bims-hemali Biomed News
on Hematologic malignancies
Issue of 2026–09–13
fifteen papers selected by
Alexandros Alexandropoulos, Γενικό Νοσοκομείο Αθηνών Λαϊκό
  1. Road to treatment-free remission in chronic myeloid leukemia.
  2. Flow Cytometry Assessment of CD26+ Leukemic Stem Cells in Chronic Myeloid Leukemia.
  3. Treatment-Free Remission in Chronic Myeloid Leukemia: Toward Precision and Personalized Approaches to Functional Cure.
  4. Revisiting Asciminib Resistance: From Binding Affinity to Allosteric Disruption in BCR::ABL1 Leukemias.
  5. First line asciminib in chronic myeloid leukemia: a quest for the "Holy Grail" of tolerability.
  6. Durable CNS remission with elranatamab and intrathecal therapy in relapsed/refractory multiple myeloma.
  7. CPX-351 in combination with ruxolitinib for advanced-phase myeloproliferative neoplasms: results of a phase 1 study.
  8. Peripheral CD8⁺ T-cell clonality and NK-cell expansion mark early response to mosunetuzumab in indolent B-cell lymphoma.
  9. Successful desensitization to bosutinib in chronic myeloid leukemia.
  10. Chemotherapy-free regimens for Richter transformation: a bridge, but not yet a destination.
  11. Age, anthracycline and mortality in 28,000 classic Hodgkin lymphoma patients: cohort study of a complete population.
  12. Induction and extended consolidation with daratumumab, cyclophosphamide, bortezomib, lenalidomide, and dexamethasone in patients with high-risk multiple myeloma (OPTIMUM/MUKnine): 5-year follow-up of a multicentre, externally controlled, phase 2 trial.
  13. Efficacy and safety of mitapivat in adults with transfusion-dependent α-thalassaemia or β-thalassaemia (ENERGIZE-T): a double-blind, randomised, multicentre, placebo-controlled, phase 3 trial.
  14. WNK1: an atypical kinase vulnerability in T-ALL.
  15. Does it really have to hurt? All-oral treatment for acute myeloid leukemia.
  1. Int J Hematol. 2026 Sep 11.
    Road to treatment-free remission in chronic myeloid leukemia.
    Hiroshi Ureshino.
      The development of BCR::ABL1 tyrosine kinase inhibitors (TKIs) has transformed chronic myeloid leukemia into a chronic disease with near-normal life expectancy. More recently, treatment-free remission (TFR), defined as sustained molecular remission even after TKI discontinuation, has emerged as a realistic therapeutic goal and a type of functional cure. Landmark studies, including STIM1, A-STIM, EURO-SKI, ENESTfreedom, DADI, and J-SKI, have established the feasibility and safety of TFR. Their results showed that approximately half of eligible patients can successfully discontinue therapy. However, the reliable prediction of TFR success remains a major challenge. Accumulating evidence indicates that durable TFR reflects a dynamic equilibrium between residual leukemic stem cells (LSCs) and host immune surveillance. Natural killer cells and T-cell immunity contribute to maintaining remission after TKI discontinuation. Conversely, immune exhaustion and the persistence of LSCs are associated with molecular relapse. Emerging biomarkers, including immune profiling, immunogenetic markers, and minimal residual disease kinetics, may improve relapse-risk stratification. To increase the proportion of patients who achieve durable TFR, future efforts should focus on the development of risk-adapted consolidation strategies incorporating optimized TKI therapy, immune modulation, and LSC-targeted approaches.
    Keywords:  Chronic myeloid leukemia; Immune surveillance; Leukemic stem cells; Treatment-free remission; Tyrosine kinase inhibitors
    DOI:  https://doi.org/10.1007/s12185-026-04278-z
  2. Indian J Hematol Blood Transfus. 2026 Sep;42(5): 1674-1680
    Flow Cytometry Assessment of CD26+ Leukemic Stem Cells in Chronic Myeloid Leukemia.
    Sarjana, Jasmita Dass, Ganesh Kumar Vishwanathan, Manoranjan Mahapatra.
