Leukemia最新文献

{"title":"NPM1-fusion proteins promote myeloid leukemogenesis through XPO1-dependent HOX activation","authors":"Yuko Shimosato, Keita Yamamoto, Yuhan Jia, Wenyu Zhang, Norio Shiba, Yasuhide Hayashi, Shuichi Ito, Toshio Kitamura, Susumu Goyama","doi":"10.1038/s41375-024-02438-w","DOIUrl":"https://doi.org/10.1038/s41375-024-02438-w","url":null,"abstract":"<p>Nucleophosmin (<i>NPM1</i>) is a nucleolar protein and one of the most frequently mutated genes in acute myeloid leukemia (AML). In addition to the commonly detected frameshift mutations in exon12 (NPM1c), previous studies have identified <i>NPM1</i> gene rearrangements leading to the expression of NPM1-fusion proteins in pediatric AML. However, whether the NPM1-fusions are indeed oncogenic and how the NPM1-fusions cause AML have been largely unknown. In this study, we investigated the subcellular localization and leukemogenic potential of two rare NPM1-fusion proteins, NPM1::MLF1 and NPM1::CCDC28A. NPM1::MLF1 is present in both the nucleus and cytoplasm and occasionally induces AML in the mouse transplantation assay. NPM1::CCDC28A is more localized to the cytoplasm, immortalizes mouse bone marrow cells in vitro and efficiently induces AML in vivo. Mechanistically, both NPM1-fusions bind to the <i>HOX</i> gene cluster and, like NPM1c, cause aberrant upregulation of <i>HOX</i> genes in cooperation with XPO1. The XPO1 inhibitor selinexor suppressed <i>HOX</i> activation and colony formation driven by the NPM1-fusions. <i>NPM1::CCDC28A</i> cells were also sensitive to menin inhibition. Thus, our study provides experimental evidence that both <i>NPM1::MLF1</i> and <i>NPM1::CCDC28A</i> are oncogenes with functions similar to NPM1c. Inhibition of XPO1 and menin may be a promising strategy for the NPM1-rearranged AML.</p>","PeriodicalId":18109,"journal":{"name":"Leukemia","volume":"62 1","pages":""},"PeriodicalIF":11.4,"publicationDate":"2024-10-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142487525","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}

