Leukemia最新文献

{"title":"Growth retardation and adult height in pediatric patients with chronic-phase chronic myeloid leukemia treated with tyrosine kinase inhibitors","authors":"Haruko Shima, Chikako Tono, Akihiko Tanizawa, Masaki Ito, Akihiro Watanabe, Yuki Yuza, Kazuko Hamamoto, Hideki Muramatsu, Masahiko Okada, Shoji Saito, Hiroaki Goto, Masaru Imamura, Akiko M. Saito, Souichi Adachi, Eiichi Ishii, Hiroyuki Shimada","doi":"10.1038/s41375-024-02488-0","DOIUrl":"https://doi.org/10.1038/s41375-024-02488-0","url":null,"abstract":"<p>Although tyrosine kinase inhibitors (TKIs) have substantially improved chronic myeloid leukemia (CML) prognosis, long-term TKI exposure remains a major concern, especially among children. One critical challenge specific to the treatment of children with TKIs is growth retardation [1,2,3,4]. Recently, both first-generation TKI imatinib and second-generation TKI dasatinib were reported to impact growth in patients with Philadelphia chromosome-positive acute lymphoblastic leukemia [5]. We have previously reported growth retardation in children with CML treated with imatinib, particularly those treated before reaching puberty [3]. Although patients often experience catch-up growth during puberty, the extent of this catch-up and the long-term impact of TKI exposure on adult height remain poorly understood.</p><p>We prospectively collected data from children diagnosed with chronic phase CML enrolled in the Japan Pediatric Leukemia and Lymphoma Study Group (JPLSG) CML-08 study. Height data were collected annually, starting two years before diagnosis. Adult height was defined as the maximum height measured when the height increase velocity was &lt;1 cm/year. Height-standard deviation scores (SDS) were adjusted using age- and sex-adjusted Japanese norms [6], with data from 17 years and six months of age used for adult height-SDS. Puberty was defined as a testicular size ≥3 mL for males and breast Tanner 2 for females. Peak height velocity was defined as the increase in height velocity during the growth spurt, and age at peak height velocity was calculated from the growth curves [7]. The duration of TKI exposure before the growth spurt was defined as the duration of TKI exposure until peak height velocity. Parental height data were collected to predict adult height and range. Target height (TH), representing a child’s predicted adult height from parental heights, and target range (TR), a 95% confidence interval of target height, were calculated as follows (cm): males, TH = (mother’s height + father’s height + 13)/2, TR = TH ± 9; females, (mother’s height + father’s height − 13)/2, TR = TH ± 8 [8].</p>","PeriodicalId":18109,"journal":{"name":"Leukemia","volume":"25 1","pages":""},"PeriodicalIF":11.4,"publicationDate":"2024-12-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142809636","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 associated RUNX1 variants induce aberrant expression of transcription factor TCF4","authors":"Mylène Gerritsen, Florentien E. M. in ’t Hout, Ruth Knops, Bas L. R. Mandos, Melanie Decker, Tim Ripperger, Bert A. van der Reijden, Joost H. A. Martens, Joop H. Jansen","doi":"10.1038/s41375-024-02470-w","DOIUrl":"https://doi.org/10.1038/s41375-024-02470-w","url":null,"abstract":"&lt;p&gt;Disruption of RUNX1 contributes to malignant transformation and consequently, &lt;i&gt;RUNX1&lt;/i&gt; variants (&lt;i&gt;RUNX1&lt;/i&gt;&lt;sup&gt;var&lt;/sup&gt;) are found in various myeloid hematological malignancies and associated with a poor prognosis. RUNX1 can either activate or repress transcription, depending on its interaction with co-activators or co-repressors and the promoter context. Genetic variants in &lt;i&gt;RUNX1&lt;/i&gt; can be found in the entire gene. N-terminal missense and nonsense variants mostly affect the RUNT domain, while truncating variants often lead to deletion of the transactivation domain, or result in decreased protein