Blood Cancer Journal最新文献

{"title":"Long-term outcomes of low-dose dasatinib in older patients with chronic myeloid leukemia in chronic phase: an extended follow-up of the DAVLEC phase 2 trial.","authors":"Hiroshi Ureshino, Kazunori Murai, Takashi Kumagai, Tatsuji Mino, Kaichi Nishiwaki, Satoshi Wakita, Tomoharu Takeoka, Masayuki Mita, Chikashi Yoshida, Nobuhiko Uoshima, Toshihiro Fukushima, Junya Kuroda, Takeshi Kondo, Masahiro Chiba, Takuya Miyazaki, Katsuhiro Io, Tomoaki Ueda, Takaaki Ono, Kensuke Usuki, Takahiro Yamauchi, Katsumichi Fujimaki, Takayuki Ikezoe, Atsushi Kawaguchi, Shinya Kimura","doi":"10.1038/s41408-026-01526-7","DOIUrl":"10.1038/s41408-026-01526-7","url":null,"abstract":"","PeriodicalId":8989,"journal":{"name":"Blood Cancer Journal","volume":"16 1","pages":""},"PeriodicalIF":13.8,"publicationDate":"2026-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13219402/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148052257","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":"Chronic myeloid leukemia: incorporation of recent advances into current treatment algorithms.","authors":"Fadi G Haddad, Hagop Kantarjian","doi":"10.1038/s41408-026-01527-6","DOIUrl":"10.1038/s41408-026-01527-6","url":null,"abstract":"<p><p>Several approved and investigational BCR::ABL1 tyrosine kinase inhibitors (TKIs) and STAMP inhibitors are used for the treatment of chronic myeloid leukemia in chronic phase (CML-CP). In the frontline setting, multiple factors affect selection of therapy including the goal of treatment, cost of TKIs, CML risk, and patient's comorbidities. Achieving a complete cytogenetic response (BCR::ABL1 transcripts on the International Scale [IS] <1%) with TKI therapy within the first year is associated with normalization of survival, whereas achieving a deeper molecular response (BCR::ABL1 transcripts < 0.01% [IS]) may allow for treatment discontinuation with the possibility of treatment-free remission. Although standard doses are approved for each TKI, post approval studies have demonstrated that an optimal biologic dose is safer than and as effective as the approved dose. In cases of TKI toxicities, reducing the dose rather than switching TKIs is recommended unless the patient experiences a prohibitive toxicity, in which case the treatment should be changed. In patients experiencing failure of frontline therapy due to resistance or intolerance, multiple second- and third-line options are available, including second-generation TKIs, ponatinib, and asciminib, as well as novel investigational agents, including the ABL1 kinase domain inhibitors olverembatinib and ELVN-001 and the STAMP inhibitors TGRX-678 and TERN-701. In this review, we discuss the recent advances in the treatment of CML-CP and challenge some established management practices.</p>","PeriodicalId":8989,"journal":{"name":"Blood Cancer Journal","volume":" ","pages":""},"PeriodicalIF":13.8,"publicationDate":"2026-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13402834/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148052283","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":"Ultra-high-sensitivity next-generation sequencing-based MRD predicts outcome in intensively treated older patients with acute myeloid leukemia: results from the ALFA-1200 cohort.","authors":"Augustin Boudry, Laurène Fenwarth, Raphaël Itzykson, Thorsten Braun, Lionel Adès, Élise Fournier, Céline Berthon, Delphine Lebon, Stéphane De Botton, Régis Peffault de Latour, Cécile Pautas, Hervé Dombret, Emmanuel Raffoux, Claude Gardin, Karine Celli-Lebras, Claude Preudhomme, Nicolas Duployez","doi":"10.1038/s41408-026-01530-x","DOIUrl":"10.1038/s41408-026-01530-x","url":null,"abstract":"","PeriodicalId":8989,"journal":{"name":"Blood Cancer Journal","volume":"16 1","pages":""},"PeriodicalIF":13.8,"publicationDate":"2026-05-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13219387/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148052254","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":"Gene- and subtype-dependent prognostic impact of ras pathway mutations in acute myeloid leukemia: a cohort study of 2,500 patients.","authors":"Heng Shen, Yan Hui, Yuntao Liu, Shouyun Li, Dong Lin, Qiuyun Fang, Ying Wang, Benfa Gong, Chunlin Zhou, Kaiqi Liu, Guangji Zhang, Xiaoyuan Gong, Shaowei Qiu, Bingcheng Liu, Ying Wang, Yingchang Mi, Yan Li, Jianxiang Wang, Hui Wei","doi":"10.1038/s41408-026-01532-9","DOIUrl":"10.1038/s41408-026-01532-9","url":null,"abstract":"","PeriodicalId":8989,"journal":{"name":"Blood Cancer Journal","volume":"16 1","pages":""},"PeriodicalIF":13.8,"publicationDate":"2026-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13216541/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148041151","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":"Prevalence of monoclonal gammopathy of undetermined significance (MGUS) using a sensitive mass spectrometry assay in young individuals 10-49 years of age: a population-based study from the National Health and Nutritional Examination Survey.","authors":"Shaji Kumar, David Murray, Dirk R Larson, Ola Landgren, P Leif Bergsagel, James R Cerhan, S Vincent Rajkumar","doi":"10.1038/s41408-026-01518-7","DOIUrl":"10.1038/s41408-026-01518-7","url":null,"abstract":"<p><p>The prevalence of monoclonal gammopathy of undetermined significance (MGUS) increases with age, but