      Flow cytometry based assessment of CD26+ leukemic stem cells (LSCs), a recently described diagnostic marker, has emerged as a promising tool for diagnosis of chronic myeloid leukemia (CML). In this prospective observational study, peripheral blood samples from suspected CML patients were evaluated by flow cytometry to assess the expression of CD26 on stem cell compartment (CD45+CD34+CD38-).Molecular confirmation of diagnosis was done by RT-PCR for BCR::ABL1 transcript. Patients initiated on tyrosine kinase inhibitors(TKIs) were followed upto twelve months to evaluate the kinetics of CD26+ LSCs. Out of the eighty six cases enrolled, CD26 expression was detectable in seventy five cases. All these seventy five cases were confirmed positive for BCR::ABL1 transcript by RT-qPCR. Eleven cases lacking CD26 expression were uniformally negative for BCR::ABL1.There was no significant correlation of the CD26 levels with age, sex, percentage of blasts, total leucocyte count, basophils, Sokal score or ELTS score. At twelve months, seven patients achieved major molecular response; of these two became negative for CD26+ LSCs, while five demonstrated a non significant decline. Flow cytometric assessment of CD26+ LSCs is a rapid, cost effective and robust diagnostic tool for diagnosis of CML. Monitoring CD26+ LSC kinetics during TKI therapy may provide a surrogate marker for monitoring response, warranting validation in larger cohorts.
    Supplementary Information: The online version contains supplementary material available at https://doi.org/10.1007/s12288-025-02182-w.
    Keywords:  CD26; CML; Leukemic stem cells
    DOI:  https://doi.org/10.1007/s12288-025-02182-w
  3. Cancer Sci. 2026 Sep 06.
    Treatment-Free Remission in Chronic Myeloid Leukemia: Toward Precision and Personalized Approaches to Functional Cure.
    Hiroshi Ureshino, Shinya Kimura.
      Treatment-free remission (TFR), defined as the maintenance of molecular remission without resumption of therapy after tyrosine kinase inhibitor (TKI) discontinuation, represents the clinical manifestation of functional cure in chronic-phase chronic myeloid leukemia (CML-CP), in which durable disease control is maintained without ongoing therapy despite the potential persistence of residual leukemic stem cells (LSCs). Emerging evidence supports a model in which outcomes after TKI discontinuation are determined by the balance between residual LSC persistence and coordinated host immune surveillance. Natural killer (NK)-cell abundance and maturation have shown the most consistent associations with TFR, while killer immunoglobulin-like receptor (KIR)-human leukocyte antigen (HLA) immunogenetics may further influence NK-cell education and antileukemic activity. Adaptive and regulatory mechanisms-including leukemia-associated antigen-specific cytotoxic T lymphocytes, T-cell receptor repertoire dynamics, T-cell exhaustion, plasmacytoid dendritic cells, and regulatory T cells-are increasingly implicated in residual disease control. Neutrophil abundance and maturation have also emerged as readily accessible candidate biomarkers. In parallel, persistent LSCs exploit BCR::ABL1-independent survival programs, immune-evasion mechanisms, and the protective bone marrow niche, providing a reservoir for molecular relapse. These observations argue against reliance on any single biomarker and instead support integrated models incorporating clinical variables, molecular residual disease, immune competence, immunogenetics, and LSC biology. Most candidate biomarkers remain exploratory and require independent prospective validation. Such multidimensional approaches may enable a transition from empiric TKI discontinuation toward precision, biomarker-guided TFR and extend durable functional cure to a broader population of patients with CML. Trail Registration: N/A.
    Keywords:  chronic myeloid leukemia; leukemic stem cells; natural killer cells; treatment‐free remission; tyrosine kinase inhibitor
    DOI:  https://doi.org/10.1111/cas.70532
  4. Turk J Haematol. 2026 Sep 08.
    Revisiting Asciminib Resistance: From Binding Affinity to Allosteric Disruption in BCR::ABL1 Leukemias.
    Müge Sayitoğlu, Yücel Erbilgin, İbrahim C Haznedaroğlu.