expression due to nonsense mediated RNA-decay. In addition, more than a dozen different chromosomal translocations have been described in hematological malignancies that involve either &lt;i&gt;RUNX1&lt;/i&gt; or &lt;i&gt;CBFB&lt;/i&gt;. One of the most common translocations in AML is t(8;21)(q22;q22), leading to the fusion protein RUNX1::RUNX1T1, which accounts for approximately 10% of adult AML [1]. The &lt;i&gt;RUNX1::RUNX1T1&lt;/i&gt; is recognized as a AML-defining genetic abnormality in the latest WHO and ICC classifications [2] and defined as favorable risk AML in the European Leukemia Net (ELN) recommendations. In contrast, AML with a &lt;i&gt;RUNX1&lt;/i&gt;&lt;sup&gt;var&lt;/sup&gt; has been categorized as AML with myelodysplasia-related gene mutations in the WHO 2022 classification [3] and as an adverse risk genetic abnormality by the ELN 2022 [4]. The different prognostic value of &lt;i&gt;RUNX1&lt;/i&gt; variants versus &lt;i&gt;RUNX1&lt;/i&gt; translocations is intriguing, but the underlying mechanisms have not been fully elucidated. We have previously identified &lt;i&gt;Transciption factor 4&lt;/i&gt; (&lt;i&gt;TCF4&lt;/i&gt;, E2-2) expression as an independent prognostic factor in AML [5] and found that &lt;i&gt;TCF4&lt;/i&gt; expression is a dominant prognostic factor in multivariate analysis over the presence of &lt;i&gt;RUNX1&lt;/i&gt;&lt;sup&gt;&lt;i&gt;var&lt;/i&gt;&lt;/sup&gt; or t(8;21) in AML, suggesting that &lt;i&gt;TCF4&lt;/i&gt; mediates the prognostic effect of &lt;i&gt;RUNX1&lt;/i&gt; aberrations in AML. The exact mechanism how the expression of &lt;i&gt;TCF4&lt;/i&gt; is linked to RUNX1 aberrations is still unclear.&lt;/p&gt;&lt;p&gt;To identify the region of the &lt;i&gt;TCF4&lt;/i&gt; promoter which is essential for RUNX1 binding, we divided the RUNX1 binding region into three different parts of similar size (Fig. 1C). Assessing the transcriptional activity of the different parts revealed that the isolated part 3 did not show transcriptional activity. In contrast, both part 1 and 2 showed transcriptional activity, where part 2 displayed higher activity (Supplementary Fig. 1D). Addition of RUNX1&lt;sup&gt;wt&lt;/sup&gt; reduced &lt;i&gt;TCF4&lt;/i&gt; promoter activity via both regions (Supplementary Fig. 1E). Interestingly, the sum of luciferase activity of the separate parts was limited when compared to the activity of the full promoter, indicating a synergistic effect in the presence of the combined parts. We further cloned the precise region covering the RUNX1 binding region most proximal to the transcriptional start site, containing a TG","PeriodicalId":18109,"journal":{"name":"Leukemia","volume":"19 1","pages":""},"PeriodicalIF":11.4,"publicationDate":"2024-12-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142809620","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":"Prognostic relevance of treatment deviations in children with relapsed acute lymphoblastic leukemia who were treated in the ALL-REZ BFM 2002 study","authors":"Eleni A. Argyriadi, Ingo G. Steffen, Christiane Chen-Santel, Andrej Lissat, Andishe Attarbaschi, Jean-Pierre Bourquin, Guenter Henze, Arend von Stackelberg","doi":"10.1038/s41375-024-02474-6","DOIUrl":"https://doi.org/10.1038/s41375-024-02474-6","url":null,"abstract":"<p>Relapsed Acute Lymphoblastic Leukemia (ALL) is among the most common causes of cancer-associated deaths in children. However, little is known about the implications of deviations from ALL treatment protocols on survival rates. The present study elucidates the various characteristics of treatment deviations in children with relapsed ALL included in the ALL-REZ BFM 2002 (i.e., Relapse Berlin-Frankfurt- Münster) trial and determines their prognostic relevance for relapse and death rates. Among 687 patients, 100 were identified with treatment deviations, further classified, and examined by occurrence time, cause and type. Protocol deviation was considered