 and RUNX3 activation and BCL11B downregulation are hallmarks of MNKPL. Although NK cells have been classically considered to be lymphoid lineage-derived, our single-cell analysis using MNKPL cells suggested that NK cells and myeloid cells share common progenitor cells. Our retrospective case study uncovered that outcomes of MNKPL are unsatisfactory, even with hematopoietic cell transplantation. Multi-omics analysis and in vitro drug sensitivity assays revealed increased sensitivity to L-asparaginase and reduced levels of asparagine synthetase, supporting the clinically observed effectiveness of L-asparaginase.</p>","PeriodicalId":93844,"journal":{"name":"[Rinsho ketsueki] The Japanese journal of clinical hematology","volume":"65 9","pages":"1179-1189"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142367819","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
[Update on treatment strategies for mantle cell lymphoma]. [套细胞淋巴瘤治疗策略的最新进展]。
[Rinsho ketsueki] The Japanese journal of clinical hematology Pub Date : 2024-01-01 DOI: 10.11406/rinketsu.65.1012
Suguru Fukuhara
{"title":"[Update on treatment strategies for mantle cell lymphoma].","authors":"Suguru Fukuhara","doi":"10.11406/rinketsu.65.1012","DOIUrl":"https://doi.org/10.11406/rinketsu.65.1012","url":null,"abstract":"<p><p>Mantle cell lymphoma (MCL) is a type of lymphoid malignancy that is rare in Japan. MCL is refractory to conventional chemotherapy and has dismal outcomes. Nonetheless, the prognosis of MCL has gradually improved with the advent of autologous stem cell transplantation and BTK inhibitors. First-line therapies incorporating BTK inhibitors are currently under development, and are expected to further improve the prognosis. Nevertheless, subsets with poor prognosis have been identified, including p53 abnormalities (TP53 mutations or deletions), blastoid variant, high MIPI-c, and POD24, and these show resistance to conventional treatments including BTK inhibitors. To overcome these challenges, novel therapies such as CAR-T therapy and combination therapy with BTK and BCL2 inhibitors are being developed, and should soon become clinically available in Japan. The therapeutic landscape for MCL is evolving dynamically, and this article will discuss the future of MCL treatment strategies in Japan.</p>","PeriodicalId":93844,"journal":{"name":"[Rinsho ketsueki] The Japanese journal of clinical hematology","volume":"65 9","pages":"1012-1018"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142367735","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
[Rinsho ketsueki] The Japanese journal of clinical hematology Pub Date : 2024-01-01 DOI: 10.11406/rinketsu.65.1245
{"title":"","authors":"","doi":"10.11406/rinketsu.65.1245","DOIUrl":"https://doi.org/10.11406/rinketsu.65.1245","url":null,"abstract":"","PeriodicalId":93844,"journal":{"name":"[Rinsho ketsueki] The Japanese journal of clinical hematology","volume":"65 10","pages":"1245"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142592184","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
[Genetic abnormalities in bone marrow failure]. [骨髓衰竭的遗传异常]。
[Rinsho ketsueki] The Japanese journal of clinical hematology Pub Date : 2024-01-01 DOI: 10.11406/rinketsu.65.1277
Kohei Hosokawa
{"title":"[Genetic abnormalities in bone marrow failure].","authors":"Kohei Hosokawa","doi":"10.11406/rinketsu.65.1277","DOIUrl":"https://doi.org/10.11406/rinketsu.65.1277","url":null,"abstract":"<p><p>Bone marrow (BM) failure is a condition characterized by peripheral pancytopenia resulting from decreased hematopoiesis in the BM. It includes congenital disorders such as Fanconi anemia (FA), as well as acquired conditions such as acquired aplastic anemia (AA), myelodysplastic syndrome (MDS), and paroxysmal nocturnal hemoglobinuria (PNH). AA presents with pancytopenia and BM hypoplasia, primarily triggered by an autoimmune mechanism involving T cells that damage hematopoietic stem cells (HSCs). Genomic investigations utilizing next-generation sequencing or SNP arrays have revealed that clonal hematopoiesis by HSCs with genetic aberrations, including PIGA, DNMT3A, ASXL1, BCOR/BCORL1, copy-number neutral LOH of chromosome 6p (6pLOH), and somatic mutations in HLA class I alleles are prevalent in AA patients. Recent studies have identified somatic mutations in genes associated with the JAK-STAT and MAPK pathways in T cells of AA patients. Genomic abnormalities in AA differ from those observed in MDS and age-related clonal hematopoiesis. Notably, the presence of PNH-type cells and HLA class I allele-lacking cells represent two major instances of escape hematopoiesis, which indicate the presence of HSCs evading autoimmune T cell attacks. These findings provide crucial insights into the immune pathophysiology of BM failure.