LeukemiaPub Date : 2024-09-05DOI: 10.1038/s41375-024-02382-9
Jianxiang Wang, Bin Jiang, Jian Li, Ligen Liu, Xin Du, Hao Jiang, Jianda Hu, Menghe Yuan, Taishi Sakatani, Takeshi Kadokura, Masato Takeuchi, Masanori Kosako, Xiao Ma, Larisa Girshova, Jerome Tan, Sergey Bondarenko, Lily Wong Lee Lee, Archrob Khuhapinant, Elena Martynova, Nahla Hasabou
{"title":"Phase 3 study of gilteritinib versus salvage chemotherapy in predominantly Asian patients with relapsed/refractory FLT3-mutated acute myeloid leukemia","authors":"Jianxiang Wang, Bin Jiang, Jian Li, Ligen Liu, Xin Du, Hao Jiang, Jianda Hu, Menghe Yuan, Taishi Sakatani, Takeshi Kadokura, Masato Takeuchi, Masanori Kosako, Xiao Ma, Larisa Girshova, Jerome Tan, Sergey Bondarenko, Lily Wong Lee Lee, Archrob Khuhapinant, Elena Martynova, Nahla Hasabou","doi":"10.1038/s41375-024-02382-9","DOIUrl":"10.1038/s41375-024-02382-9","url":null,"abstract":"The phase 3 COMMODORE trial evaluated gilteritinib versus salvage chemotherapy (SC) in a predominantly Asian relapsed/refractory (R/R) FLT3-mutated (FLT3mut+) acute myeloid leukemia (AML) patient population. The primary endpoint was overall survival (OS); secondary endpoints included event-free survival (EFS) and complete remission (CR) rate. As of June 30, 2020 (interim analysis: 32.2 months after study initiation), 234 patients were randomized (gilteritinib, n = 116; SC, n = 118). Median OS was significantly longer with gilteritinib versus SC (9.6 vs. 5.0 months; HR 0.566 [95% CI: 0.392, 0.818]; p = 0.00211) with a median follow-up of 10.3 months. Median EFS was also significantly longer with gilteritinib (2.8 vs. 0.6 months; HR 0.551 [95% CI: 0.395, 0.769]; p = 0.00004). CR rates with gilteritinib and SC were 16.4% and 10.2%, respectively; composite CR rates were 50.0% and 20.3%, respectively. Exposure-adjusted grade ≥3 adverse event (AE) rates were lower with gilteritinib (58.38 events/patient-year [E/PY]) versus SC (168.30 E/PY). Common AEs with gilteritinib were anemia (77.9%) and thrombocytopenia (45.1%). Gilteritinib plasma concentration peaked ~4 h postdose; ~3-fold accumulation occurred with multiple dosing. The COMMODORE trial demonstrated that gilteritinib significantly improved OS and EFS in predominantly Asian patients, validating the outcomes of gilteritinib from the ADMIRAL trial in R/R FLT3mut+ AML.","PeriodicalId":18109,"journal":{"name":"Leukemia","volume":null,"pages":null},"PeriodicalIF":12.8,"publicationDate":"2024-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s41375-024-02382-9.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142138026","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
LeukemiaPub Date : 2024-09-04DOI: 10.1038/s41375-024-02403-7
Cédric G. van der Ham, Lianne C. Suurenbroek, Michelle M. Kleisman, Željko Antić, Stefan H. Lelieveld, Marley Yeong, Liset Westera, Edwin Sonneveld, Peter M. Hoogerbrugge, Vincent H. J. van der Velden, Frank N. van Leeuwen, Roland P. Kuiper
{"title":"Mutational mechanisms in multiply relapsed pediatric acute lymphoblastic leukemia","authors":"Cédric G. van der Ham, Lianne C. Suurenbroek, Michelle M. Kleisman, Željko Antić, Stefan H. Lelieveld, Marley Yeong, Liset Westera, Edwin Sonneveld, Peter M. Hoogerbrugge, Vincent H. J. van der Velden, Frank N. van Leeuwen, Roland P. Kuiper","doi":"10.1038/s41375-024-02403-7","DOIUrl":"10.1038/s41375-024-02403-7","url":null,"abstract":"Pediatric acute lymphoblastic leukemia (ALL) is marked by low mutational load at initial diagnosis, which increases at relapse. To determine which processes are active in (relapsed) ALL and how they behave during disease progression before and after therapy, we performed whole genome sequencing on 97 tumor samples of 29 multiply relapsed ALL patients. Mutational load increased upon relapse in 