a time-dependent variable and its impact on Disease Free Survival (DFS) and Overall Survival (OS) was examined using the time-dependent model Mantel Byar. Five years after the relapse diagnosis, deviations were significantly related to both inferior DFS (38%) and OS (57%) rates compared to protocol conformed treatment (DFS = 61%; OS = 70%, <i>P</i> &lt; 0.001). Based on multivariate analyses, protocol deviation proved to be an independent adverse prognostic factor of DFS. Moreover, deviations triggered by chemotherapy-induced toxicity were associated with a higher relapse rate compared to deviations due to insufficient response. Therefore, to avoid impairment of results by deviations, future clinical trials, and treatment strategies should focus on less toxic treatments and stricter protocol compliance.</p>","PeriodicalId":18109,"journal":{"name":"Leukemia","volume":"40 1","pages":""},"PeriodicalIF":11.4,"publicationDate":"2024-12-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142809726","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":"Surrogate endpoints in mature B-cell neoplasms – meaningful or misleading?","authors":"Florian Simon, Othman Al-Sawaf, John F. Seymour, Barbara Eichhorst","doi":"10.1038/s41375-024-02483-5","DOIUrl":"https://doi.org/10.1038/s41375-024-02483-5","url":null,"abstract":"<p>Indolent mature B-cell neoplasms are a group of diseases in which recent therapeutic advances have led to an improved overall survival (OS) extending beyond several years. While cause of celebration for patients and caregivers, the increasingly long observation periods necessary to capture treatment effects are complicating trial design and possibly hindering swift access to more effective therapies. Surrogate endpoints are a tool with the potential of earlier study readouts, however, their validity needs to be proven in each individual disease and therapeutic setting. The validation of surrogate endpoints and available data for mature B-cell neoplasms are discussed within this perspective article, followed by an outlook on the potential of precise tools such as measurable residual disease assessment as novel surrogate candidates.</p>","PeriodicalId":18109,"journal":{"name":"Leukemia","volume":"9 1","pages":""},"PeriodicalIF":11.4,"publicationDate":"2024-12-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142796999","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":"Incidence of Richter transformation of chronic lymphocytic leukemia/small lymphocytic lymphoma in the targeted therapy era","authors":"Paul J. Hampel, Kari G. Rabe, Yucai Wang, Steven R. Hwang, Saad S. Kenderian, Eli Muchtar, Jose F. Leis, Amber B. Koehler, Mazie Tsang, Talal Hilal, Ricardo Parrondo, Rachel J. Bailen, Susan M. Schwager, Curtis A. Hanson, Esteban Braggio, Susan L. Slager, Min Shi, Cinthya J. Zepeda-Mendoza, Daniel L. Van Dyke, Tait D. Shanafelt, Rebecca L. King, Timothy G. Call, Neil E. Kay, Wei Ding, Sameer A. Parikh","doi":"10.1038/s41375-024-02492-4","DOIUrl":"https://doi.org/10.1038/s41375-024-02492-4","url":null,"abstract":"<p>Richter transformation (RT) is the histologic transformation of chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL) into an aggressive lymphoma, most commonly diffuse large B-cell lymphoma (DLBCL). RT has devastating consequences with survival after transformation typically &lt;1 year [1]. Estimates of RT frequency vary by study design, setting, and duration of follow-up. In several large studies from time periods when chemoimmunotherapy (CIT) was used to treat patients with CLL, RT rates have been reported between 2 and 10% after a median follow-up of 4–6 years from the time of diagnosis; these studies included patients with both newly diagnosed CLL and treated CLL [2,3,4,5,6]. Targeted therapies, including Bruton tyrosine kinase inhibitors (BTKi) and B-cell lymphoma 2 inhibitors (BCL2i), are now standard of care treatment for patients with CLL. High