      Tyrosine kinase inhibitors (TKIs) have reshaped the treatment of BCR::ABL1 positive leukemias. The first-in-class STAMP (Specifically Targeting the ABL Myristoyl Pocket) inhibitor, asciminib introduces a distinct therapeutic paradigm by targeting the myristoyl pocket and avoids direct competition with ATP. However, resistance to asciminib has been reported in 4-10% of chronic myeloid leukemia (CML) cases. Asciminib resistance is predominantly driven by impaired allosteric regulations: 1) Expanded spectrum of kinase domain mutations "pre-activate" the kinase and confer resistance despite retained drug affinity; 2) Intrinsic primary resistance, from b2(e13)a3 and b3(e14)a3 transcript variants; and 3) Isoform-specific (p190 vs. p210) resistance, with common Ploop mutations exhibit greater resistance in p190 than in p210. This paradigm shift from an "affinity" problem to an "allostery" problem necessitates a corresponding evolution in clinical and laboratory practice. This includes expanding mutational screening, incorporating pre-treatment screening of the BCR::ABL1 isoforms, and transcript types to appropriately guide therapeutic selection.
    Keywords:  Allosteric Disruption; Asciminib; BCR::ABL1; Chronic Myeloid Leukemia (CML); Drug Resistance; STAMP Inhibitor
    DOI:  https://doi.org/10.4274/tjh.galenos.2026.86383
  5. Haematologica. 2026 Sep 10.
    First line asciminib in chronic myeloid leukemia: a quest for the "Holy Grail" of tolerability.
    Delphine Rea.
      Not available.
    DOI:  https://doi.org/10.3324/haematol.2026.301753
  6. Ann Hematol. 2026 Aug 07. pii: 408. [Epub ahead of print]105(9):
    Durable CNS remission with elranatamab and intrathecal therapy in relapsed/refractory multiple myeloma.
    Sinan Mersin, Ömür Gökmen Sevindik.
      Central nervous system (CNS) involvement in multiple myeloma (MM) is a rare but devastating complication associated with poor prognosis and limited therapeutic options. We report a 73-year-old woman with high-risk IgG kappa MM harboring TP53 [del(17p)] and 13q deletion who developed extramedullary and CNS disease after six prior lines of therapy, including two autologous stem cell transplants, and was triple-class refractory to proteasome inhibitors, immunomodulatory agents, and anti-CD38 monoclonal antibodies. At CNS relapse, cerebrospinal fluid (CSF) cytology demonstrated abundant atypical and binucleated plasma cells, and MRI showed diffuse leptomeningeal enhancement. Elranatamab was initiated using a standard step-up dosing schedule, combined with intrathecal methotrexate and dexamethasone. Within two months, MRI showed complete resolution of leptomeningeal disease and CSF became acellular. Systemic evaluation confirmed a complete response by IMWG criteria, with normalization of serum immunofixation, protein electrophoresis, and free light chains. No cytokine release syndrome or neurotoxicity was observed. The remission has been sustained and remains ongoing at 18 months. This case suggests that BCMA-targeted bispecific antibodies, combined with CNS-directed therapy, may induce deep and durable CNS remission in heavily pretreated MM, and supports further investigation of bispecific antibodies in CNS-involved myeloma.
    Keywords:  BCMA; Bispecific antibody; Central nervous system; Elranatamab; Leptomeningeal disease; Multiple myeloma
    DOI:  https://doi.org/10.1007/s00277-026-07226-3
  7. Blood Neoplasia. 2026 Nov;3(4): 100274
    CPX-351 in combination with ruxolitinib for advanced-phase myeloproliferative neoplasms: results of a phase 1 study.
    Shivani Handa, Yazan Madanat, Kelly Pugh, Kaitlyn Dvorak-Kornaus, Qiuhong Zhao, Alice Mims, Kristin Koenig, Andrew Srisuwananukorn, Rachel Cook, Ronan Swords, Uma Borate.
      
    DOI:  https://doi.org/10.1016/j.bneo.2026.100274
  8. Blood Adv. 2026 Sep 10. pii: bloodadvances.2026021450. [Epub ahead of print]
    Peripheral CD8⁺ T-cell clonality and NK-cell expansion mark early response to mosunetuzumab in indolent B-cell lymphoma.
    Charles J Milrod, Anna Dorota Chorzalska, Dennis M Bonal, John Morgan, Makayla Pardo, Thomas A Ollila, Ari Pelcovits, Christina Raker, Diana Olguta Treaba, Jessica McMahon, Stephen Donnelly, Caylee Carmody, Jeannine Margolis, Matthew J Matasar, Scott F Huntington, Patrycja M Dubielecka, Adam J Olszewski.