28 patients and upon every subsequent relapse in 22 patients. In addition to two clock-like mutational processes, we identified UV-like damage, APOBEC activity, reactive oxygen species, thiopurine-associated damage and an unknown therapy component as drivers of mutagenesis. Mutational processes often affected patients over longer time periods, but could also occur in isolated events, suggesting the requirement of additional triggers. Thiopurine exposure was the most prominent source of new mutations in relapse, affecting over half of the studied patients in first and/or later relapse and causing potential relapse-driving mutations in multiple patients. Our data demonstrate that multiple mutational processes frequently act in parallel as prominent secondary drivers with dynamic activity during ALL development and progression.","PeriodicalId":18109,"journal":{"name":"Leukemia","volume":null,"pages":null},"PeriodicalIF":12.8,"publicationDate":"2024-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s41375-024-02403-7.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142133167","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
LeukemiaPub Date : 2024-09-02DOI: 10.1038/s41375-024-02385-6
Elias Jabbour, Jane Apperley, Jorge Cortes, Delphine Rea, Michael Deininger, Elisabetta Abruzzese, Charles Chuah, Daniel J. DeAngelo, Andreas Hochhaus, Jeffrey H. Lipton, Michael Mauro, Franck Nicolini, Javier Pinilla-Ibarz, Gianantonio Rosti, Philippe Rousselot, Neil P. Shah, Moshe Talpaz, Alexander Vorog, Xiaowei Ren, Hagop Kantarjian
{"title":"Correction: Dose modification dynamics of ponatinib in patients with chronic-phase chronic myeloid leukemia (CP-CML) from the PACE and OPTIC trials","authors":"Elias Jabbour, Jane Apperley, Jorge Cortes, Delphine Rea, Michael Deininger, Elisabetta Abruzzese, Charles Chuah, Daniel J. DeAngelo, Andreas Hochhaus, Jeffrey H. Lipton, Michael Mauro, Franck Nicolini, Javier Pinilla-Ibarz, Gianantonio Rosti, Philippe Rousselot, Neil P. Shah, Moshe Talpaz, Alexander Vorog, Xiaowei Ren, Hagop Kantarjian","doi":"10.1038/s41375-024-02385-6","DOIUrl":"10.1038/s41375-024-02385-6","url":null,"abstract":"","PeriodicalId":18109,"journal":{"name":"Leukemia","volume":null,"pages":null},"PeriodicalIF":12.8,"publicationDate":"2024-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s41375-024-02385-6.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142120205","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
LeukemiaPub Date : 2024-09-02DOI: 10.1038/s41375-024-02396-3
Simon Husby, Morten Tulstrup, Mads Harsløf, Christian Nielsen, Eva Haastrup, Lene Hyldahl Ebbesen, Mette Klarskov Andersen, Maroulio Pertesi, Christian Brieghel, Carsten U. Niemann, Björn Nilsson, Agoston Gyula Szabo, Niels Frost Andersen, Niels Abildgaard, Annette Vangsted, Kirsten Grønbæk
{"title":"Mosaic chromosomal alterations in hematopoietic cells and clinical outcomes in patients with multiple myeloma","authors":"Simon Husby, Morten Tulstrup, Mads Harsløf, Christian Nielsen, Eva Haastrup, Lene Hyldahl Ebbesen, Mette Klarskov Andersen, Maroulio Pertesi, Christian Brieghel, Carsten U. Niemann, Björn Nilsson, Agoston Gyula Szabo, Niels Frost Andersen, Niels Abildgaard, Annette Vangsted, Kirsten Grønbæk","doi":"10.1038/s41375-024-02396-3","DOIUrl":"10.1038/s41375-024-02396-3","url":null,"abstract":"Mosaic chromosomal alterations (mCAs) in hematopoietic cells increase mortality and risk of hematological cancers and infections. We investigated the landscape of mCAs and their clinical consequences in 976 patients with multiple myeloma undergoing high-dose chemotherapy and autologous stem cell support (ASCT) with median 6.4 years of follow-up. mCAs were detected in the stem cell harvest product of 158 patients (16.2%). Autosomal aberrations were