Leukemia research最新文献

{"title":"Eltrombopag treatment in thrombocytopenia following hematopoietic stem cell transplantation: A multicenter real-world experience","authors":"Ebru Kilic Gunes ,&nbsp;Sureyya Yigit Kaya ,&nbsp;Fatih Yaman ,&nbsp;Mustafa Kemal Yeniay ,&nbsp;Kurtulus Vural ,&nbsp;Melda Comert ,&nbsp;Omur Gokmen Sevindik ,&nbsp;Neslihan Andic ,&nbsp;Simten Dagdas ,&nbsp;Ilknur Nizam Ozen ,&nbsp;Leylagul Kaynar ,&nbsp;Filiz Yavasoglu ,&nbsp;Gulsum Ozet ,&nbsp;Volkan Karakus ,&nbsp;Meltem Ayli","doi":"10.1016/j.leukres.2024.107484","DOIUrl":"10.1016/j.leukres.2024.107484","url":null,"abstract":"<div><h3>Introduction</h3><p>Thrombocytopenia is among the most common complications following hematopoietic stem cell transplantation and is associated with increased mortality and morbidity with no standard treatment yet. In this multicenter and retrospective study, we aim to present our multi-center experience of Eltrombopag treatment in patients with isolated thrombocytopenia following HSCT.</p></div><div><h3>Material-method</h3><p>A total of 73 patients from 5 centers who underwent autologous or allogeneic stem cell transplantation, had no primary disease relapse, all of whom had neutrophil engraftment, complete chimerism, and who were diagnosed with Prolonged Isolated Thrombocytopenia (PIT) or Secondary Failure Of Platelet Recovery (SFPR) were included in the study. The patients were initiated on Eltrombopag at a dose of 50–150 mg. Complete response was defined as a platelet count &gt;50×10⁹/L for 7 consecutive days with no transfusion support.</p></div><div><h3>Results</h3><p>A total of 50.3% of the patients underwent Autologous and 49.7% Allogeneic Stem Cell Transplantation, 54.8% were diagnosed with PIT, and 45.2% were diagnosed with SFPR, and the treatment with 50–150 mg/day Eltrombopag was initiated on the median day +42. Complete response was achieved in 71.2% of these patients on the median day 23 of the treatment. No significant effects of the initial dose (50–150 mg/day) were detected in the Complete Response in the multivariate analysis on response. An insufficient number of Megakaryocytes in the bone marrow before Eltrombopag treatment was determined as an independent risk factor in determining the response (OR 3.57, 95% CI 1.21–10.55). The overall survival of the patients who did not respond to Eltrombopag was found to be significantly worse than that of patients who responded (p=0.022, HR:2.74, 95% CI 1.12–6.54).</p></div><div><h3>Conclusion</h3><p>As a result of the present study, Eltrombopag treatment was found to be effective and safe in thrombocytopenia that develops following hematopoietic stem cell transplantation. It was concluded that its use may be more effective in patients with sufficient bone marrow megakaryocytes before the treatment and an initial dose of 50 mg/day may be appropriate in terms of cost, effectiveness, and toxicity. Large-scale randomized and controlled prospective studies are needed to determine the roles of Eltrombopag treatment in patients with post-transplant PIT and SFPR.</p></div>","PeriodicalId":18051,"journal":{"name":"Leukemia research","volume":"140 ","pages":"Article 107484"},"PeriodicalIF":2.7,"publicationDate":"2024-03-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140149420","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Clinical validation of a 10-color flow cytometry panel to detect measurable residual disease in acute myeloid leukemia","authors":"Maura R.V. Ikoma-Colturato ,&nbsp;Alef Rafael Severino ,&nbsp;Juliana Fernanda dos Santos Tosi ,&nbsp;Camila Marques Bertolucci ,&nbsp;Yeda Midori Nakamura Cuoco ,&nbsp;Ederson Roberto de Mattos ,&nbsp;Iago Colturato ,&nbsp;Fernanda Barbieri Rodrigues Silva ,&nbsp;Mair Pedro de Souza ,&nbsp;Anderson João Simione ,&nbsp;Vergilio Antonio Rensi Colturato","doi":"10.1016/j.leukres.2024.107482","DOIUrl":"10.1016/j.leukres.2024.107482","url":null,"abstract":"","PeriodicalId":18051,"journal":{"name":"Leukemia