      Mosunetuzumab is highly effective against many B-cell lymphomas, but longitudinal immune changes induced by intermittently dosed CD20×CD3 bispecific antibodies remain incompletely characterized. We performed immune profiling of peripheral blood samples from patients receiving fixed-duration (6 months) subcutaneous mosunetuzumab for previously untreated follicular or marginal zone lymphoma on a phase 2 clinical trial (NCT04792502). Analyses included flow cytometry, cytokine profiling, and RNA-seq of isolated CD8+ T-cells with TCR repertoire inference. Early (at 3 weeks) on-treatment samples showed broad cytokine induction, CD8+ T-cell redistribution with decreased TEMRA cells and increased CD27+CD62L+ transitional effector memory-like cells, increased PD-1 and LAG-3 expression, and induction of CD8+ transcriptional programs consistent with activation, proliferation, exhaustion priming, and SREBF2-regulated cholesterol metabolism. By mid-treatment (at 3 months), activation-associated features contracted toward baseline, with no evidence of phenotypic exhaustion, though with persistent overexpression of LAG3, HAVCR2, and LAYN on RNA-seq, as well as sustained SREBF2 activation. CD8+ T-cell clonality increased at mid-treatment compared with baseline and higher clonality was associated with early clinical complete response. Mosunetuzumab also induced indirect NK-cell activation and expansion, including skewing toward CD56dimCD16bright effector state. HLA-DR upregulation on NK cells correlated with early increases in NK-activating plasma cytokines, and higher NK-cell count at mid-treatment was associated with complete response. Together, these findings define a CD8+ effector-remodeling state on mosunetuzumab therapy, characterized by clonal expansion, selective inhibitory receptor expression, sustained activation of cholesterol biosynthesis, and cytokine-linked engagement of innate immune mechanisms, providing a framework for potential strategies to support T-cell function and enhance bispecific antibody efficacy.
    DOI:  https://doi.org/10.1182/bloodadvances.2026021450
  9. Leuk Res Rep. 2026 ;26 100603
    Successful desensitization to bosutinib in chronic myeloid leukemia.
    Catarina Guedes, Ricardo Geraldes, Sara Regalo, Margarida Alves, João Lopes, Ana Todo-Bom, Carmelita Ribeiro.
      Hypersensitivity reactions (HSRs) to antineoplastic agents may compromise optimal cancer treatment and lead to drug discontinuation. Although tyrosine kinase inhibitors (TKIs) are generally well tolerated, HSRs can occur, and standardized diagnostic and desensitization strategies are lacking. We report a 69-year-old woman with chronic myeloid leukemia who developed facial and oropharyngeal angioedema nine days after starting bosutinib. Symptoms resolved after drug withdrawal, with no alternative trigger identified. As no other TKIs were tolerated and continued therapy was essential for disease control, a rapid drug desensitization protocol was designed. A 14-step, single-day inpatient protocol with incremental dosing was completed without adverse reactions. Bosutinib was then reintroduced through short stepwise dose escalation and maintained at the full therapeutic dose. After one year, the patient remains asymptomatic, without recurrence of angioedema, and with sustained hematologic control. This is the first published desensitization protocol for bosutinib, enabling continuation of first-line therapy.
    Keywords:  Chronic myeloid leukemia; Drug desensitization; Hypersensitivity reactions; Tyrosine kinase inhibitors
    DOI:  https://doi.org/10.1016/j.lrr.2026.100603
  10. Haematologica. 2026 Sep 10.
    Chemotherapy-free regimens for Richter transformation: a bridge, but not yet a destination.
    Hannah Goulart, Matthew S Davids, Nitin Jain.
      Not available.
    DOI:  https://doi.org/10.3324/haematol.2026.301437
  11. Haematologica. 2026 Sep 10.
    Age, anthracycline and mortality in 28,000 classic Hodgkin lymphoma patients: cohort study of a complete population.
    Aisling Barrett, Zhe Wang, Paul McGale, John Broggio, Andrew Challenger, David Jones, Kavya Kayiparambil Harish, Lorna Roden, Graham P Collins, Sarah Darby, David J Cutter.
      Classic Hodgkin lymphoma (CHL) has an excellent prognosis in younger patients but outcomes are poorer in those aged ≥60 years at diagnosis. We used routinely collected English data to assess baseline characteristics, survival and treatment approaches in 28 175 patients with CHL registered between 1997 and 2020 with a particular focus on 1 958 patients aged 60 to 79 years at diagnosis with known first-line chemotherapy regimens. Mortality rates (all causes, lymphoma-specific and other causes) were calculated first without and then with adjustment for available characteristics to identify factors associated with survival. Survival outcomes for younger patients were better than older (p.
