bims-hemali Biomed News
on Hematologic malignancies
Issue of 2026–07–12
fourteen papers selected by
Alexandros Alexandropoulos, Γενικό Νοσοκομείο Αθηνών Λαϊκό



  1. Blood Adv. 2026 Jul 10. pii: bloodadvances.2025017565. [Epub ahead of print]
      In EPCORE® NHL-1 (NCT03625037), the CD3×CD20 bispecific antibody epcoritamab demonstrated promising efficacy and manageable safety in patients with relapsed/refractory (R/R) follicular lymphoma (FL) after ≥2 prior lines of therapy. Using the clonoSEQ® assay, we evaluated minimal residual disease (MRD) status using peripheral blood mononuclear cells (PBMCs) and/or circulating tumor DNA (ctDNA) at prespecified time points and investigated correlation with clinical outcomes. Epcoritamab induced rapid conversion to MRD-negativity, with most MRD-evaluable patients reaching MRD-negativity by cycle (C) 3 day (D) 1 as measured by either analyte. MRD-negativity at C3D1 landmark by either analyte correlated with prolonged progression-free survival (PFS; median not reached) irrespective of radiographic response status. PFS was comparable among patients with overall MRD-negativity by PBMCs or ctDNA, regardless of challenging-to-treat disease features. By C3D1 and C5D1 landmarks, patients with complete or partial response as assessed by positron emission tomography/computed tomography (PET/CT) who were MRD-positive had a shorter PFS compared with those who were MRD-negative. In multivariable analyses at week 12 and week 18 PET/CT landmarks, MRD-negative responders by PBMC assessment (week 12) and by both PBMC and ctDNA assessment (week 18) had significantly improved PFS when adjusted for baseline clinical risk factors. These analyses demonstrate that MRD-negativity is associated with rapid molecular responses to epcoritamab and prolonged PFS in patients with R/R FL, underscoring the value of MRD analysis to complement conventional response assessment. These findings may aid future clinical trial design or clinical practices in FL.
    DOI:  https://doi.org/10.1182/bloodadvances.2025017565
  2. Lancet. 2026 Jul 09. pii: S0140-6736(26)01204-3. [Epub ahead of print]
       BACKGROUND: Venetoclax-rituximab (VR) following covalent Bruton tyrosine kinase (BTK) inhibitor therapy is the fixed-duration standard of care for patients with chronic lymphocytic leukaemia (including small lymphocytic lymphoma). Pirtobrutinib, a non-covalent BTK inhibitor, is approved for use after treatment with a covalent BTK inhibitor as a continuous therapy option. We aimed to evaluate the addition of pirtobrutinib to VR as a fixed-duration regimen in patients with relapsed or refractory chronic lymphocytic leukaemia.
    METHODS: This open-label, multicentre, randomised, controlled, phase 3 trial was conducted at 152 sites (comprising community hospitals and academic centres) across 22 countries. Eligible patients were aged 18 years or older, had a confirmed diagnosis of chronic lymphocytic leukaemia (including small lymphocytic lymphoma), and had previously been treated with at least one line of therapy that could include a covalent BTK inhibitor. Patients who had previously received a non-covalent BTK inhibitor, venetoclax, or another BCL2 inhibitor were not eligible. Enrolled patients were randomly assigned (1:1) using an interactive web-based randomisation system, stratified by del(17p) status and previous exposure to covalent BTK inhibitors, and assigned to receive either pirtobrutinib plus VR (PVR) or VR. Both groups received oral venetoclax (25 cycles) and intravenous rituximab (six cycles); the PVR group also received oral pirtobrutinib for 28 cycles, with a three-cycle pirtobrutinib-rituximab lead-in before venetoclax initiation. For this prespecified interim analysis, the primary endpoint was progression-free survival in the intention-to-treat population, assessed by a masked independent review committee (IRC) as per 2018 International Workshop on Chronic Lymphocytic Leukemia guidelines. Safety analyses were conducted in the safety population, defined as all randomly assigned patients who took at least one dose of any study treatment. All analyses were based on a data cutoff date of Feb 2, 2026. The trial is registered at ClinicalTrials.gov, NCT04965493, and is ongoing but no longer recruiting.