research","volume":"140 ","pages":"Article 107482"},"PeriodicalIF":2.7,"publicationDate":"2024-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140148869","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Investigations of the prognostic value of RUNX1 mutation in acute myeloid leukemia patients: Data from a real-world study","authors":"Chao-Ling Wan ,&nbsp;Yuan-Hong Huang ,&nbsp;Si-Man Huang ,&nbsp;Yan-Li Xu ,&nbsp;Kai-Wen Tan ,&nbsp;Yan-Qiu ,&nbsp;Xiang-Dong Shen ,&nbsp;Shuai-Shuai Ge ,&nbsp;Han-Yu Cao ,&nbsp;Yan-Yan Li ,&nbsp;Song-Bai Liu ,&nbsp;Jia-Jun Qi ,&nbsp;Hai-Ping Dai ,&nbsp;Sheng-Li Xue","doi":"10.1016/j.leukres.2024.107483","DOIUrl":"https://doi.org/10.1016/j.leukres.2024.107483","url":null,"abstract":"<div><p><em>RUNX1</em> is one of the recurrent mutated genes in newly diagnosed acute myeloid leukemia (AML). Although historically recognized as a provisional distinct entity, the AML subtype with <em>RUNX1</em> mutations (AML-<em>RUNX1</em>^mut) was eliminated from the 2022 WHO classification system. To gain more insight into the characteristics of AML-<em>RUNX1</em>^mut, we retrospectively analyzed 1065 newly diagnosed adult AML patients from the First Affiliated Hospital of Soochow University between January 2017 and December 2021. <em>RUNX1</em> mutations were identified in 112 patients (10.5%). The presence of <em>RUNX1</em> mutation (<em>RUNX1</em>^mut) conferred a lower composite complete remission (CRc) rate (40.2% vs. 58.4%, <em>P</em>＜0.001), but no significant difference was observed in the 5-year overall survival (OS) rate (50.2% vs. 53.9%; HR=1.293; <em>P</em>=0.115) and event-free survival (EFS) rate (51.5% vs. 49.4%; HR=1.487, <em>P</em>=0.089), even within the same risk stratification. Multivariate analysis showed that <em>RUNX1</em>^mut was not an independent prognostic factor for OS (HR=1.352, <em>P</em>=0.068) or EFS (HR=1.129, <em>P</em>=0.513). When patients were stratified according to induction regimen, <em>RUNX1</em>^mut was an unfavorable factor for CRc both on univariate and multivariate analysis in patients receiving conventional chemotherapy, and higher risk stratification predicted worse OS. In those who received venetoclax plus hypomethylating agents, <em>RUNX1</em>^mut was not predictive of CRc and comparable OS and EFS were seen between intermediate-risk and adverse-risk groups. The results of this study revealed that the impact of <em>RUNX1</em>^mut is limited. Its prognostic value depended more on treatment and co-occurrent abnormalities. VEN-HMA may abrogate the prognostic impact of <em>RUNX1</em>, which merits a larger prospective cohort to illustrate.</p></div>","PeriodicalId":18051,"journal":{"name":"Leukemia research","volume":"139 ","pages":"Article 107483"},"PeriodicalIF":2.7,"publicationDate":"2024-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140138722","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pracinostat combined with azacitidine in newly diagnosed adult acute myeloid leukemia (AML) patients unfit for standard induction chemotherapy: PRIMULA phase III study","authors":"Guillermo Garcia-Manero ,&nbsp;Maciej Kazmierczak ,&nbsp;Agnieszka Wierzbowska ,&nbsp;Chun Yew Fong ,&nbsp;Michael K. Keng ,&nbsp;Gianluca Ballinari ,&nbsp;Francesco Scarci ,&nbsp;Lionel Adès","doi":"10.1016/j.leukres.2024.107480","DOIUrl":"10.1016/j.leukres.2024.107480","url":null,"abstract":"<div><p>Non-intensive therapies such as the hypomethylating agent (HMA) azacitidine (AZA) have been used in patients with AML ineligible for intensive induction chemotherapy (IC) or stem cell transplant due to advanced age, comorbidities, and/or risk factors. However, response rates and survival remain dismal. Pre-clinical studies indicate the epigenetic combination of HMAs and HDAC inhibitors induce re-expression of silenced genes synergistically. The activity of pracinostat, an oral pan-HDAC inhibitor, has been shown in xenograft tumor models of AML and