Blood Research最新文献

{"title":"End of induction MRD assessment based early treatment intensification with novel agents in ETP-ALL- may be the way forward.","authors":"Pritish Chandra Patra, Sujay Rainchwar, Reema Singh, Rohan Halder, Pallavi Mehta, Megha Verma, Rayaz Ahmed, Jyoti Shankar Raichaudhuri, Dinesh Bhurani, Narendra Agrawal, Suman Pramanik","doi":"10.5045/br.2023.2022241","DOIUrl":"https://doi.org/10.5045/br.2023.2022241","url":null,"abstract":"TO THE EDITOR: Early T-cell precursor acute lymphoblastic leukemia (ETP-ALL) arises from early thymic progenitor cells that migrate from the bone marrow to the thymus and have the potential to differentiate into myeloid/dendritic or T cells. Gene expression profiling has revealed that ETP cells share similarities with hematopoietic stem cells and myeloid progenitor cells. ETP leukemic cells do not express CD1a, CD8, and CD5 (negative to dim). Instead, these cells express ≥1 stem cell/myeloid markers. However, in addition to other ETP-ALL diagnostic criteria, near-ETP-ALL usually shows brighter CD5 [1]. In the literature, the data on ETP-ALL varies markedly, ranging from outcomes poorer than those of other T-ALL to comparable outcomes, with complete remission (CR) rates ranging from 70% to more than 90% [2-5]. Combination chemotherapy is the mainstay treatment. ETP-ALL represents a high-risk subtype of ALL. These outcomes highlight the need for alternative therapeutic approaches that are prognosis-based, and ideally, aiming for minimal residual disease (MRD)negative remission, which may help in preventing relapse. Here, we present the results of a retrospective study on ETP/near-ETP-ALL in the Department of Hemato-Oncology of a dedicated cancer hospital in North India.","PeriodicalId":46224,"journal":{"name":"Blood Research","volume":"58 2","pages":"112-115"},"PeriodicalIF":2.2,"publicationDate":"2023-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/7a/7a/br-58-2-112.PMC10310492.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10110838","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"An alternative approach to confirm mixed lineage involvement in acute leukemia with <i>KMT2A</i> rearrangement-an illustrative report.","authors":"Debadrita Ray,&nbsp;Sreejesh Sreedharanunni,&nbsp;Anand Balakrishnan,&nbsp;Praveen Sharma,&nbsp;Nabhajit Mallik,&nbsp;Srinivasan Peyam,&nbsp;Man Updesh Singh Sachdeva","doi":"10.5045/br.2023.2023084","DOIUrl":"https://doi.org/10.5045/br.2023.2023084","url":null,"abstract":"REFERENCES 1. Munker R, Labopin M, Esteve J, Schmid C, Mohty M, Nagler A. Mixed phenotype acute leukemia: outcomes with allogeneic stem cell transplantation. A retrospective study from the Acute Leukemia Working Party of the EBMT. Haematologica 2017; 102:2134-40. 2. Shimoni A. Relapse of acute leukemia after a second allogeneic stemcell transplantation; is there any hope for cure? Bone Marrow Transplant 2022;57:336-7. 3. DiNardo CD, Jonas BA, Pullarkat V, et al. Azacitidine and venetoclax in previously untreated acute myeloid leukemia. N Engl J Med 2020;383:617‐29. 4. Schuler E, Wagner-Drouet EM, Ajib S, et al. Treatment of myeloid malignancies relapsing after allogeneic hematopoietic stem cell transplantation with venetoclax and hypomethylating agents-a retrospective multicenter analysis on behalf of the German Cooperative Transplant Study Group. Ann Hematol 2021;100:959‐68. 5. Qasrawi A, Gomes V, Chacko CA, et al. Acute undifferentiated leukemia: data on incidence and outcomes from a large population-based database. Leuk Res 2020;89:106301. 6. Pan R, Hogdal LJ, Benito JM, et al. Selective BCL-2 inhibition by ABT-199 causes on-target cell death in acute myeloid leukemia. Cancer Discov 2014;4:362‐75. 7. Fleischmann M, Scholl S, Frietsch JJ, et al. Clinical experience with venetoclax in patients with newly diagnosed, relapsed, or refractory acute myeloid leukemia. J Cancer Res Clin Oncol 2022;148:3191‐202. 8. Pratz KW, Jonas BA, Pullarkat V, et al. Measurable residual disease response and prognosis in treatment-naïve acute myeloid leukemia with venetoclax and azacitidine. J Clin Oncol 2022; 40:855‐65. 