found in 60 patients (6.1%) and affected all chromosomes. Loss of chromosome X was found in 51 females (12.7%) and loss of chromosome Y in 55 males (9.6%). Overall survival and progression were similar between carriers of autosomal mCAs and non-carriers. In contrast, female patients with loss of the X chromosome had longer overall survival (age-adjusted[a.a.] HR 0.54, 95% CI 0.32–0.93, p = 0.02), lower risk of progression (a.a. HR 0.55, 95% CI 0.35–0.87; p = 0.01), and better post-transplant response (higher degree of complete response (CR) or very good partial response (VGPR)). The reason for this substantial effect is unknown. Additionally, myeloma clones in the stem cell product was confirmed by mCA analysis in the few patients with multiple mCAs (n = 12 patients). Multiple mCAs conferred inferior overall survival (a.a. HR 2.0, 95% CI 1.02–3.84; p = 0.04) and higher risk of myeloma progression (a.a. HR 3.36, 95% CI 1.67–6.81; p < 0.001), which is presumed to be driven by suspected myeloma contaminants.","PeriodicalId":18109,"journal":{"name":"Leukemia","volume":null,"pages":null},"PeriodicalIF":12.8,"publicationDate":"2024-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s41375-024-02396-3.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142120206","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
LeukemiaPub Date : 2024-09-02DOI: 10.1038/s41375-024-02369-6
Monika M. Toma, Tomasz Skorski
{"title":"Star wars against leukemia: attacking the clones","authors":"Monika M. Toma, Tomasz Skorski","doi":"10.1038/s41375-024-02369-6","DOIUrl":"10.1038/s41375-024-02369-6","url":null,"abstract":"Leukemia, although most likely starts as a monoclonal genetic/epigenetic anomaly, is a polyclonal disease at manifestation. This polyclonal nature results from ongoing evolutionary changes in the genome/epigenome of leukemia cells to promote their survival and proliferation advantages. We discuss here how genetic and/or epigenetic aberrations alter intracellular microenvironment in individual leukemia clones and how extracellular microenvironment selects the best fitted clones. This dynamic polyclonal composition of leukemia makes designing an effective therapy a challenging task especially because individual leukemia clones often display substantial differences in response to treatment. Here, we discuss novel therapeutic approach employing single cell multiomics to identify and eradicate all individual clones in a patient.","PeriodicalId":18109,"journal":{"name":"Leukemia","volume":null,"pages":null},"PeriodicalIF":12.8,"publicationDate":"2024-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s41375-024-02369-6.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142118056","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
LeukemiaPub Date : 2024-08-30DOI: 10.1038/s41375-024-02389-2
Irene Pastor-Galán, Arturo Pereira, Eduardo Arellano-Rodrigo, Iván Martín, Adrián Mosquera-Orgueira, María-Teresa Gómez-Casares, Alberto Hernández-Sánchez, Francisca Ferrer-Marín, Elvira Mora, Patricia Velez, Rosa Ayala, Anna Angona, Natalia de las Heras, Elena Magro, María-Isabel Mata-Vázquez, María-Laura Fox, Sonia González de Villambrosía, María-José Ramírez, Ana García, Valentín García-Gutiérrez, Amparo Cáceres, María-Antonia Durán, María-Alicia Senín, José-María Raya, José Antonio González, Beatriz Cuevas, Blanca Xicoy, Marta Garrote, Blanca Ferrer, Manuel Pérez-Encinas, Jesús María Hernández-Rivas, Beatriz Bellosillo, Alberto Álvarez-Larrán, Juan Carlos Hernández-Boluda