    DOI:  https://doi.org/10.3324/haematol.2026.301079
  12. Lancet Oncol. 2026 Sep 07. pii: S1470-2045(26)00286-X. [Epub ahead of print]
    Induction and extended consolidation with daratumumab, cyclophosphamide, bortezomib, lenalidomide, and dexamethasone in patients with high-risk multiple myeloma (OPTIMUM/MUKnine): 5-year follow-up of a multicentre, externally controlled, phase 2 trial.
    Martin F Kaiser, Rachel H Phillip, Sarah R Brown, Amy Holroyd, Elsa Ferris, Ruth M de Tute, Sadie Roberts, Laura Clayton, Kristian Bowles, Mamta Garg, Anand Lokare, Christina Messiou, Richard S Houlston, Graham Jackson, Gordon Cook, Roger G Owen, Mark T Drayson, Guy Pratt, Andrew Hall, Matthew W Jenner.
       BACKGROUND: High-risk multiple myeloma, defined by two or more high-risk cytogenetic abnormalities (HRCAs), high-risk gene expression profiling (GEP), or plasma cell leukaemia, remains associated with poor long-term outcomes despite quadruplet induction therapy. OPTIMUM showed that intensified induction, extended consolidation, and maintenance therapy after autologous stem-cell transplantation (ASCT) improved progression-free survival for patients with high-risk multiple myeloma. Here we report the 5-year follow-up of survival outcomes across molecular subgroups.
    METHODS: The multicentre, externally controlled, phase 2 OPTIMUM trial was conducted at 22 centres in the UK and enrolled patients aged 18 or older with newly diagnosed high-risk multiple myeloma or plasma cell leukaemia, measurable disease according to IMWG criteria, up to two previous induction cycles, and an Eastern Cooperative Oncology Group Performance Status of 2 or less. Participants received intravenous or subcutaneous daratumumab, oral cyclophosphamide, subcutaneous bortezomib, oral lenalidomide, and oral or intravenous dexamethasone induction at protocol specified doses before and after ASCT; melphalan-bortezomib during ASCT; consolidation part 1: daratumumab, bortezomib, lenalidomide, and dexamethasone; consolidation part 2: bortezomib, lenalidomide, and daratumumab; and maintenance lenalidomide and daratumumab until disease progression, unacceptable toxicity, or withdrawal. The trial used a Bayesian design and activity of treatment was compared with a molecularly matched external control cohort from the Myeloma XI trial. The primary endpoint was 18-month progression-free survival and has been previously reported. In this analysis, we report progression-free survival, progression-free survival 2 (time from registration until second disease progression or death, whichever occurred first), and overall survival at 5 years follow-up; and subgroup analyses by high-risk multiple myeloma features at entry (≥2 HRCAs, high-risk GEP, ≥2 HRCAs and high-risk GEP; and plasma cell leukaemia; subgroups selected post-hoc). OPTIMUM was registered with ClinicalTrials.gov (NCT03188172; active [not recruiting], with ongoing follow-up and maintenance).
    FINDINGS: Between Sept 29, 2017, and Sept 24, 2019, 108 participants with high-risk multiple myeloma were recruited to OPTIMUM and 107 were included in the analysis, with 120 genetically matched patients from the Myeloma XI trial (external control). Median follow-up was 71·1 months (IQR 66·9-77·7) for OPTIMUM and 117·8 months (98·3-128·6) for Myeloma XI. Progression-free survival (not reached [NR; 70·6-NR] vs 24·4 months [19·7-30·4]; HR 0·32 [95% CI 0·22-0·45]; p<0·0001) and overall survival (NR [NR-NR] vs 57·4 months [47·3-74·2]; HR 0·43 [95% CI 0·28-0·65]; p<0·0001) was longer in OPTIMUM than in Myeloma XI. Median progression-free survival 2 was NR (NR-NR) in OPTIMUM and 43·9 months (38·3-51·5) in Myeloma XI (HR 0·26 [95% CI 0·17-0·41]; p<0·0001). The survival benefit was consistent across high-risk multiple myeloma subgroups, except for patients with three or more HRCAs.