    FINDINGS: Between Oct 13, 2021, and Oct 28, 2024, 784 patients were screened, of whom 639 were randomly assigned: 321 to the PVR group and 318 to the VR group. The median age of patients was 68·0 years (IQR 60·0-74·0), of whom 439 (69%) were male and 200 (31%) were female. The median number of previous therapies was 2 (IQR 1-3); 510 (80%) of 639 patients had previous exposure to covalent BTK inhibitors, of whom 362 (71%) discontinued their most recent drug of this class owing to progressive disease. At a median follow-up of 27·3 months (IQR 19·5-38·7), PVR showed a significant improvement in IRC-assessed progression-free survival compared with VR (hazard ratio 0·547 [95% CI 0·400-0·748]; p=0·0001). The median 24-month progression-free survival rate was 87% (95% CI 82·3-90·4) in the PVR group versus 72% (65·7-77·0) in the VR group, and the median progression-free survival was not reached (IQR 31·7-not estimable) in the PVR group versus 39·7 months (21·5-50·0) in the VR group. This benefit was consistent across prespecified subgroups, including patients with previous exposure to covalent BTK inhibitors. The most frequent treatment-emergent adverse event of any grade in both groups was diarrhoea, reported in 106 (34%) of 316 patients in the PVR group and 110 (35%) of 311 patients in the VR group. The frequency of treatment-emergent adverse events of grade 3 or higher was similar in both groups (249 [79%] of 316 patients in the PVR group vs 227 [73%] of 311 patients in the VR group); the rate of tumour lysis syndrome of grade 3 or higher was lower in the PVR group (1%; three of 316) than in the VR group (4%; 12 of 311). Rates of atrial fibrillation or flutter of any grade were low (11 [3%] of 316 patients in the PVR group vs eight [3%] of 311 patients in the VR group). Rates of treatment discontinuation owing to treatment-emergent adverse events deemed as related to any of the study drugs were similar: 5% (17 of 316 patients) in the PVR group versus 5% (16 of 311 patients) in the VR group. There were five treatment-related deaths: one in the PVR group and four in the VR group.
    INTERPRETATION: In patients with previously treated chronic lymphocytic leukaemia, PVR showed significant improvement in progression-free survival compared with VR, with consistent results in patients who had previously received covalent BTK inhibitors and no new safety signals. To our knowledge, these results represent the first randomised phase 3 evidence comparing a novel fixed-duration regimen to the current standard of VR in relapsed or refractory chronic lymphocytic leukaemia, supporting PVR as a potential new standard of care.
    FUNDING: Eli Lilly and Company.
    DOI:  https://doi.org/10.1016/S0140-6736(26)01204-3
  3. J Clin Oncol. 2026 Jul 06. JCO2502849
       PURPOSE: Patients with relapsed or refractory (R/R) diffuse large B-cell lymphoma (DLBCL) face an unfavorable prognosis once first-line treatment fails; therefore, there is an unmet need for new treatment options. We evaluated the efficacy and safety of polatuzumab vedotin plus rituximab, gemcitabine, and oxaliplatin (Pola-R-GemOx) as an alternative therapy in patients with transplant-ineligible R/R DLBCL.
    METHODS: The phase III POLARGO trial was a randomized, open-label, global study. Following a Pola-R-GemOx safety run-in (n = 15), patients with R/R DLBCL (not otherwise specified or transformed indolent lymphoma) ineligible for autologous stem cell transplant were randomly assigned 1:1 to receive Pola-R-GemOx or R-GemOx alone every 21 days for up to eight cycles. The primary end point was overall survival (OS).