9. Wang N, He J, Liu F. Venetoclax in combination with hypomethylating agents for the treatment of treatment-naive B/myeloid mixed-phenotype acute leukemia and relapsed/refractory acute myeloid leukemia: a report of 3 cases. Chemotherapy 2022;67:178-82. 10. Klocke H, Dong ZM, O'Brien C, et al. Venetoclax and decitabine for T/myeloid mixed-phenotype acute leukemia not otherwise specified (MPAL NOS). Case Rep Hematol 2020;2020:8811673. 11. Zhao P, Ni M, Ma D, et al. Venetoclax plus azacitidine and donor lymphocyte infusion in treating acute myeloid leukemia patients who relapse after allogeneic hematopoietic stem cell transplantation. Ann Hematol 2022;101:119‐30. 12. Lasica M, Anderson MA. Review of venetoclax in CLL, AML and multiple myeloma. J Pers Med 2021;11:463. 13. Mei M, Aldoss I, Marcucci G, Pullarkat V. Hypomethylating agents in combination with venetoclax for acute myeloid leukemia: update on clinical trial data and practical considerations for use. Am J Hematol 2019;94:358-62. 14. Rausch CR, DiNardo CD, Maiti A, et al. Venetoclax dosing in combination with antifungal agents: real world experience in patients with acute myeloid leukemia. Blood (ASH Annual Meeting Abstracts) 2019;134(Suppl 1):2640.","PeriodicalId":46224,"journal":{"name":"Blood Research","volume":"58 2","pages":"120-123"},"PeriodicalIF":2.2,"publicationDate":"2023-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/50/e0/br-58-2-120.PMC10310490.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9791403","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Overexpression of S100A9 in donor T cells is associated with reconstitution of gut microbiota and outcome of allogeneic hematopoietic stem cell transplantation.","authors":"Sena Kim, Sora Lim, Farnaz Razmkhah, Jaebok Choi","doi":"10.5045/br.2023.2022238","DOIUrl":"10.5045/br.2023.2022238","url":null,"abstract":"","PeriodicalId":46224,"journal":{"name":"Blood Research","volume":"58 2","pages":"105-111"},"PeriodicalIF":2.3,"publicationDate":"2023-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/76/68/br-58-2-105.PMC10310486.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10109762","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"WITHDRAWN: Mutational analysis of the <i>F8</i> gene and phenotypic characterization of Hemophilia A.","authors":"Suresh Hanagavadi,&nbsp;Priyanka Indoria,&nbsp;K S Rajashekar,&nbsp;Rajat Hegde,&nbsp;Smita Hegde,&nbsp;Sujayendra Kulkarni,&nbsp;Chanda Varshini Sindhiya,&nbsp;Vardendra Kulkarni,&nbsp;Suyamindra S Kulkarni,&nbsp;Pramod B Gai","doi":"10.5045/br.2023.2022237","DOIUrl":"https://doi.org/10.5045/br.2023.2022237","url":null,"abstract":"<p><p>This article has been withdrawn as the request of the author(s) and/or Editors. The Publisher apologizes for any inconvenience this may cause.</p>","PeriodicalId":46224,"journal":{"name":"Blood Research","volume":" ","pages":""},"PeriodicalIF":2.2,"publicationDate":"2023-06-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9675490","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}

{"title":"Asciminib: the first-in-class allosteric inhibitor of BCR::ABL1 kinase.","authors":"Eun-Ji Choi","doi":"10.5045/br.2023.2023017","DOIUrl":"https://doi.org/10.5045/br.2023.2023017","url":null,"abstract":"<p><p>The prognosis of patients with chronic phase (CP) chronic myeloid leukemia (CML) has significantly improved due to the development of potent BCR::ABL1 tyrosine kinase inhibitors (TKIs). However, approximately 15‒20% of patients ultimately experience treatment failure due to resistance or intolerance to TKI therapy. As the prognosis of patients in whom multiple TKIs fail remains poor, an optimal therapeutic approach is required to treat the condition. Asciminib, an allosteric inhibitor that targets ABL1 myristoyl pocket, has been approved by the Food and Drug Administration for use in patients with CP-CML resistant or intolerant to ≥2 prior TKIs or those with T315I mutation. In a phase 1 trial, asciminib monotherapy showed a relatively favorable safety profile and potent efficacy in patients with and without the T315I mutation. In a subsequent phase 3 trial, asciminib treatment was associated with a significantly higher major molecular response rate and lower discontinuation rate than bosutinib in patients with CP-CML for whom two previous TKIs failed. Several clinical trials are being performed in various clinical settings to evaluate the role of asciminib as a frontline treatment for newly diagnosed CP-CML, either as a single agent or in combination with other TKIs as a second-line or additive treatment to improve treatment-free or deep remission. This review summarizes the incidence, available therapies, and outcomes of patients with CP-CML who experienced treatment failure, the mechanism of action, preclinical and clinical data, and ongoing trials for asciminib.