the study of age of onset and the prevalence of MGUS in younger individuals has been limited by lack of sensitive serum protein testing methods. In addition, there is marked racial disparity in the prevalence in Black individuals compared with White individuals and it is important to determine if MGUS has an earlier age of onset in Black individuals. In this first large mass spectrometry-based population-based screening study of MGUS, we evaluated 12,378 individuals (3598 White, 4075 Black, 4147 Mexican Americans, and 558 others) aged 10-49 years of age. The study used serum samples from the National Health and Nutritional Examination Survey (NHANES) III. MGUS was identified in 177 persons (1.28%, 95% CI 0.95, 1.60). MGUS was detectable in 0.2% of individuals age 10-19 years and the prevalence increased with age to 0.88%, 1.46%, and 2.82% in individuals ages 20-29, 30-39, and 40-49, respectively. The age-adjusted prevalence of MGUS was significantly higher in Black individuals compared with White individuals, 1.49% (1.13, 1.95) versus 0.82% (0.57, 1.18), P = < 0.01. MGUS had an earlier age of onset in Black individuals; the increased prevalence of MGUS among Black compared with White individuals was apparent at age 30-39 years, 2.94% vs 1.42%, and this disparity increased further in the age group 40-49 years to 5.2% vs 2.8%, respectively. There was no significant difference in the prevalence of MGUS between White individuals and Mexican American individuals in the overall cohort, or within any specific age group. The study using a highly sensitive mass spectrometry-based assay demonstrates onset of monoclonal gammopathy in the second decade of life, with a higher prevalence among the Black individuals with comparable prevalence among the White and Mexican individuals, a disparity that increases with advancing age.</p>","PeriodicalId":8989,"journal":{"name":"Blood Cancer Journal","volume":" ","pages":""},"PeriodicalIF":13.8,"publicationDate":"2026-05-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13291244/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148013315","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":"Clinical outcomes of CD3xCD20 bispecific antibodies in patients with central nervous system involvement by lymphoma.","authors":"Karan L Chohan, Rina L Welkie, James Godfrey, Steven Bair, Lorenzo Falchi, Manali Kamdar, Ajay Major, Wendy Dixon, Jennifer Crombie, Reid Merryman, Sonia Godbole, Gilles Salles, Omnia Farahat, Amy Ayers, Ayushi Chauhan, Alex Herrera, Geoffrey Shouse, Sairah Ahmed, Yazeed Sawalha","doi":"10.1038/s41408-026-01519-6","DOIUrl":"10.1038/s41408-026-01519-6","url":null,"abstract":"","PeriodicalId":8989,"journal":{"name":"Blood Cancer Journal","volume":"16 1","pages":""},"PeriodicalIF":13.8,"publicationDate":"2026-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13197401/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148004461","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":"CHIP clinics: a practical overview of structure and function.","authors":"Shyam A Patel, Abhishek A Mangaonkar","doi":"10.1038/s41408-026-01514-x","DOIUrl":"10.1038/s41408-026-01514-x","url":null,"abstract":"<p><p>Modern knowledge about the principles of clonal hematopoiesis of indeterminate potential (CHIP) has paved way for numerous clinical efforts aimed at managing this pre-malignant condition. The emergence of various CHIP clinics across the globe attests to collaborative attempts to formalize clinical management of CHIP and its entities. However, translational science in this field is limited to date, partly due to nascent therapeutic concepts with limited understanding of natural history and longitudinal follow up. Here, we explore the structure and function of existing CHIP clinics and propose a working model to materialize future CHIP clinics at academic and community health care systems. We discuss the critical elements in conceptualizing and operationalizing CHIP clinic workflows, including pinpointing unmet clinical needs, prospective and retrospective identification of patients with CHIP, and recruitment of key CHIP clinic personnel toward creation of an effective multidisciplinary team. We underscore the clinical utility of CHIP clinics with regard to value creation in preventive hematology, real-world risk assessment using evidence-based models, provision of clinical trial enrollment opportunities, establishment of curated research registries and tissue biorepositories, and development of community outreach efforts. Finally, we shed light onto prospects of continued multi-center participation in collaborative science related to emerging therapeutic options in CHIP. These concepts may have a favorable impact on previvorship in hematology in the coming years.