    RESULTS: In total, 255 patients were randomly assigned to receive Pola-R-GemOx (n = 129) or R-GemOx (n = 126). After a median follow-up of 24.6 months, patients receiving Pola-R-GemOx versus R-GemOx had a significantly lower risk of death (hazard ratio, 0.6 [95% CI, 0.43 to 0.83]; P = .0017) with a median OS of 19.5 months (95% CI, 13.3 to not estimable) versus 12.5 months (95% CI, 8.9 to 15.8). The most common grade 3/4 adverse events (AEs) were thrombocytopenia and neutropenia. Peripheral neuropathy was more common with Pola-R-GemOx (n = 73 [57%]) versus R-GemOx (n = 36 [29%]) and was primarily grade 1. Fatal AEs occurred in 15 (12%) and five (4%) patients in the Pola-R-GemOx and R-GemOx groups, respectively, and were largely driven by infections (including COVID-19).
    CONCLUSION: Pola-R-GemOx significantly improved OS compared with R-GemOx, offering an additional treatment option in patients with transplant-ineligible R/R DLBCL.
    DOI:  https://doi.org/10.1200/JCO-25-02849
  4. Blood. 2026 Jul 07. pii: blood.2026033906. [Epub ahead of print]
      Blastic plasmacytoid dendritic cell neoplasm (BPDCN) is an orphan, aggressive hematologic malignancy characterized by high CD123 expression. Tagraxofusp (TAG), a CD123-directed toxin, is the only approved therapy. Prior studies demonstrated BPDCN dependence on BCL2, sensitivity to venetoclax (VEN), and reversal of TAG resistance with azacitidine (AZA). We conducted a phase 2 study evaluating combination therapy with TAG, AZA, and VEN in patients with BPDCN (NCT03113643). Patients with previously untreated (1L) or relapsed/refractory (R/R) BPDCN received 28-day cycles of AZA (75 mg/m² days 1-7), VEN (400 mg days 1-21), and TAG (12 µg/kg days 4-6). Eligibility followed TAG guidelines to mitigate risk of capillary leak syndrome (CLS). Twenty-seven patients were enrolled (16 1L, 11 R/R), with median age of 70 years (range 21-81). Composite complete remission (CR/CRi/CRc) rates were 88% in 1L and 64% in R/R cohorts. Median duration of response was not reached in 1L and was 7.2 months in R/R patients. CLS occurred in 15% of patients; most were grade 2. In the 1L cohort, median overall and progression-free survival were not reached; the 2-year overall survival was 65% and 2-year progression-free survival was 53%. Median overall survival in R/R patients was 8.4 months. A high proportion of patients proceeded to allogeneic stem cell transplantation in remission (63% 1L, including 10 of 11 patients age 75 or younger; and 55% R/R). TAG-AZA-VEN is highly active in both untreated and relapsed BPDCN with a predictable and manageable safety profile, supporting its use as a new therapeutic option.
    DOI:  https://doi.org/10.1182/blood.2026033906
  5. Br J Haematol. 2026 Jul 09.
      Treatment-free remission (TFR) is now a key goal for chronic-phase chronic myeloid leukaemia (CML-CP) after achievement of a prolonged deep molecular response. About half of these patients can remain in remission without treatment, whereas those who relapse must resume lifelong therapy. This study investigated whether patients who previously failed tyrosine kinase inhibitor discontinuation could achieve TFR after receiving ponatinib as maintenance therapy. Patients who had relapsed after prior tyrosine kinase inhibitor (TKI) discontinuation and subsequently regained molecular response 4.5 (MR4.5; defined as a BCR-ABL1 transcript level ≤0.0032% on the International Scale [IS]) were enrolled, switched to ponatinib (15 mg/day) for 12 months and those who maintained MR4.5 discontinued TKI therapy. The primary end-point was the proportion of patients with TFR at 12 months. Patients losing major molecular response (MMR) resumed ponatinib or their prior TKI. Of 50 enrolled patients, 49 received ponatinib and 41 proceeded to TKI discontinuation. At 12 months, the proportion of patients with TFR was 36.6% (90% confidence interval: 24.1-50.6). Univariate analysis identified favourable factors for TFR: first discontinuation of imatinib, longer initial TKI therapy and longer first TFR duration. In conclusion, ponatinib maintenance followed by a second attempt at TKI discontinuation may facilitate successful TFR in selected CML patients. However, the risk of adverse events highlights the need for careful patient selection.