{"title":"MSI2 mediates WNT/β-Catenin pathway function in hematopoietic stem cells","authors":"Huifang Zhang, Ruixue Guo, Zhenfen Li, Rui Ma, Shina Xu, Le Yin, Hongkai Zhu, Zineng Huang, Cheng Xing, Yunlong Yang, Yulin Pu, Zhao Cheng, Jing Liu, Hongling Peng, Yue Sheng","doi":"10.1038/s41375-024-02447-9","DOIUrl":"https://doi.org/10.1038/s41375-024-02447-9","url":null,"abstract":"&lt;p&gt;First, we sorted out hematopoietic stem cells (HSCs) and hematopoietic stem and progenitor cells (HSPCs) from wildtype (WT) and &lt;i&gt;Apc&lt;/i&gt; knockout (Apc KO, Apc&lt;sup&gt;−/−&lt;/sup&gt;) mice, which are Apc&lt;sup&gt;fl/fl&lt;/sup&gt; and Apc&lt;sup&gt;fl/fl&lt;/sup&gt;Mx1Cre respectively. The &lt;i&gt;Apc&lt;/i&gt; deletion was induced by Poly(I:C) injection. Quantitative PCR (qPCR) demonstrated a significant decrease of &lt;i&gt;Msi2&lt;/i&gt; expression in the HSCs (lin&lt;sup&gt;−&lt;/sup&gt;c-Kit&lt;sup&gt;+&lt;/sup&gt; Sca1&lt;sup&gt;+&lt;/sup&gt;CD150&lt;sup&gt;+&lt;/sup&gt;CD48&lt;sup&gt;−&lt;/sup&gt;) and HSPCs (lin&lt;sup&gt;−&lt;/sup&gt;c-Kit&lt;sup&gt;+&lt;/sup&gt;) of Apc KO mice (Fig. 1B, C). To investigate the role of MSI2 in the WNT signaling pathway, MSI2 was re-expressed in Apc&lt;sup&gt;−/−&lt;/sup&gt; HSPCs by retrovirus infection, and western blot (WB) confirmed Msi2 was successfully overexpressed (Supplementary Fig. 1). The colony-forming assay showed that restoring MSI2 expression could partially rescue the diminished colony-forming ability observed in Apc&lt;sup&gt;+/−&lt;/sup&gt; and Apc&lt;sup&gt;−/−&lt;/sup&gt; cells (Fig. 1D, E). Next, we collected colony cells from the above colony-forming assay, and found that restoration of MSI2 expression can significantly reduce the high apoptosis rate induced by &lt;i&gt;Apc&lt;/i&gt; KO (Fig. 1F and Supplementary Fig. 2).&lt;/p&gt;&lt;p&gt;To further investigate the relationship between MSI2 and WNT signaling pathway, we performed in vivo transplantation experiments following the restoration of MSI2 expression in &lt;i&gt;Apc&lt;/i&gt; KO cells. Five days after the 5-FU injection, HSPCs from WT (Apc&lt;sup&gt;fl/fl&lt;/sup&gt;) or Apc&lt;sup&gt;fl/fl&lt;/sup&gt; Mx1Cre mice were infected with MigR1 vector or MSI2, and then were transplanted into CD45.1 recipient mice irradiated lethally (10 Gray). One month later, pIpC was injected intra-peritoneally at bi-daily intervals to induce the expression of Mx1Cre to knock out &lt;i&gt;Apc&lt;/i&gt;. Seven days after the third pIpC injection, the mice were euthanized, and bone marrow cells were gathered for detection (Fig. 1G). The restoration of MSI2 expression considerably increased the populations of HSCs (Lin&lt;sup&gt;−&lt;/sup&gt;c-Kit&lt;sup&gt;+&lt;/sup&gt;Sca1&lt;sup&gt;+&lt;/sup&gt;CD48&lt;sup&gt;−&lt;/sup&gt;CD150&lt;sup&gt;+&lt;/sup&gt;), LSK (Lin&lt;sup&gt;−&lt;/sup&gt;c-Kit&lt;sup&gt;+&lt;/sup&gt;Sca1&lt;sup&gt;+&lt;/sup&gt;) and HPCs (Lin&lt;sup&gt;−&lt;/sup&gt;c-Kit&lt;sup&gt;+&lt;/sup&gt;Sca1&lt;sup&gt;−&lt;/sup&gt;) compared to cells from &lt;i&gt;Apc&lt;/i&gt; KO mice (Fig. 1H and Supplementary Fig. 3). Furthermore, the proportion of granulocyte-monocyte progenitors (GMP) and common myeloid progenitors (CMP) in the HPC population returned to normal. The megakaryocyte-erythroid progenitors (MEP) also changed, but not significantly (Fig. 1I and Supplementary Fig. 4). &lt;i&gt;Apc&lt;/i&gt; deletion can induce a significant increase in apoptosis, which is one of the main reasons for the decline of HSPCs [7]. We found that the restoration of MSI2 expression can significantly inhibit the increase of apoptosis caused by &lt;i&gt;Apc&lt;/i&gt; deletion (Fig. 1J and Supplementary Fig. 5A, B), suggesting that MSI2 can partially rescue the decline of HSPCs induced by &lt;i&gt;Apc&lt;/i&gt; loss through inhibiting apoptosis. In addition to HSPCs, w","PeriodicalId":18109,"journal":{"name":"Leukemia","volume":"9 1","pages":""},"PeriodicalIF":11.4,"publicationDate":"2024-10-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142487526","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}