</p>","PeriodicalId":93844,"journal":{"name":"[Rinsho ketsueki] The Japanese journal of clinical hematology","volume":"65 10","pages":"1277-1284"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142592248","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
[Recent advances in bone marrow pathology for myeloproliferative neoplasms diagnosis]. [骨髓病理学在骨髓增生性肿瘤诊断中的最新进展]。
[Rinsho ketsueki] The Japanese journal of clinical hematology Pub Date : 2024-01-01 DOI: 10.11406/rinketsu.65.778
Masafumi Ito
{"title":"[Recent advances in bone marrow pathology for myeloproliferative neoplasms diagnosis].","authors":"Masafumi Ito","doi":"10.11406/rinketsu.65.778","DOIUrl":"10.11406/rinketsu.65.778","url":null,"abstract":"<p><p>Identification of driver genes and pathological bone marrow diagnosis were considered essential for subclassification of MPN in the revised 4th edition of the WHO classification, and this remained nearly unchanged in the 5th edition. Pathological diagnosis of primary myelofibrosis/pre-fibrotic stage by biopsy is now feasible and is becoming standardized. Progressive myelofibrosis and blast transformation are the advanced forms of MPN, and various therapeutic interventions for these forms have been devised. Observation of activated megakaryocytes on evaluation of megakaryocyte morphology could predict the progression of myelofibrosis. This paper describes recent progress in pathological diagnosis of MPN and how it is performed in practice.</p>","PeriodicalId":93844,"journal":{"name":"[Rinsho ketsueki] The Japanese journal of clinical hematology","volume":"65 8","pages":"778-783"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142134707","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
[Treatment strategies for low-risk polycythemia vera]. [低风险红细胞增多症的治疗策略]。
[Rinsho ketsueki] The Japanese journal of clinical hematology Pub Date : 2024-01-01 DOI: 10.11406/rinketsu.65.810
Shuichi Ota
{"title":"[Treatment strategies for low-risk polycythemia vera].","authors":"Shuichi Ota","doi":"10.11406/rinketsu.65.810","DOIUrl":"10.11406/rinketsu.65.810","url":null,"abstract":"<p><p>Treatment selection for patients with polycythemia vera (PV) is based on patient age and history of thrombosis. The standard treatment is low-dose aspirin and phlebotomy for low-risk PV, with cytoreductive therapy added for high-risk PV. Thrombotic events and disease progression due to PV clone expansion affect the prognosis of PV. Although phlebotomy is effective in controlling hematocrit level, it has no effect on disease progression or PV-related symptoms. In Western countries, interferon (IFN) has been used as a cytoreductive therapy for PV. Long-term IFN therapy has been shown to result in sustained hematologic remission and molecular responses. Ropeginterferon-α-2b (ropeg-IFN), which is administered every two weeks, has recently become available. Clinical trials in patients with PV have shown that ropeg-IFN treatment is safe and efficacious, reducing JAK2V617F allele burden. Ropeg-IFN could ultimately affect long-term hematologic remission and molecular response in younger patients with low-risk PV, and may even offer a cure.</p>","PeriodicalId":93844,"journal":{"name":"[Rinsho ketsueki] The Japanese journal of clinical hematology","volume":"65 8","pages":"810-818"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142134709","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
[Appropriate use of the ELN guidelines based on results of real-world genetic analysis in Japanese patients with AML]. [根据日本急性髓细胞性白血病患者的实际基因分析结果合理使用 ELN 指南]。
[Rinsho ketsueki] The Japanese journal of clinical hematology Pub Date : 2024-01-01 DOI: 10.11406/rinketsu.65.676
Satoshi Wakita