    Keywords:  chronic myeloid leukaemia; ponatinib; second discontinuation attempt; treatment‐free remission; tyrosine kinase inhibitor
    DOI:  https://doi.org/10.1111/bjh.70678
  6. Oncology. 2026 Jul 09. 1-11
      Hydroxyurea-based cytoreduction before tyrosine kinase inhibitor (TKI) initiation remains common in newly diagnosed chronic-phase chronic myeloid leukemia (CML), yet its contemporary value is uncertain. This critical narrative review examines the historical rationale, biologic basis, clinical evidence, and guideline positions relevant to hydroxyurea use before or immediately around frontline TKI therapy. Hydroxyurea can lower leukocyte and platelet counts rapidly and may provide short-term symptomatic relief while diagnostic confirmation is pending or when definitive treatment access is briefly delayed. However, contemporary evidence does not support routine pretreatment in clinically stable chronic-phase CML. Observational studies have shown no improvement in European LeukemiaNet response milestones, no acceleration of molecular response kinetics, and possible disadvantages including delayed TKI initiation, greater hematologic toxicity, and more treatment interruptions. Randomized studies evaluating early hydroxyurea together with imatinib likewise have not demonstrated meaningful molecular or hematologic benefit over TKI therapy alone. Current guidelines consistently position hydroxyurea as a selective, time-limited bridging option rather than a standard pretreatment strategy. In modern practice, the priority should be rapid initiation of definitive BCR::ABL1-directed therapy once the diagnosis is confirmed and access is secured. Hydroxyurea retains a limited role in selected situations such as symptomatic proliferative burden, suspected leukostasis, clinically important thrombocytosis, or short unavoidable logistical delay to TKI initiation.
    DOI:  https://doi.org/10.1159/000553465
  7. Br J Haematol. 2026 Jul 06.
      Bortezomib, lenalidomide and dexamethasone (VRd) and carfilzomib, lenalidomide and dexamethasone (KRd) regimens have been widely used for induction in transplant-eligible newly diagnosed multiple myeloma (NDMM), yet direct comparisons between these regimens have been limited and inconsistent. We retrospectively analysed 1129 NDMM patients who received KRd (n = 364) or VRd (n = 765) before upfront autologous haematopoietic stem cell transplantation at a single-centre between 2006 and 2021. KRd-treated patients more often had high-risk cytogenetics and advanced Second revision of the International Staging System (R2-ISS) stage. Pretransplant complete response (CR) and ≥very good partial response (VGPR) rates were higher with KRd (23% and 71%) than VRd (16% and 61%; p = 0.002), with superior best post-transplant ≥CR (71% vs. 60%; p = 0.001) and higher pretransplant measurable residual disease (MRD) negativity (49% vs. 42%; p = 0.027). After a median follow-up of 38.6 months, median progression-free survival (PFS) was 62.2 versus 48.7 months (hazard ratio [95% confidence interval] 0.74 [0.59-0.93], p = 0.009) and median overall survival (OS) was not reached versus 122.7 months (0.86 [0.59-1.25], p = 0.43) for KRd and VRd respectively. In inverse probability-weighted multivariable analysis, KRd remained associated with improved PFS (0.76 [0.60-0.97], p = 0.025), with no OS difference. The PFS benefit was most pronounced in standard-risk, younger and male patients, and those with fewer comorbidities. Overall, KRd induction led to deeper responses and improved PFS compared with VRd.