{"title":"Impact of somatic gene mutations on the risk of thrombosis in myelofibrosis","authors":"Irene Pastor-Galán, Arturo Pereira, Eduardo Arellano-Rodrigo, Iván Martín, Adrián Mosquera-Orgueira, María-Teresa Gómez-Casares, Alberto Hernández-Sánchez, Francisca Ferrer-Marín, Elvira Mora, Patricia Velez, Rosa Ayala, Anna Angona, Natalia de las Heras, Elena Magro, María-Isabel Mata-Vázquez, María-Laura Fox, Sonia González de Villambrosía, María-José Ramírez, Ana García, Valentín García-Gutiérrez, Amparo Cáceres, María-Antonia Durán, María-Alicia Senín, José-María Raya, José Antonio González, Beatriz Cuevas, Blanca Xicoy, Marta Garrote, Blanca Ferrer, Manuel Pérez-Encinas, Jesús María Hernández-Rivas, Beatriz Bellosillo, Alberto Álvarez-Larrán, Juan Carlos Hernández-Boluda","doi":"10.1038/s41375-024-02389-2","DOIUrl":"10.1038/s41375-024-02389-2","url":null,"abstract":"","PeriodicalId":18109,"journal":{"name":"Leukemia","volume":null,"pages":null},"PeriodicalIF":12.8,"publicationDate":"2024-08-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142100840","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
LeukemiaPub Date : 2024-08-30DOI: 10.1038/s41375-024-02391-8
Jennifer Sun, Stefan Corradini, Feda Azab, Monica Shokeen, Barbara Muz, Katerina E. Miari, Mina Maksimos, Camila Diedrich, Obed Asare, Kinan Alhallak, Chaelee Park, Berit Lubben, Yixuan Chen, Ola Adebayo, Hannah Bash, Sarah Kelley, Mark Fiala, Diane E. Bender, Haibin Zhou, Shaomeng Wang, Ravi Vij, Mark T. S. Williams, Abdel Kareem Azab
{"title":"IL-10R inhibition reprograms tumor-associated macrophages and reverses drug resistance in multiple myeloma","authors":"Jennifer Sun, Stefan Corradini, Feda Azab, Monica Shokeen, Barbara Muz, Katerina E. Miari, Mina Maksimos, Camila Diedrich, Obed Asare, Kinan Alhallak, Chaelee Park, Berit Lubben, Yixuan Chen, Ola Adebayo, Hannah Bash, Sarah Kelley, Mark Fiala, Diane E. Bender, Haibin Zhou, Shaomeng Wang, Ravi Vij, Mark T. S. Williams, Abdel Kareem Azab","doi":"10.1038/s41375-024-02391-8","DOIUrl":"10.1038/s41375-024-02391-8","url":null,"abstract":"Multiple myeloma (MM) is the cancer of plasma cells within the bone marrow and remains incurable. Tumor-associated macrophages (TAMs) within the tumor microenvironment often display a pro-tumor phenotype and correlate with tumor proliferation, survival, and therapy resistance. IL-10 is a key immunosuppressive cytokine that leads to recruitment and development of TAMs. In this study, we investigated the role of IL-10 in MM TAM development as well as the therapeutic application of IL-10/IL-10R/STAT3 signaling inhibition. We demonstrated that IL-10 is overexpressed in MM BM and mediates M2-like polarization of TAMs in patient BM, 3D co-cultures in vitro, and mouse models. In turn, TAMs promote MM proliferation and drug resistance, both in vitro and in vivo. Moreover, inhibition of IL-10/IL-10R/STAT3 axis using a blocking IL-10R monoclonal antibody and STAT3 protein degrader/PROTAC prevented M2 polarization of TAMs and the consequent TAM-induced proliferation of MM, and re-sensitized MM to therapy, in vitro and in vivo. Therefore, our findings suggest that inhibition of IL-10/IL-10R/STAT3 axis is a novel therapeutic strategy with monotherapy efficacy and can be further combined with current anti-MM therapy, such as immunomodulatory drugs, to overcome drug resistance. Future investigation is warranted to evaluate the potential of such therapy in MM patients.","PeriodicalId":18109,"journal":{"name":"Leukemia","volume":null,"pages":null},"PeriodicalIF":12.8,"publicationDate":"2024-08-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s41375-024-02391-8.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142100841","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
LeukemiaPub Date : 2024-08-28DOI: 10.1038/s41375-024-02393-6
Karan L. Chohan, Rajiv K. Pruthi, Saurabh Zanwar, Jonas Paludo, Ronald Go, Animesh Pardanani, Aneel Ashrani, Joselle M. Cook, Carrie A. Thompson, Asher Chanan-Khan, Sikander Ailawadhi, Thomas M. Habermann, Thomas E. Witzig, Morie A. Gertz, David Dingli, Fransis K. Buadi, Angela Dispenzieri, Nelson Leung, Shaji K. Kumar, Vincent Rajkumar, William L. Nichols, Robert A. Kyle, Stephen M. Ansell, Prashant Kapoor, Meera Sridharan, Jithma P. Abeykoon