promising efficacy was seen in a Phase 2 study. This Phase 3 study (NCT03151408) evaluated the efficacy/safety of pracinostat administered with AZA in adult patients with newly diagnosed AML ineligible to receive IC. Patients were randomized to either pracinostat plus AZA or placebo/AZA and stratified by cytogenetic risk and ECOG status. As planned, an interim analysis was performed when 232/390 events (deaths) occurred. A total of 406 patients were randomized (203/group) at the time of the analysis. Median overall survival was 9.95 months for both treatment groups (p=0.8275). There was no significant difference between treatments in secondary efficacy endpoints, reflecting a lack of clinical response. This study did not show a benefit of adding pracinostat to AZA in elderly patients unfit for IC.</p></div>","PeriodicalId":18051,"journal":{"name":"Leukemia research","volume":"140 ","pages":"Article 107480"},"PeriodicalIF":2.7,"publicationDate":"2024-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140148793","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Efficacy and safety of bosutinib in patients treated with prior imatinib and/or dasatinib and/or nilotinib: Subgroup analyses from the phase 4 BYOND study","authors":"B. Douglas Smith ,&nbsp;Tim H. Brümmendorf ,&nbsp;Gail J. Roboz ,&nbsp;Carlo Gambacorti-Passerini ,&nbsp;Aude Charbonnier ,&nbsp;Andrea Viqueira ,&nbsp;Eric Leip ,&nbsp;Simon Purcell ,&nbsp;Erinn Hoag Goldman ,&nbsp;Francis Giles ,&nbsp;Thomas Ernst ,&nbsp;Andreas Hochhaus ,&nbsp;Gianantonio Rosti","doi":"10.1016/j.leukres.2024.107481","DOIUrl":"https://doi.org/10.1016/j.leukres.2024.107481","url":null,"abstract":"<div><p>The BYOND study evaluated the efficacy and safety of bosutinib 500 mg once daily in patients with chronic myeloid leukemia (CML) resistant/intolerant to prior tyrosine kinase inhibitors (TKIs). These post-hoc analyses assessed the efficacy and safety of bosutinib by resistance or intolerance to prior TKIs (imatinib-resistant vs dasatinib/nilotinib-resistant vs TKI-intolerant), and cross-intolerance between bosutinib and prior TKIs (imatinib, dasatinib, nilotinib), in patients with Philadelphia chromosome–positive chronic phase CML. Data are reported after ≥3 years’ follow-up. Of 156 patients with Philadelphia chromosome–positive chronic phase CML, 53 were imatinib-resistant, 29 dasatinib/nilotinib-resistant, and 74 intolerant to all prior TKIs; cumulative complete cytogenetic response rates at any time were 83.7%, 61.5%, and 86.8%, and cumulative major molecular response rates at any time were 72.9%, 40.7%, and 82.4%, respectively. Of 141, 95, and 79 patients who received prior imatinib, dasatinib, and nilotinib, 64 (45.4%), 71 (74.7%), and 60 (75.9%) discontinued the respective TKI due to intolerance; of these, 2 (3.1%), 5 (7.0%), and 0 had cross-intolerance with bosutinib. The response rates observed in TKI-resistant and TKI-intolerant patients, and low cross-intolerance between bosutinib and prior TKIs, further support bosutinib use for patients with Philadelphia chromosome–positive chronic phase CML resistant/intolerant to prior TKIs.</p></div><div><h3>Trial registration</h3><p>ClinicalTrials.gov: NCT02228382</p></div>","PeriodicalId":18051,"journal":{"name":"Leukemia research","volume":"139 ","pages":"Article 107481"},"PeriodicalIF":2.7,"publicationDate":"2024-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140123305","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CD38 and BCL2 expression guides treatment with daratumumab and venetoclax in tagraxofusp-refractory blastic plasmacytoid dendritic cell neoplasm (BPDCN) featuring dynamic loss of CD123","authors":"Xiaoyi Hu ,&nbsp;Asiri Ediriwickrema ,&nbsp;Atif Saleem ,&nbsp;Brent Tan ,&nbsp;Naveen Pemmaraju ,&nbsp;Gabriel N. Mannis","doi":"10.1016/j.leukres.2024.107479","DOIUrl":"https://doi.org/10.1016/j.leukres.2024.107479","url":null,"abstract":"","PeriodicalId":18051,"journal":{"name":"Leukemia