    Keywords:  autologous; bortezomib; carfilzomib; myeloma; transplant
    DOI:  https://doi.org/10.1111/bjh.70642
  8. Blood Adv. 2026 Jul 10. pii: bloodadvances.2025018199. [Epub ahead of print]
      High-grade B cell lymphoma (HGBCL) is an aggressive clinical entity characterized by poor overall survival and high rates of CNS relapse. HGCBL traditionally includes cases harboring MYC rearrangement with concurrent BCL2 and/or BCL6 rearrangements (R). However, the prognostic implications of different combinations of rearrangements (MYC/BCL2, MYC/BCL6, or MYC/BCL2/BCL6) remain an open question with differing reports in the literature, and our knowledge of the clinical characteristics, response to treatment, and patterns of relapse remains incomplete. We identified clinical data from 124 cases of advanced-stage HGBCL treated at Memorial Sloan Kettering Cancer Center (69 MYC/BCL2-R, 34 MYC/BCL2/BCL6-R ('triple hit') and 21 MYC/BCL6-R). Thirty-six cases were subjected to targeted next-generation sequencing with MSK-IMPACT HEME. We confirm the poor prognosis of HGBCL, with low complete response rates (44%), poor overall survival (59.8% at 2 years) and high rates of CNS relapse (10.1%). Intensive regimens such as dose-adjusted R-EPOCH were associated with improved overall survival compared to R-CHOP based regimens. Unexpectedly, patients with MYC/BCL6-R disease had increased incidence of CNS relapse and rapid progression to death after relapse; we observed differing cell-of-origin in these cases compared to BCL2-R disease. In addition, counter to prior reports in DLBCL, HGBCL transformed from low-grade lymphoma was associated with improved survival in our cohort. Mutational profiling of HGBCL cases demonstrated enrichment for mutations associated with DLBCL, particularly GC-derived cases, as well as a high proportion of MYC mutations. Our results support the poor prognosis of HGBCL and the recent separation of MYC/BCL6 disease as a distinct clinical entity.
    DOI:  https://doi.org/10.1182/bloodadvances.2025018199
  9. Rinsho Ketsueki. 2026 ;67(6): 558-565
      Iron excretion from the body is minimal due to lack of an active excretion mechanism, and absorption is limited as well, making iron metabolism a semi-closed system. However, loss of iron-containing red blood cells through persistent gastrointestinal or gynecological bleeding depletes iron stores. If the bleeding progresses further, iron stores become insufficient for erythropoiesis, leading to iron deficiency anemia (IDA). IDA accounts for approximately 70% of all anemia cases. Furthermore, it is increasingly recognized that iron deficiency causes various symptoms even in the absence of anemia. Recent research has also revealed that iron-related tests are being underutilized in diagnosis and treatment. In recent years, ferric citrate hydrate has been added as a new oral iron preparation, along with ferric carboxymaltose and ferric derisomaltose as new intravenous options. Multiple clinical trials conducted in Japan have expanded the body of evidence. Alongside established agents, iron preparations are contributing to IDA treatment across a broad range of clinical areas.
    Keywords:  Ferric carboxymaltose; Ferric citrate hydrate; Ferric derisomaltose; Iron deficiency anemia
    DOI:  https://doi.org/10.11406/rinketsu.67.558
  10. Blood Cancer J. 2026 Jul 04.
      Outcomes in B-cell acute lymphoblastic leukemia (ALL) have improved over time due to therapeutic advances, and improved disease monitoring and prognostication. The BCR::ABL1 tyrosine kinase inhibitors (TKIs) were the first targeted therapies to significantly impact the therapeutic trajectory and outcomes of Philadelphia chromosome-positive (Ph-positive) ALL. Similarly, antibodies targeting CD19/20/22 and engineered chimeric antigen receptor (CAR) T-cell immunotherapies have drastically changed the therapeutic landscape and outcomes of B-cell ALL. Incorporation of the bispecific T-cell engager (BiTE) blinatumomab has demonstrated a significant survival advantage in patients with both newly diagnosed Philadelphia chromosome-negative (Ph-negative) and Ph-positive ALL. Inotuzumab ozogamicin, the anti-CD22 antibody drug conjugate (ADC), has also been safely integrated into the frontline treatment backbones in both younger and older patients. CAR T-cell therapy has resulted in durable remissions in relapsed/refractory (R/R) ALL, especially with lower disease burden. CAR T-cell therapy consolidation in the frontline setting is being pursued with the goal of reducing the need for allogeneic stem cell transplantation (alloSCT). Future research is focusing on treatment optimization through replacement of chemotherapy with immunotherapies with the goal of reducing toxicities, minimizing the need for alloSCT, and shortening the intensity and duration of therapy while improving long-term outcomes.