{"title":"The clinical impact of acquired von Willebrand syndrome secondary to Waldenström macroglobulinemia: an underrecognized source of major bleeding events","authors":"Karan L. Chohan, Rajiv K. Pruthi, Saurabh Zanwar, Jonas Paludo, Ronald Go, Animesh Pardanani, Aneel Ashrani, Joselle M. Cook, Carrie A. Thompson, Asher Chanan-Khan, Sikander Ailawadhi, Thomas M. Habermann, Thomas E. Witzig, Morie A. Gertz, David Dingli, Fransis K. Buadi, Angela Dispenzieri, Nelson Leung, Shaji K. Kumar, Vincent Rajkumar, William L. Nichols, Robert A. Kyle, Stephen M. Ansell, Prashant Kapoor, Meera Sridharan, Jithma P. Abeykoon","doi":"10.1038/s41375-024-02393-6","DOIUrl":"10.1038/s41375-024-02393-6","url":null,"abstract":"","PeriodicalId":18109,"journal":{"name":"Leukemia","volume":null,"pages":null},"PeriodicalIF":12.8,"publicationDate":"2024-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142084724","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
LeukemiaPub Date : 2024-08-27DOI: 10.1038/s41375-024-02370-z
Agata Pastorczak, Zuzanna Urbanska, Borys Styka, Karolina Miarka-Walczyk, Lukasz Sedek, Kamila Wypyszczak, Anna Wakulinska, Zuzanna Nowicka, Tomasz Szczepański, Marcin Stańczak, Wojciech Fendler, Jerzy Kowalczyk, Wojciech Młynarski, Monika Lejman
{"title":"Genetic hallmarks and clinical implications of chromothripsis in childhood T-cell acute lymphoblastic leukemia","authors":"Agata Pastorczak, Zuzanna Urbanska, Borys Styka, Karolina Miarka-Walczyk, Lukasz Sedek, Kamila Wypyszczak, Anna Wakulinska, Zuzanna Nowicka, Tomasz Szczepański, Marcin Stańczak, Wojciech Fendler, Jerzy Kowalczyk, Wojciech Młynarski, Monika Lejman","doi":"10.1038/s41375-024-02370-z","DOIUrl":"10.1038/s41375-024-02370-z","url":null,"abstract":"Chromothripsis (cth) is a form of genomic instability leading to massive de novo structural chromosome rearrangements in a one-time catastrophic event. It can cause cancer-promoting alterations, such as loss of sequences for tumor-suppressor genes, formation of oncogenic fusions, and oncogene amplifications. We investigated the genetic background and clinical significance of cth in childhood T-cell acute lymphoblastic leukemia (T-ALL) patients. For this purpose, whole-genome copy number alterations were analyzed in 173 children with newly diagnosed T-ALL using high-density microarrays. Cth was identified in 10 T-ALL samples (5.78%). In six of them, cth occurred in a constitutional background of Nijmegen breakage syndrome (n = 5) or Li-Fraumeni syndrome (n = 1). Cth generated alterations, including deletions of CDKN2A/B (n = 4) and EZH2 (n = 4), amplifications of CDK6 (n = 2), and NUP214::ABL1 and TFG::GPR128 fusions. Cth-positive leukemias exhibited deletions involving the tumor-suppressor genes RB1 (n = 3), TP53 (n = 1) and MED12 (n = 2). Cth-positive T-ALL patients had a lower probability of 5-year overall survival (OS) [0.56 vs. 0.81; hazard ratio (HR) = 4.14 (1.42–12.02) p = 0.017] as did 5-year event-free survival [0.45 vs. 0.74; HR = 3.91 (1.52–10.08); p = 0.012]. Chromothripsis is an infrequent genomic phenomenon in pediatric T-ALL but is significantly associated with cancer-predisposing syndromes and may associate with inferior prognosis.","PeriodicalId":18109,"journal":{"name":"Leukemia","volume":null,"pages":null},"PeriodicalIF":12.8,"publicationDate":"2024-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s41375-024-02370-z.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142080798","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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