{"title":"[Appropriate use of the ELN guidelines based on results of real-world genetic analysis in Japanese patients with AML].","authors":"Satoshi Wakita","doi":"10.11406/rinketsu.65.676","DOIUrl":"10.11406/rinketsu.65.676","url":null,"abstract":"<p><p>Researchers in the field of acute myeloid leukemia have long sought to establish a prognostic stratification system for clinical use that combines multiple genetic mutations. In 2022, the European LeukemiaNet (ELN) proposed a new prognostic model incorporating new genetic mutations. However, Japanese National Health insurance only recently began covering clinical genetic analysis for AML. We established the Multi-center Collaborative Program for Gene Sequencing of Japanese AML (GS-JAML) to contribute to clinical practice by providing rapid genetic analysis results. Retrospective analysis of this research program revealed (1) the clinical significance of CEBPA-bZIP mutations, and (2) the clinical significance of DNMT3A mutations in NPM1 mutated AML.</p>","PeriodicalId":93844,"journal":{"name":"[Rinsho ketsueki] The Japanese journal of clinical hematology","volume":"65 7","pages":"676-683"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141891234","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
[Budd-Chiari syndrome and JAK2 gene mutation]. [布德-奇异综合征与 JAK2 基因突变]。
[Rinsho ketsueki] The Japanese journal of clinical hematology Pub Date : 2024-01-01 DOI: 10.11406/rinketsu.65.790
Shuichi Shirane
{"title":"[Budd-Chiari syndrome and JAK2 gene mutation].","authors":"Shuichi Shirane","doi":"10.11406/rinketsu.65.790","DOIUrl":"10.11406/rinketsu.65.790","url":null,"abstract":"<p><p>Budd-Chiari syndrome (BCS) is a rare vascular disorder characterized by obstruction of hepatic venous outflow, culminating in elevated hepatic and portal venous pressure. BCS is associated with myeloproliferative neoplasms (MPN) in 40% of cases, which is significantly higher than the rate observed in other venous thrombotic conditions, and suggests that MPN may contribute to the etiology of BCS. In particular, the JAK2 V617F mutation has recently attracted substantial attention, given its profound association with thrombogenesis, mechanically implicated through endothelial damage, increased blood cell adhesion, and facilitation of neutrophil extracellular trap formation. A common treatment approach consists of anticoagulation for prevention and treatment of thrombosis, and cytoreductive therapy targeting MPN. However, as no definitive evidence exists for this approach, a bespoke therapeutic strategy tailored to individual patient profiles is required.</p>","PeriodicalId":93844,"journal":{"name":"[Rinsho ketsueki] The Japanese journal of clinical hematology","volume":"65 8","pages":"790-797"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142134697","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
[Development and prospects of bispecific antibodies for multiple myeloma]. [多发性骨髓瘤双特异性抗体的发展与前景]。
[Rinsho ketsueki] The Japanese journal of clinical hematology Pub Date : 2024-01-01 DOI: 10.11406/rinketsu.65.1049
Junichiro Yuda
{"title":"[Development and prospects of bispecific antibodies for multiple myeloma].","authors":"Junichiro Yuda","doi":"10.11406/rinketsu.65.1049","DOIUrl":"10.11406/rinketsu.65.1049","url":null,"abstract":"<p><p>Patients with triple-class refractory multiple myeloma once had a poor prognosis, but recently developed bispecific antibodies (bsAbs) targeting B-cell maturation antigen (BCMA), G protein-coupled receptor 5D (GPRC5D), and Fc receptor-homolog 5 (FcRH5) have shown significant clinical activity in these patients. However, responses to bsAbs are not universal, and resistance often develops during therapy. Mechanisms that mediate resistance may be tumor-intrinsic or immune-dependent. Tumor-intrinsic factors include antigen loss (biallelic or functional) due to deletion or mutation of target genes, increased soluble BCMA (for BCMA targeting bsAbs), high tumor burden, and extramedullary disease. Immune-mediated resistance highly depends on T cell fitness and the resistant immune environment. This article describes bispecific antibodies against multiple myeloma that are currently being developed.</p>","PeriodicalId":93844,"journal":{"name":"[Rinsho ketsueki] The Japanese journal of clinical hematology","volume":"65 9","pages":"1049-1057"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142367803","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
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