    DOI:  https://doi.org/10.1038/s41408-026-01566-z
  11. J Immunother Cancer. 2026 Jul 07. pii: e014311. [Epub ahead of print]14(7):
       BACKGROUND: Tetraspanin CD37, highly expressed in mature B-cells, represents an opportunity for therapeutic targeting in B-cell malignancies. GEN3009 (DuoHexaBody-CD37), a humanized biparatopic IgG1 antibody with an E430G hexamerization-enhancing mutation targeting two non-overlapping CD37 epitopes, was shown to induce potent tumor cell killing through enhanced complement-dependent cytotoxicity (CDC) and other fragment crystallizable-mediated effector functions, including antibody-dependent cellular cytotoxicity (ADCC) and antibody-dependent cellular phagocytosis (ADCP), in vitro and in vivo. GEN3009 was assessed in non-clinical studies and a phase 1 dose-escalation study of B-cell non-Hodgkin's lymphoma (B-NHL).
    METHODS: After a non-clinical toxicity study was conducted in cynomolgus monkeys, a phase 1, first-in-human, open-label, multicenter dose-escalation trial of GEN3009 monotherapy enrolled adults with relapsed/refractory (R/R) B-NHL (NCT04358458). A modified Bayesian optimal interval design informed dose escalation and de-escalation with dose levels ranging from 6 mg to 2000 mg. Primary endpoints were the rate of dose-limiting toxicities (DLTs) to determine the recommended phase 2 dose (RP2D) and safety and tolerability.
    RESULTS: In the toxicity study, 10 mg/kg GEN3009 weekly was identified as the highest non-severely toxic dose. In the phase 1 study, from March 13, 2020, to July 28, 2023, 46 patients with R/R B-NHL received intravenous GEN3009 infusions. Median duration of treatment was 1.2 months (range, 0.0-14.5). No DLTs were observed up to 1600 mg. The most common treatment-emergent adverse events were neutropenia (n=41 (89.1%)), infusion-related reactions (n=39 (84.8%)), and thrombocytopenia (n=18 (39.1%)). Plasma GEN3009 concentrations increased over time with increasing GEN3009 doses, with no apparent accumulation of GEN3009 observed over the course of treatment. Antitumor activity was observed at dose levels of ≥180 mg in both aggressive and indolent NHL. GEN3009 treatment reduced total hemolytic complement activity (CH50) levels in serum, and peak changes in CH50 levels were significantly correlated with clinical response (p=0.008 by Wilcoxon rank-sum test).
    CONCLUSIONS: Based on safety, efficacy, and pharmacokinetics, the RP2D of GEN3009 was determined to be 1200 mg. Preliminary data suggest that GEN3009 monotherapy demonstrated an acceptable safety profile at the RP2D of 1200 mg, with modest clinical activity. These findings provide the first clinical proof-of-concept for hexamerization-potentiated molecules that induce antitumor activity through enhanced CDC.