</p>","PeriodicalId":46224,"journal":{"name":"Blood Research","volume":"58 S1","pages":"S29-S36"},"PeriodicalIF":2.2,"publicationDate":"2023-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/2f/45/br-58-s1-s29.PMC10133857.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9455553","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"T-large granular lymphocytic leukemia.","authors":"Sang Hyuk Park,&nbsp;Yoo Jin Lee,&nbsp;Youjin Kim,&nbsp;Hyun-Ki Kim,&nbsp;Ji-Hun Lim,&nbsp;Jae-Cheol Jo","doi":"10.5045/br.2023.2023037","DOIUrl":"https://doi.org/10.5045/br.2023.2023037","url":null,"abstract":"<p><p>T-cell large granular lymphocyte (T-LGL) leukemia is characterized by clonal expansion of cytotoxic T cells resulting in cytopenia. The proliferation of clonal LGLs is caused by prolonged antigenic stimulation, which leads to apoptotic dysregulation owing mainly to the constitutive activation of survival pathways, notably the JAK/STAT pathway. Understanding how leukemic T-LGL persists can aid in the development of future immunosuppressive therapies. In this review, we summarize the diagnosis and current standard of therapy for T-LGL leukemia, as well as recent advances in clinical trials.</p>","PeriodicalId":46224,"journal":{"name":"Blood Research","volume":"58 S1","pages":"S52-S57"},"PeriodicalIF":2.2,"publicationDate":"2023-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/52/2c/br-58-s1-s52.PMC10133854.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9456509","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Transfusion support in hematopoietic stem cell transplantation.","authors":"Dong Wook Jekarl,&nbsp;Jae Kwon Kim,&nbsp;Jay Ho Han,&nbsp;Howon Lee,&nbsp;Jaeeun Yoo,&nbsp;Jihyang Lim,&nbsp;Yonggoo Kim","doi":"10.5045/br.2023.2023004","DOIUrl":"10.5045/br.2023.2023004","url":null,"abstract":"<p><p>Transfusion support for hematopoietic stem cell transplantation (HSCT) is an essential part of supportive care, and compatible blood should be transfused into recipients. As leukocyte antigen (HLA) matching is considered first and as the blood group does not impede HSCT, major, minor, bidirectional, and RhD incompatibilities occur that might hinder transfusion and cause adverse events. Leukocyte reduction in blood products is frequently used, and irradiation should be performed for blood products, except for plasma. To mitigate incompatibility and adverse events, local transfusion guidelines, hospital transfusion committees, and patient management should be considered.</p>","PeriodicalId":46224,"journal":{"name":"Blood Research","volume":"58 S1","pages":"S1-S7"},"PeriodicalIF":2.2,"publicationDate":"2023-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/be/ad/br-58-s1-s1.PMC10133853.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10294836","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Practical issues in CAR T-cell therapy.","authors":"Ja Min Byun","doi":"10.5045/br.2023.2023015","DOIUrl":"https://doi.org/10.5045/br.2023.2023015","url":null,"abstract":"<p><p>Chimeric antigen receptor (CAR) T-cell therapy presents a revolutionary advancement in personalized cancer treatment. During the production process, the patient's own T-cells are genetically engineered to express a synthetic receptor that binds to a tumor antigen. CAR T-cells are then expanded for clinical use and infused back into the patient's body to attack cancer cells. Although CAR T-cell therapy is considered a major breakthrough in cancer immunotherapy, it is not without limitations. In this review, we discuss the barriers to effective CAR T-cell therapy in Korea.</p>","PeriodicalId":46224,"journal":{"name":"Blood Research","volume":"58 S1","pages":"S11-S12"},"PeriodicalIF":2.2,"publicationDate":"2023-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/3e/5f/br-58-s1-s11.PMC10133847.