{"title":"Robust anti-myeloma effect of TAS0612, an RSK/AKT/S6K inhibitor, with venetoclax regardless of cytogenetic abnormalities","authors":"Haruya Okamoto, Shinsuke Mizutani, Taku Tsukamoto, Yoko Katsuragawa-Taminishi, Yuka Kawaji-Kanayama, Kentaro Mizuhara, Ayako Muramatsu, Reiko Isa, Takahiro Fujino, Yuji Shimura, Koji Ichikawa, Junya Kuroda","doi":"10.1038/s41375-024-02439-9","DOIUrl":"https://doi.org/10.1038/s41375-024-02439-9","url":null,"abstract":"<p>Multiple myeloma (MM) remains a difficult-to-treat disease even with the latest therapeutic advances due to the complex, overlapping, and heterogeneous cytogenetic, genetic, and molecular abnormalities. To address this challenging problem, we previously identified the universal and critical roles of RSK2 and AKT, the effector signaling molecules downstream of PDPK1, regardless of cytogenetic and genetic profiles. Based on this, in this study, we investigated the anti-myeloma potency of TAS0612, a triple inhibitor against RSK, including RSK2, AKT, and S6K. Treatment with TAS0612 exerted the anti-proliferative effect <i>via</i> cell cycle blockade and the induction of apoptosis in human myeloma-derived cell lines (HMCLs) with diverse cytogenetic and genetic profiles. Ex vivo treatment with TAS0612 also significantly reduced the viability of patient-derived primary myeloma cells with diverse cytogenetic profiles. TAS0612 simultaneously caused the upregulation of several tumor suppressor genes, modulated prognostic genes according to the MMRF CoMMpass data, and downregulated a series of Myc- and mTOR-related genes. Moreover, the combination of TAS0612 with venetoclax (VEN) showed the synergy in inducing apoptosis in HMCLs irrespective of the t(11;14) translocation status. TAS0612 alone and combined with VEN are new potent candidate therapeutic strategies for MM, regardless of cytogenetic/genetic profiles, facilitating its future clinical development.</p>","PeriodicalId":18109,"journal":{"name":"Leukemia","volume":"222 1","pages":""},"PeriodicalIF":11.4,"publicationDate":"2024-10-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142486851","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}

{"title":"The BIM deletion polymorphism potentiates the survival of leukemia stem and progenitor cells and impairs response to targeted therapies","authors":"Mengge Yu, Giselle Sek Suan Nah, Vaidehi Krishnan, Fatin Nasha Bte Sulaimi, King Pan Ng, Chuqi Wang, Shruti Bhatt, Charles Chuah, David E. Bergstrom, S. Tiong Ong","doi":"10.1038/s41375-024-02418-0","DOIUrl":"https://doi.org/10.1038/s41375-024-02418-0","url":null,"abstract":"<p>One sixth of human cancers harbor pathogenic germline variants, but few studies have established their functional contribution to cancer outcomes. Here, we developed a humanized mouse model harboring a common East Asian polymorphism, the <i>BIM</i> deletion polymorphism (BDP), which confers resistance to oncogenic kinase inhibitors through generation of non-apoptotic splice isoforms. However, despite its clear role in mediating bulk resistance in patients, the BDP’s role in cancer stem and progenitor cells, which initiate disease and possess altered BCL-2 rheostats compared to differentiated tumor cells, remains unknown. To study the role of the BDP in leukemia initiation, we crossed the BDP mouse into a chronic myeloid leukemia (CML) model. We found that the BDP greatly enhanced the fitness of CML cells with a three-fold greater competitive advantage, leading to more aggressive disease. The BDP conferred almost complete resistance to cell death induced by imatinib in CML stem and progenitor cells (LSPCs). Using BH3 profiling, we identified a novel therapeutic vulnerability of BDP LSPCs to MCL-1 antagonists, which we confirmed in primary human LSPCs, and in vivo. Our findings demonstrate the impact of human polymorphisms on the survival of LSPCs and highlight their potential as companion diagnostics for tailored therapies.</p>","PeriodicalId":18109,"journal":{"name":"Leukemia","volume":"22 1","pages":""},"PeriodicalIF":11.4,"publicationDate":"2024-10-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142486994","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}

{"title":"Retraction Note: SAR650984 directly induces multiple myeloma cell death via lysosomal-associated and apoptotic pathways, which is further enhanced by pomalidomide","authors":"H. Jiang,&nbsp;C. Acharya,&nbsp;G. An,&nbsp;M. Zhong,&nbsp;X. Feng,&nbsp;L. Wang,&nbsp;N. Dasilva,&nbsp;Z. Song,&nbsp;G. Yang,&nbsp;F. Adrian,&nbsp;L. Qiu,&nbsp;P. Richardson,&nbsp;N. C. Munshi,&nbsp;Y. -T. Tai,&nbsp;K. C. Anderson","doi":"10.1038/s41375-024-02443-z","DOIUrl":"10.1038/s41375-024-02443-z","url":null,"abstract":"","PeriodicalId":18109,"journal":{"name":"Leukemia","volume":"38 12","pages":"2739-2739"},"PeriodicalIF":12.8,"publicationDate":"2024-10-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s41375-024-02443-z.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142503170","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}