research","volume":"139 ","pages":"Article 107479"},"PeriodicalIF":2.7,"publicationDate":"2024-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140134425","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Expression of the chemokine receptor CCR1 decreases sensitivity to bortezomib in multiple myeloma cell lines","authors":"Mara N. Zeissig ,&nbsp;Duncan R. Hewett ,&nbsp;Krzysztof M. Mrozik ,&nbsp;Vasilios Panagopoulos ,&nbsp;Craig T. Wallington-Gates ,&nbsp;Andrew Spencer ,&nbsp;Sandra M. Dold ,&nbsp;Monika Engelhardt ,&nbsp;Kate Vandyke ,&nbsp;Andrew C.W. Zannettino","doi":"10.1016/j.leukres.2024.107469","DOIUrl":"10.1016/j.leukres.2024.107469","url":null,"abstract":"<div><h3>Background</h3><p>The proteasome inhibitor bortezomib is one of the primary therapies used for the haematological malignancy multiple myeloma (MM). However, intrinsic or acquired resistance to bortezomib, via mechanisms that are not fully elucidated, is a barrier to successful treatment in many patients. Our previous studies have shown that elevated expression of the chemokine receptor CCR1 in MM plasma cells in newly diagnosed MM patients is associated with poor prognosis. Here, we hypothesised that the poor prognosis conferred by CCR1 expression is, in part, due to a CCR1-mediated decrease in MM plasma cell sensitivity to bortezomib.</p></div><div><h3>Methods</h3><p>In order to investigate the role of CCR1 in MM cells, CCR1 was knocked out in human myeloma cell lines OPM2 and U266 using CRISPR-Cas9. Additionally, CCR1 was overexpressed in the mouse MM cell line 5TGM1. The effect of bortezomib on CCR1 knockout or CCR1-overexpressing cells was then assessed by WST-1 assay, with or without CCL3 siRNA knockdown or addition of recombinant human CCL3. NSG mice were inoculated intratibially with OPM2-CCR1^KO cells and were treated with 0.7 mg/kg bortezomib or vehicle twice per week for 3 weeks and GFP⁺ tumour cells in the bone marrow were quantitated by flow cytometry. The effect of CCR1 overexpression or knockout on unfolded protein response pathways was assessed using qPCR for <em>ATF4</em>, <em>HSPA5</em>, <em>XBP1</em>, <em>ERN1</em> and <em>CHOP</em> and Western blot for IRE1α and p-Jnk.</p></div><div><h3>Results</h3><p>Using CCR1 overexpression or CRIPSR-Cas9-mediated CCR1 knockout in MM cell lines, we found that CCR1 expression significantly decreases sensitivity to bortezomib <em>in vitro</em>, independent of the CCR1 ligand CCL3. In addition, CCR1 knockout rendered the human MM cell line OPM2 more sensitive to bortezomib in an intratibial MM model in NSG mice <em>in vivo.</em> Moreover, CCR1 expression negatively regulated the expression of the unfolded protein response receptor IRE1 and downstream target gene <em>XBP1</em>, suggesting this pathway may be responsible for the decreased bortezomib sensitivity of CCR1-expressing cells.</p></div><div><h3>Conclusions</h3><p>Taken together, these studies suggest that CCR1 expression may be associated with decreased response to bortezomib in MM cell lines.</p></div>","PeriodicalId":18051,"journal":{"name":"Leukemia research","volume":"139 ","pages":"Article 107469"},"PeriodicalIF":2.7,"publicationDate":"2024-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0145212624000353/pdfft?md5=fcdeab6521f153c54f015f88cbb46d30&pid=1-s2.0-S0145212624000353-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140100203","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A critical evaluation of the EFS endpoint in AML: Does induction treatment failure timing have a profound impact on study design and results?","authors":"Yulia Sidi ,&nbsp;Cassie Dong ,&nbsp;Yujun Wu ,&nbsp;Douglas V. Faller","doi":"10.1016/j.leukres.2024.107465","DOIUrl":"10.1016/j.leukres.2024.107465","url":null,"abstract":"<div><p>Despite emerging novel therapies, treating acute myeloid leukemia (AML) remains challenging. Complexities persist in designing pivotal clinical trials and establishing acceptable endpoints for AML. Recent