    INTERPRETATION: OPTIMUM shows sustained progression-free survival and overall survival improvement with risk-stratified extended therapy, supporting implementation of molecular diagnostics and tailored treatment in patients with newly diagnosed high-risk multiple myeloma.
    FUNDING: Myeloma UK, BMS, and Johnson & Johnson.
    DOI:  https://doi.org/10.1016/S1470-2045(26)00286-X
  13. Lancet. 2026 Sep 12. pii: S0140-6736(26)00874-3. [Epub ahead of print]408(10559): 1010-1018
    Efficacy and safety of mitapivat in adults with transfusion-dependent α-thalassaemia or β-thalassaemia (ENERGIZE-T): a double-blind, randomised, multicentre, placebo-controlled, phase 3 trial.
    ENERGIZE-T Investigators
       BACKGROUND: The absence of disease-modifying therapies for patients with α-thalassaemia and oral disease-modifying therapies for patients with β-thalassaemia has been a substantial unmet need in these patients. We assessed the efficacy and safety of mitapivat, an oral allosteric activator of pyruvate kinase, in adults with transfusion-dependent thalassaemia.
    METHODS: ENERGIZE-T is a global, double-blind, randomised, placebo-controlled, phase 3 trial, conducted across 19 countries in North America, Europe, Asia-Pacific, South America, and the Middle East. Patients aged 18 years or older with transfusion-dependent α-thalassaemia or β-thalassaemia were randomly allocated (2:1) with a central interactive response technology system, stratified by geographical region and thalassaemia genotype, to receive 100 mg mitapivat or placebo orally twice a day for 48 weeks. The primary endpoint was transfusion reduction response (TRR), defined as a reduction of at least 50% in transfused red blood cell units with a reduction of at least two units in any consecutive 12-week period until week 48 compared with baseline. Efficacy was analysed in the full analysis set, comprising all randomly allocated patients. Type, severity, and relationship of adverse events and serious adverse events were assessed in patients who received at least one dose of study treatment. This study is registered with ClinicalTrials.gov (NCT04770779) and is active but not recruiting.
    FINDINGS: Between Nov 30, 2021 and May 2, 2023, 305 patients were screened, of whom 258 were randomly allocated (median age 33·5 years [IQR 27·0-44·0]; 136 [53%] female and 122 [47%] male participants). Of 258 patients allocated, 238 (92%) completed the double-blind treatment period. All patients were required to have a safety follow-up approximately 4 weeks after the final dose of study drug, regardless of completion of the double-blind period or continuation into the open-label extension period. In the full analysis set, TRRs occurred in 52 (30%) of 171 patients in the mitapivat group and 11 (13%) of 87 in the placebo group (adjusted difference 18 percentage points [95% CI 8-27]; two-sided p=0·0003). The safety analysis set comprised 172 patients in the mitapivat group (including one patient allocated to the placebo group who received one dose of mitapivat in error) and 85 in the placebo group. Adverse events were reported in 155 (90%) patients treated with mitapivat and 71 (84%) treated with placebo; the most common events with mitapivat were headache, upper respiratory tract infection, initial insomnia, diarrhoea, and fatigue. Serious adverse events were reported in 19 (11%) patients treated with mitapivat and 13 (15%) treated with placebo. Ten (6%) patients who received mitapivat and one (1%) who received placebo discontinued study treatment due to adverse events. No deaths were reported.
    INTERPRETATION: Mitapivat significantly reduced the transfusion burden and was generally well tolerated, showing a favourable benefit-risk profile. These findings support mitapivat as the first oral disease-modifying therapy for adults with transfusion-dependent α-thalassaemia or β-thalassaemia, providing a new treatment option to reduce transfusion burden in this patient population.
    FUNDING: Agios Pharmaceuticals, Inc.
    DOI:  https://doi.org/10.1016/S0140-6736(26)00874-3
  14. Blood. 2026 Sep 10. 148(11): 1369-1371
    WNK1: an atypical kinase vulnerability in T-ALL.
    Cristina Borin, Panagiotis Ntziachristos.
      
    DOI:  https://doi.org/10.1182/blood.2026034652
  15. Haematologica. 2026 Sep 10.
    Does it really have to hurt? All-oral treatment for acute myeloid leukemia.
    Christoph Rummelt, Michael Lübbert.
      Not available.
    DOI:  https://doi.org/10.3324/haematol.2026.301795
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