RT rates (up to 25%) reported in early studies with BTKi and BCL2i in relapsed CLL patients likely reflect increased RT risk among heavily pre-treated patients rather than risk due to these therapies themselves [7, 8]. Comparison of risk after specific treatment exposures from first-line clinical trials with CIT and targeted therapy arms is limited by the low numbers of RT events reported [9,10,11,12,13]. As the treatment paradigm for CLL has changed and CLL patients are living longer, we aimed to assess the current risk of developing RT and the potential impact of targeted therapies on that risk by comparing cohorts of patients with newly diagnosed CLL across different time periods.</p><p>Following IRB approval, we identified patients with previously untreated CLL in the Mayo Clinic CLL Database who were seen within 12 months of diagnosis. Only cases of biopsy proven DLBCL with histopathologic confirmation at Mayo Clinic were considered an RT event. Cumulative incidence methodology was used to display the time to development of RT, both from time of initial CLL diagnosis and from start of CLL-directed therapy, with death as a competing risk. We defined the period prior to February 2014 (FDA approval of ibrutinib for CLL) as the pre-targeted therapy era and the period after February 2014 as the targeted therapy era. Using Cox proportional hazards regression analysis, we compared the incidence of RT between patients diagnosed with CLL in the pre-targeted therapy era versus the targeted therapy era. Cox regression analysis was also used to investigate the association of effects of type of treatment exposure (time-dependent variable) on risk of RT. Statistical analyses were conducted using SAS 9.4 (SAS Institute, Cary, NC, USA).</p>","PeriodicalId":18109,"journal":{"name":"Leukemia","volume":"93 1","pages":""},"PeriodicalIF":11.4,"publicationDate":"2024-12-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142796997","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":"Allogeneic hematopoietic stem cell transplantation in adult acute myeloid leukemia with t(16;21)(p11;q22)/FUS::ERG","authors":"Satoshi Mitsuyuki, Yoshimitsu Shimomura, Hiroki Mizumaki, Masamitsu Yanada, Shohei Mizuno, Naoyuki Uchida, Noriko Doki, Ayumu Ito, Masatsugu Tanaka, Tetsuya Nishida, Yuta Katayama, Satoshi Yoshihara, Tetsuya Eto, Satoru Takada, Shuichi Ota, Masako Toyosaki, Yuta Hasegawa, Hirohisa Nakamae, Koji Kawamura, Makoto Onizuka, Takahiro Fukuda, Marie Ohbiki, Yoshiko Atsuta, Takaaki Konuma","doi":"10.1038/s41375-024-02495-1","DOIUrl":"https://doi.org/10.1038/s41375-024-02495-1","url":null,"abstract":"&lt;p&gt;The t(16;21)(p11;q22) translocation is a rare but non-random chromosomal abnormality that accounts for approximately 1% of cases of acute myeloid leukemia (AML) [1, 2]. This chromosomal translocation produces a fusion gene between the &lt;i&gt;FUS&lt;/i&gt; gene at chromosome 16p11 and the &lt;i&gt;ERG&lt;/i&gt; gene at chromosome 21q22. Recent cytogenetic stratification classifies the sole abnormality of t(16;21)(p11;q22) as intermediate risk [1]. However, previous reports [2,3,4] suggest that the prognosis for AML patients with t(16;21)(p11;q22) is generally significantly worse, and evidence regarding allogeneic hematopoietic stem cell transplantation (HSCT) for AML patients with t(16;21)(p11;q22) is still lacking. Therefore, this study evaluated the survival outcomes of AML with t(16;21)(p11;q22) after allogeneic HSCT and compared them with those of other AML patients using Japanese transplant registry data.