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9826121","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Novel therapeutic strategies for essential thrombocythemia/polycythemia vera.","authors":"Seug Yun Yoon,&nbsp;Jong-Ho Won","doi":"10.5045/br.2023.2023013","DOIUrl":"https://doi.org/10.5045/br.2023.2023013","url":null,"abstract":"<p><p>Myeloproliferative neoplasms (MPNs) are clonal disorders of hematopoietic stem cells; these include polycythemia vera (PV), essential thrombocythemia (ET), and primary myelofibrosis (PMF). MPNs are inflammatory cancers, wherein the malignant clone generates cytokines that sustain the inflammatory drive in a self-perpetuating vicious cycle. The course of MPNs follows a biological continuum, that is, from early cancer stages (ET/PV) to advanced myelofibrosis as well as impending leukemic transformation. MPN-related symptoms, e.g., fatigue, general weakness, and itching, are caused by inflammatory cytokines. Thrombosis and bleeding are also exacerbated by inflammatory cytokines in patients with MPN. Until recently, the primary objective of ET and PV therapy was to increase survival rates by preventing thrombosis. However, several medications have recently demonstrated the ability to modify the course of the disease; symptom relief is expected for most patients. In addition, there is increasing interest in the active treatment of patients at low risk with PV and ET. This review focuses on the ET/PV treatment strategies as well as novel treatment options for clinical development.</p>","PeriodicalId":46224,"journal":{"name":"Blood Research","volume":"58 S1","pages":"83-89"},"PeriodicalIF":2.2,"publicationDate":"2023-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/15/30/br-58-s1-s83.PMC10133851.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9723124","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Management of adverse events in young adults and children with acute B-cell lymphoblastic leukemia receiving anti-CD19 chimeric antigen receptor (CAR) T-cell therapy.","authors":"Jae Won Yoo","doi":"10.5045/br.2023.2023026","DOIUrl":"https://doi.org/10.5045/br.2023.2023026","url":null,"abstract":"<p><p>With impressive clinical advancements in immune effector cell therapies targeting CD19, chimeric antigen receptor (CAR) T-cell therapy has emerged as a new paradigm for treating relapsed/refractory B-cell malignancies. Currently, three second-generation CAR T-cell therapies have been approved, of which only tisagenlecleucel (tisa-cel) is approved for treating children and young adults with B-cell acute lymphoblastic leukemia (ALL) with durable remission rates of approximately 60‒90%. Although CAR T-cell therapies are considered to treat refractory B-ALL, they are associated with unique toxicities such as cytokine release syndrome (CRS) and immune effector cell-associated neurotoxicity syndrome (ICANS). The severity of CAR T-cell therapy toxicities can vary according to several clinical factors. In rare cases, severe CRS can progress to a fulminant hyperinflammatory syndrome known as hemophagocytic lymphohistiocytosis, which has a poor prognosis. The first-line treatments for CRS/ICANS include tocilizumab and corticosteroids. When severe CAR T-cell toxicity is resistant to first-line treatment, an additional approach is required to manage the persistent inflammation. In addition to CRS/ICANS, CAR T-cell therapy can cause early and delayed hematological toxicity, which can predispose patients to severe infections. The use of growth factors and anti-infective prophylaxis should follow institutional guidelines according to patient-specific risk factors. This review provides a thorough summary of updated practical recommendations for managing acute and delayed adverse effects following anti-CD19 CAR T-cell therapy in adults and children.</p>","PeriodicalId":46224,"journal":{"name":"Blood Research","volume":"58 S1","pages":"S20-S28"},"PeriodicalIF":2.2,"publicationDate":"2023-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/ba/7a/br-58-s1-s20.PMC10133856.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9449205","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}