    Keywords:  B cell; Lymphoma; Monoclonal antibody; Pharmacodynamics - PD; Pharmacokinetics - PK
    DOI:  https://doi.org/10.1136/jitc-2025-014311
  12. Haematologica. 2026 Jul 09.
      Olverembatinib (HQP1351) is a potent third-generation (3G) tyrosine kinase inhibitor (TKI) that binds to both the active and inactive conformations of native ABL1 and mutant BCR::ABL1. It was developed as a potent inhibitor with activity against wild-type and mutated BCR::ABL1 for chronic myeloid leukemia (CML) patients. It is effective against the T315I mutation, which confers resistance to first and second generation TKIs. The results of clinical trials in China have led to olverembatinib approval by China's regulatory authority, National Medical Products Administration (NMPA), for adult patients with TKIresistant chronic phase (CP) or accelerated phase (AP) CML harboring the T315I mutation and for adult CP CML patients with resistance or intolerance to imatinib or 2G TKIs. Olverembatinib has also received breakthrough therapy designation by the NMPA in combination with low intensity chemotherapy for the first-line treatment of Philadelphia chromosome-positive acute lymphoblastic leukemia (Ph+ ALL). Global studies of olverembatinib are underway in CML and Ph +ALL, with the results of the US phase 1b study published in 2025. This review will summarize the safety, tolerability, and efficacy of olverembatinib in CML and Ph+ ALL in China and globally and discuss the role of olverembatinib among existing therapeutics and its future development.
    DOI:  https://doi.org/10.3324/haematol.2026.300834
  13. Cancer Cell. 2026 Jul 09. pii: S1535-6108(26)00295-3. [Epub ahead of print]
      Menin inhibition, an approved therapy for KMT2A-rearranged and NPM1 mutant acute leukemia, is accompanied by decreased platelet counts in 15-20% of heavily pre-treated patients. While studying the mechanism underlying this effect, we discovered that menin inhibition reduced the numbers of megakaryocyte progenitors in human CD34+ cultures and in mice. Because megakaryocytes are key drivers of myeloproliferative neoplasms (MPNs), we investigated the extent to which menin inhibition ameliorates MPN phenotypes. We found that the menin inhibitor revumenib has potent anti-tumor activity, synergizes with ruxolitinib, and shows only subtle effects on healthy mice. Moreover, revumenib suppressed megakaryopoiesis of primary MPN patient specimens in vitro and in vivo. Importantly, genetic knockout of MEN1 and its target MEF2C phenocopied the action of revumenib, confirming an on-target effect of the drug. Together, we reveal menin as a dependency in proliferative megakaryocytes and support further evaluation of menin inhibition as a potential therapy for MPNs.
    Keywords:  megakaryocyte; menin; myeloproliferative neoplasms; revumenib
    DOI:  https://doi.org/10.1016/j.ccell.2026.06.008
  14. Leuk Lymphoma. 2026 Jul 10. 1-13
      We conducted unanchored matching-adjusted indirect comparisons (MAICs) of the BCMA × CD3 bispecific antibodies, linvoseltamab and elranatamab, in triple-class exposed (TCE) relapsed/refractory multiple myeloma (RRMM). Patient-level data from BCMA-targeted therapy-naïve patients in LINKER-MM1 (linvoseltamab; NCT03761108; n = 107; data cutoff (DCO): 07/2024; median follow-up: 21.3 months) were matched to MagnetisMM-3 Cohort A (elranatamab; NCT04649359; N = 123; DCO: 09/2024; median follow-up: 33.9 months). Linvoseltamab demonstrated significantly (p < 0.05) higher overall response (71.5% vs. 61.0%) and complete response or better rates (50.5% vs. 37.4%), and numerically higher very good partial response or better rate (65.0% vs. 56.1%; p = 0.09) versus elranatamab. Duration of response (hazard ratio [HR] = 0.82; p = 0.54), progression-free survival (HR = 0.86; p = 0.50), and overall survival (OS) (HR = 0.67; p = 0.08) were numerically but not statistically significantly favorable for linvoseltamab. When measured using restricted mean survival time, OS significantly favored linvoseltamab (difference: 3.47 months; p = 0.04). This MAIC of linvoseltamab versus elranatamab suggests linvoseltamab offers favorable efficacy in TCE RRMM.
    Keywords:  bispecific antibodies; clinical efficacy; elranatamab; linvoseltamab; relapsed/refractory multiple myeloma
    DOI:  https://doi.org/10.1080/10428194.2026.2688561