&lt;/p&gt;&lt;p&gt;The clinical data were provided by the Transplant Registry Unified Management Program 2 of the Japan Society for Transplantation and the Cellular Therapy and the Japanese Data Center for Hematopoietic Cell Transplantation [5,6,7]. Our study included patients with AML aged ≥16 years who received their first allogeneic HSCT between 1986 and 2021. Patients with a favorable-risk karyotype were excluded, as t(16;21)(p11;q22) is not classified as favorable according to the karyotype risk classification. This study was approved by the Data Management Committee of the Japanese Data Center for Hematopoietic Cell Transplantation and the Ethics Committee of Kobe City Medical Center General Hospital. Cytogenetic information was obtained at diagnosis or before allogeneic HSCT. The cytogenetic risk was classified as favorable, intermediate, or poor in accordance with the criteria provided by the National Comprehensive Cancer Network Guidelines (Version 1.2016) [8]. Due to insufficient data, in some cases, the t(16;21) translocation was identified, but their breakpoints were unknown (t(16;21) BU [breakpoint unknown]). Chromosomal translocations involving chromosomes 16 and 21 seen in AML include t(16;21)(q24;q22), as well as t(16;21)(p11;q22) [9]. However, t(16;21)(q24;q22) is notably rare in adult AML [3, 4, 9]; therefore, we considered t(16;21) BU as t(16;21)(p11;q22) in our analysis. Additionally, we performed a sensitivity analysis comparing patient characteristics and survival data between the t(16;21) BU and t(16;21)(p11;q22) groups to identify potential misclassifications. Other detailed definitions of variables and endpoints are described in Supplementary materials. The study endpoints were progression-free survival (PFS), overall survival (OS), relapse, and non-relapse mortality (NRM). For survival analysis, the Kaplan–Meier method was used for OS and PFS, while the Gray’s method was used for relapse and NRM to account for competing risks. Multivariable analysis was performed using a Cox proportional hazard model for OS and PFS or a Fine and Gray proportional ","PeriodicalId":18109,"journal":{"name":"Leukemia","volume":"27 1","pages":""},"PeriodicalIF":11.4,"publicationDate":"2024-12-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142796998","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":"Is there really an accelerated phase of chronic myeloid leukaemia at presentation?","authors":"Sen Yang, Xiaoshuai Zhang, Robert Peter Gale, Xiaojun Huang, Qian Jiang","doi":"10.1038/s41375-024-02486-2","DOIUrl":"https://doi.org/10.1038/s41375-024-02486-2","url":null,"abstract":"<p>Whether there is really a distinct accelerated phase (AP) at diagnosis in chronic myeloid leukaemia (CML) in the context of tyrosine kinase-inhibitor (TKI)-therapy is controversial. We studied 2122 consecutive subjects in chronic phase (CP, <i>n</i> = 1837) or AP (<i>n</i> = 285) at diagnosis classified according to the 2020 European LeukemiaNet (ELN) classification. AP subjects with increased basophils only had similar transformation-free survival (TFS) and survival compared with CP subjects classified as ELTS intermediate-risk. Those with increased blasts only had worse TFS but similar survival compared with CP subjects classified as ELTS high-risk. AP subjects with decreased platelets only had similar TFS but worse survival compared with subjects classified as ELTS high-risk. Proportions of CP and AP subjects meeting the 2020 ELN TKI-response milestones were similar. However, worse TFS at 3-month and survival at 6- or 12-month were only in AP subjects failing to meet ELN milestones. Findings were similar using the 2022 International Consensus Classification (ICC) criteria for AP replacing decreased platelets with additional cytogenetic abnormalities. Our data support the 2022 WHO classification of CML eliminating AP. We suggest adding a very high-risk cohort to the ELTS score including people with increased blasts or decreased platelets and dividing CML into 2 phases at diagnosis: CP and acute or blast phases.