</p>","PeriodicalId":8989,"journal":{"name":"Blood Cancer Journal","volume":" ","pages":""},"PeriodicalIF":13.8,"publicationDate":"2026-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13342069/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147939964","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":"Impaired iron balance and erythrocytosis: a complex relationship.","authors":"Benoît Gendrot, Carole Peyssonnaux, Isabelle Plo, Sophie Vaulont, Guillemette Fouquet","doi":"10.1038/s41408-026-01516-9","DOIUrl":"10.1038/s41408-026-01516-9","url":null,"abstract":"<p><p>Erythropoiesis and iron metabolism are closely interconnected, under both physiological and pathological conditions. Polycythemia vera (PV) is a myeloproliferative neoplasm (MPN) caused by a Janus kinase-2 (JAK2) mutation, resulting in uncontrolled red blood cell production and elevated hemoglobin and hematocrit levels. In PV, iron deficiency is common and may be due to several factors, including chronic gastrointestinal bleeding, chronic inflammation, dysregulated hepcidin signaling, and therapeutic phlebotomy. Many patients exhibit low serum ferritin and low to normal hepcidin levels despite erythroid proliferation, suggesting a maladaptive iron-restricted state. This functional iron deficiency may limit erythropoiesis to some extent, but also contributes to burdensome symptoms such as fatigue, cognitive impairment, and restless leg syndrome. Novel therapeutic approaches, including hepcidin mimetics or ferroportin inhibitors, aim to restore iron homeostasis, improving quality of life and potentially reducing the need for cytoreductive therapy (drugs used to treat MPNs by reducing blood cell production) in low-risk PV patients. In secondary forms of erythrocytosis (both congenital and acquired), iron homeostasis has been less often investigated. However, exploring it may be of great interest since in these affections, iron overload could act as a hidden driver of erythrocytosis by stimulating erythroblast proliferation. Hereditary hemochromatosis (HH) is a well-known cause of iron overload. While its association with erythrocytosis has been a subject of interest, it remains incompletely understood. In this review, we will explore the complex relationship between iron (deficiency or overload, including HH) and erythrocytosis (including PV), discussing underlying mechanisms and potential therapeutic applications.</p>","PeriodicalId":8989,"journal":{"name":"Blood Cancer Journal","volume":" ","pages":""},"PeriodicalIF":13.8,"publicationDate":"2026-05-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13338261/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147926164","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":"The clinical relevance of sole loss of chromosome Y in myeloid neoplasms.","authors":"Sandra Huber, Stephan Hutter, Manja Meggendorfer, Christian Pohlkamp, Torsten Haferlach, Isolde Summerer","doi":"10.1038/s41408-026-01515-w","DOIUrl":"10.1038/s41408-026-01515-w","url":null,"abstract":"","PeriodicalId":8989,"journal":{"name":"Blood Cancer Journal","volume":"16 1","pages":""},"PeriodicalIF":13.8,"publicationDate":"2026-05-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13157478/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147863493","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":"Docirbrutinib is a pan-mutant BTK inhibitor and inhibits B-cell receptor signaling in chronic lymphocytic leukemia cells in preclinical and early clinical investigations.","authors":"Natalia Timofeeva, Breana Herrera, Hitomi Fujiwara, Tokiko Asami, Hiroko Endo, Mariko Hatakeyama, Fumio Nakajima, Hiroshi Ohmoto, Yu Nishioka, Kyoko Miyamoto, Akinori Arimura, Shady I Tantawy, Javier Pinilla-Ibarz, Catherine C Coombs, Nitin Jain, Masaaki Sawa, Varsha Gandhi","doi":"10.1038/s41408-026-01509-8","DOIUrl":"10.1038/s41408-026-01509-8","url":null,"abstract":"<p><p>BTK inhibitors (BTKi) have become standard of care for treatment of patients with chronic lymphocytic leukemia (CLL). Covalent BTKi (cBTKi) such as ibrutinib, acalabrutinib, and zanubrutinib are effective but alterations in the kinase domain at C481 or BTK gatekeeper residue T474 mutations result in development of resistance. Noncovalent BTK inhibitors (ncBTKi) such as pirtobrutinib are effective in patients with C481x mutations developed through use of cBTKi. However, resistance to ncBTKi can occur owing to second site aberrations in BTK, generating novel mutations such as L528x and T316x. Sometimes, CLL cells with double BTK mutations are also observed. These BTK aberrations underscore a need for new inhibitors that target pan-BTK-mutants. We evaluated the efficacy of a new ncBTKi, docirbrutinib (AS-1763), against 14 BTK mutants, including C481S, T474x, and L528x, as well as gatekeeper and kinase domain double mutants, using biochemical assays, cell-line models, and primary CLL lymphocytes. Docirbrutinib potently inhibited BTK autophosphorylation and mutant BTK-driven cell proliferation, with greater effects than ibrutinib and pirtobrutinib against certain mutants. In treatment-naïve and relapsed/refractory CLL samples, docirbrutinib disrupted B-cell receptor signaling and sensitized cells to apoptosis induced by venetoclax and AZD5991. In a dose-escalation trial (NCT05602363), docirbrutinib decreased CCL3/CCL4 biomarkers and inhibited the B-cell receptor pathway signaling in longitudinal samples from patients with relapsed/refractory CLL. These findings establish docirbrutinib as a pan-mutant ncBTKi with potential to improve outcomes for CLL patients, including those with disease resistant to cBTKi and other ncBTKi.</p>","PeriodicalId":8989,"journal":{"name":"Blood Cancer Journal","volume":" ","pages":""},"PeriodicalIF":13.8,"publicationDate":"2026-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13319122/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147833067","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}