{"title":"Genome-wide CRISPR screen identifies MAD2L1BP and ANAPC15 as targets for brentuximab vedotin sensitivity in CD30+ peripheral T-cell lymphoma","authors":"Keito Suto, Norio Takei, Keito Yokoyama, Masahiro Chiba, Takashi Ishio, Michiyuki Maeda, Hideki Goto, Tomoyuki Endo, Takanori Teshima, Yibin Yang, Masao Nakagawa","doi":"10.1038/s41375-024-02441-1","DOIUrl":"https://doi.org/10.1038/s41375-024-02441-1","url":null,"abstract":"<figure></figure>","PeriodicalId":18109,"journal":{"name":"Leukemia","volume":"84 1","pages":""},"PeriodicalIF":11.4,"publicationDate":"2024-10-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142452138","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}

{"title":"Single-cell transcriptomics of pediatric Burkitt lymphoma reveals intra-tumor heterogeneity and markers of therapy resistance","authors":"Clarissa Corinaldesi, Antony B. Holmes, Gaia Martire, Anna Tosato, Domenico Rizzato, Federica Lovisa, Ilaria Gallingani, Qiong Shen, Lavinia Ferrone, Marian Harris, Kimberly Davies, Luca Molinaro, Umberto Mortara, Angelo Paolo Dei Tos, Kenneth Ofori, Emanuele S. G. D’Amore, Roberto Chiarle, Bo Ngan, Elisa Carraro, Marta Pillon, Shafinaz Hussein, Govind Bhagat, Marco Pizzi, Lara Mussolin, Katia Basso","doi":"10.1038/s41375-024-02431-3","DOIUrl":"https://doi.org/10.1038/s41375-024-02431-3","url":null,"abstract":"<p>Burkitt lymphoma (BL) is the most frequent B-cell lymphoma in pediatric patients. While most patients are cured, a fraction of them are resistant to therapy. To investigate BL heterogeneity and the features distinguishing therapy responders (R) from non-responders (NR), we analyzed by single-cell (sc)-transcriptomics diagnostic EBV-negative BL specimens. Analysis of the non-tumor component revealed a predominance of immune cells and a small representation of fibroblasts, enriched in NR. Tumors displayed patient-specific features, as well as shared subpopulations that expressed transcripts related to cell cycle, signaling pathways and cell-of-origin signatures. Several transcripts were differentially expressed in R versus NR. The top candidate, Tropomyosin 2 (TPM2), a member of the tropomyosin actin filament binding protein family, was confirmed to be significantly higher in NR both at the transcript and protein level. Stratification of patients based on TPM2 expression at diagnosis significantly correlated with prognosis, independently of <i>TP53</i> mutations. These results indicate that BL displays transcriptional heterogeneity and identify candidate biomarkers of therapy resistance.</p>","PeriodicalId":18109,"journal":{"name":"Leukemia","volume":"12 1","pages":""},"PeriodicalIF":11.4,"publicationDate":"2024-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142449249","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}