</p>","PeriodicalId":18109,"journal":{"name":"Leukemia","volume":"14 1","pages":""},"PeriodicalIF":11.4,"publicationDate":"2024-12-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142763190","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":"HMX3 is a critical vulnerability in MECOM-negative KMT2A::MLLT3 acute myelomonocytic leukemia","authors":"Saioa Arza-Apalategi, Branco M. H. Heuts, Saskia M. Bergevoet, Roos Meering, Daan Gilissen, Pascal W. T. C. Jansen, Anja Krippner-Heidenreich, Peter J. M. Valk, Michiel Vermeulen, Olaf Heidenreich, Torsten Haferlach, Joop H. Jansen, Joost H. A. Martens, Bert A. van der Reijden","doi":"10.1038/s41375-024-02485-3","DOIUrl":"https://doi.org/10.1038/s41375-024-02485-3","url":null,"abstract":"<p>KMT2A::MLLT3 acute myelomonocytic leukemia (AML) comes in two clinically and biologically different subtypes. One is characterized by inferior outcome, older age, and MECOM oncogene expression. The other is mainly observed in children and young adults, associates with better clinical outcome, but lacks MECOM. To identify cell fate determining transcription factors downstream of KMT2A::MLLT3, we applied a bioinformatic algorithm that integrates gene and enhancer expression from primary MECOM-positive and -negative KMT2A::MLLT3 AML samples. This identified MECOM to be most influential in the MECOM-positive group, while neuronal transcription factor HMX3 was most influential in the MECOM-negative group. In large AML cohorts, HMX3 expression associated with a unique gene expression profile, younger age (<i>p</i> &lt; 0.002) and KMT2A-rearranged and KAT6A-CREBBP leukemia (<i>p</i> &lt; 0.00001). HMX3 was not expressed in other major genetic risk groups and healthy blood cells. RNA-sequencing analyses following forced HMX3 expression in healthy CD34+ cells and its silencing in KMT2A::MLT3 cells showed that HMX3 drives cancer-associated E2F and MYC gene programs (<i>p</i> &lt; 0.001). HMX3 expression in healthy CD34+ cells blocked monocytic but not granulocytic colony formation. Strikingly, HMX3 silencing in KMT2A::MLLT3 patient cells resulted in cell cycle arrest, monocytic differentiation and apoptosis. Thus, the neuronal transcription factor HMX3 is a leukemia-specific vulnerability in KMT2A::MLLT3 AML.</p>","PeriodicalId":18109,"journal":{"name":"Leukemia","volume":"26 1","pages":""},"PeriodicalIF":11.4,"publicationDate":"2024-12-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142763191","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":"Correction: Efficacy and safety in a 4-year follow-up of the ELEVATE-TN study comparing acalabrutinib with or without obinutuzumab versus obinutuzumab plus chlorambucil in treatment-naïve chronic lymphocytic leukemia.","authors":"Jeff P Sharman, Miklos Egyed, Wojciech Jurczak, Alan Skarbnik, John M Pagel, Ian W Flinn, Manali Kamdar, Talha Munir, Renata Walewska, Gillian Corbett, Laura Maria Fogliatto, Yair Herishanu, Versha Banerji, Steven Coutre, George Follows, Patricia Walker, Karin Karlsson, Paolo Ghia, Ann Janssens, Florence Cymbalista, Jennifer A Woyach, Emmanuelle Ferrant, William G Wierda, Veerendra Munugalavadla, Ting Yu, Min Hui Wang, John C Byrd","doi":"10.1038/s41375-024-02487-1","DOIUrl":"https://doi.org/10.1038/s41375-024-02487-1","url":null,"abstract":"","PeriodicalId":18109,"journal":{"name":"Leukemia","volume":" ","pages":""},"PeriodicalIF":12.8,"publicationDate":"2024-12-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142770615","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":"Infection-related pathway activation and vulnerability to arsenic trioxide in acute promyelocytic leukemia with TTMV::RARA.","authors":"Jiacheng Lou, Yi Zhang, Jingfen Tao, Wen Jin, Yongmei Zhu, Zhuo Wang, Min Wu, Hongmei Yi, Xiaoxiao Chen, Shuhong Shen, Junmin Li, Zhu Chen, Saijuan Chen, Yangyang Xie, Li Chen, Kankan Wang","doi":"10.1038/s41375-024-02481-7","DOIUrl":"https://doi.org/10.1038/s41375-024-02481-7","url":null,"abstract":"","PeriodicalId":18109,"journal":{"name":"Leukemia","volume":" ","pages":""},"PeriodicalIF":12.8,"publicationDate":"2024-11-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142751321","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}