FDA guidance for drug and biological products development for AML outlines considerations for trial design. The guidance defines overall survival (OS) and event-free survival (EFS) as endpoints representing clinical benefit for AML therapies without curative intent. We highlight the EFS definition, particularly the assignment of day 1 as the event date for patients with induction treatment failures (ITFs), as recommended in the guidance. Through a comprehensive simulation study, our results show that the guidance EFS definition performs adequately with high complete remission (CR) rates but may pose challenges for low CR rates. When the experimental arm CR rate is 5% or less over the control, the use of the ITF events at day 1 for EFS definition leads to a critical power decrease, hampering the ability to predict survival benefit for a moderate OS duration. We further expand upon the EFS definition with the event date at ITF period end. Our goal is to inform investigators and regulatory agencies about the implications and limitations of various EFS definitions for future pivotal trials in AML.</p></div>","PeriodicalId":18051,"journal":{"name":"Leukemia research","volume":"138 ","pages":"Article 107465"},"PeriodicalIF":2.7,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139947489","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"KRAS mutations, autoimmunity and female sex in chronic myelomonocytic leukemia","authors":"Afaf E.G. Osman ,&nbsp;Anton Rets ,&nbsp;Ami B. Patel","doi":"10.1016/j.leukres.2024.107466","DOIUrl":"10.1016/j.leukres.2024.107466","url":null,"abstract":"","PeriodicalId":18051,"journal":{"name":"Leukemia research","volume":"138 ","pages":"Article 107466"},"PeriodicalIF":2.7,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139947513","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Clinical outcomes of patients with acute myeloid leukemia and cardiovascular disease","authors":"Gabriela Sanchez-Petitto ,&nbsp;Olga G. Goloubeva ,&nbsp;Jack Masur ,&nbsp;James Childress ,&nbsp;Tahreem Iqbal ,&nbsp;Max An ,&nbsp;Safwan Muhammad ,&nbsp;Justin Lawson ,&nbsp;Grace Li ,&nbsp;Brian Barr ,&nbsp;Ashkan Emadi ,&nbsp;Jennie Y. Law ,&nbsp;Seung Tae Lee ,&nbsp;Vu H. Duong ,&nbsp;Maria R. Baer ,&nbsp;Sandrine Niyongere","doi":"10.1016/j.leukres.2024.107456","DOIUrl":"10.1016/j.leukres.2024.107456","url":null,"abstract":"<div><p>Incidence of both acute myeloid leukemia (AML) and cardiovascular disease (CVD) increases with age. We evaluated whether pre-existing CVD impacts clinical outcomes in AML. We retrospectively evaluated 291 consecutive adult AML patients treated at our institution, 2014–2020. Pretreatment comorbidities were identified by chart review. Outcomes included complete remission (CR) and CR with incomplete count recovery (CRi) rates, disease-free survival (DFS), overall survival (OS) and incidence of cardiovascular adverse events. CVD was present in 34% of patients at AML diagnosis. CVD patients had worse performance status (p=0.03) and more commonly had secondary AML (p=0.03) and received hypomethylating (HMA) agent-based therapy (72% vs 38%, p&lt; 0.001). CVD (0.45 vs 0.71, p&lt;0.001) and diabetes mellitus (HR= 0.24, 95% CI: 0.08 – 0.8, p= 0.01) were associated with lower probability of achieving CR/CRi. Accounting for age, performance status (PS), complex karyotype, secondary disease and treatment, CVD patients had shorter OS (HR=1.5, 95% CI: 1.1–2.2, p=0.002), with 1- and 3-year OS 44% vs 67% and 25% vs 40%, respectively, but there was no difference in cumulative incidence of relapse between patients with vs without CVD. Thus, CVD is an independent risk factor for lower response rate and shorter survival in AML patients.</p></div>","PeriodicalId":18051,"journal":{"name":"Leukemia research","volume":"138 ","pages":"Article 107456"},"PeriodicalIF":2.7,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139928098","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}