{"title":"CD36 cell surface expression as a surrogate marker to identify ABL/JAK-class kinase fusions in pediatric BCP-ALL","authors":"Marion Strullu, Aurélie Caye-Eude, Elie Robert, Jean-Marie Renard, Amandine Chaye, Julie Galimand, Odile Fenneteau, Chloé Arfeuille, Wendy Cuccuini, Alexandre Theron, Sandrine Thouvenin, Catherine Paillard, Arnaud Petit, Pierre-Simon Rohrlich, Hélène Cavé, André Baruchel, Elodie Lainey","doi":"10.1038/s41375-024-02421-5","DOIUrl":"https://doi.org/10.1038/s41375-024-02421-5","url":null,"abstract":"<p>Genetic alterations are the cornerstone of risk stratification in B-cell precursor acute lymphoblastic leukemia (BCP-ALL), and their accurate identification is critical for optimal treatment. Most cases with <i>ABL</i>-class fusion are classified as high-risk yet display good responses to tyrosine kinase inhibitors (TKIs). Current clinical protocols recommend adding a TKI to chemotherapy as soon as possible, making it mandatory to rapidly identify these alterations. We investigated here whether the identification of immunophenotypic features associated with these molecular alterations could be a valuable screening tool. CD36 expression was shown to be a characteristic feature of <i>ABL-</i> or <i>JAK</i>-class kinase fusions. The main genetic subgroups clustering in the subset with Philadelphia (Ph)-like features were also found to display specific immunophenotypic characteristics. A predictive multiparameter scoring system was generated, segregating genetic subtypes with aberrant kinase activation (<i>PAX5/CRLF2</i>alt<i>, BCR::ABL1, ABL/JAK-</i>class). The most robust markers identified were the TSLPR with CD19/22/9/38/81/304 and CD49f. As TKI adjunction is currently limited to the <i>ABL</i>-class kinase fusions, immunophenotypes distinguishing <i>ABL</i> from <i>JAK</i>-class were also investigated. The flow cytometry method reported here, accessible to most hematology departments, is thus a new useful tool to quickly screen for Ph-like kinase fusion with a good sensitivity (95%) and specificity (96%).</p>","PeriodicalId":18109,"journal":{"name":"Leukemia","volume":"78 1","pages":""},"PeriodicalIF":11.4,"publicationDate":"2024-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142448262","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}

{"title":"Anagrelide and idarubicin combination induces GSDME-mediated pyroptosis as a potential therapy for high-PDE3A acute myeloid leukemia","authors":"Chenwei Yang, Yixin Hu, Li Gao, Zhiheng Li, Yongping Zhang, Ran Zhuo, Yayun Du, Hu Liu, Qi Ji, Minyuan Liu, Jian Pan, Jun Lu, Peifang Xiao, Yuanyuan Tian, Sudan He, Jing Ling, Shaoyan Hu","doi":"10.1038/s41375-024-02437-x","DOIUrl":"https://doi.org/10.1038/s41375-024-02437-x","url":null,"abstract":"<p>Acute myeloid leukemia (AML) is an invasive hematopoietic malignancy requiring novel treatment strategies. In this study, we identified phosphodiesterase 3 A (PDE3A) as a potential new target for drug repositioning in AML. PDE3A was preferentially overexpressed in AML cells than in normal cells, and high expression of PDE3A was correlated with lower event-free survival (EFS) in de novo AML patients. The PDE3A inhibitor anagrelide (ANA) profoundly suppresses the proliferation of high PDE3A-expressing AML cells while exhibiting minimal impact on those with low PDE3A expression. Moreover, synergistic effect of ANA with other chemotherapeutic drugs in high PDE3A expression AML cells was observed. The ANA-idarubicin (IDA) combination showed the most remarkable synergistic effect among all ANA-chemotherapeutic drugs commonly used in AML cell line models. Mechanistically, the synergy between ANA and IDA inhibited the survival of PDE3A^high AML cell lines through pyroptosis. This mechanism was initiated by GSDME cleavage triggered by caspase-3 activation. In vivo combination treatment of leukemic animals with high PDE3A expression significantly reduced leukemia burden and prolonged survival time compared with single-drug and vehicle control treatments. Our findings suggest that combined ANA and IDA treatment is an innovative and promising therapeutic strategy for AML patients with high PDE3A expression.</p>","PeriodicalId":18109,"journal":{"name":"Leukemia","volume":"42 1","pages":""},"PeriodicalIF":11.4,"publicationDate":"2024-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142440214","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}

{"title":"Acute myeloid leukemia: does sex matter?","authors":"Jesse M. Tettero,&nbsp;Jacqueline Cloos,&nbsp;Lars Bullinger","doi":"10.1038/s41375-024-02435-z","DOIUrl":"10.1038/s41375-024-02435-z","url":null,"abstract":"","PeriodicalId":18109,"journal":{"name":"Leukemia","volume":"38 11","pages":"2329-2331"},"PeriodicalIF":12.8,"publicationDate":"2024-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s41375-024-02435-z.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142439647","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}