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        <title>Frontiers in Hematology | New and Recent Articles</title>
        <link>https://www.frontiersin.org/journals/hematology</link>
        <description>RSS Feed for Frontiers in Hematology | New and Recent Articles</description>
        <language>en-us</language>
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        <pubDate>2026-05-08T20:01:21.669+00:00</pubDate>
        <ttl>60</ttl>
        <item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/frhem.2026.1800304</guid>
        <link>https://www.frontiersin.org/articles/10.3389/frhem.2026.1800304</link>
        <title><![CDATA[Optimisation of patient-reported outcome measurement for haematological cancer patients receiving novel immunotherapies: perspectives of multi-stakeholders]]></title>
        <pubdate>2026-05-04T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Eilidh M Duncan</author><author>Jhulia Salviano</author><author>Charalampia Kyriakou</author><author>Samantha Nier</author><author>Simone Oerlemans</author><author>Sam Salek</author><author>Kate Morgan</author><author>Katie Joyner</author>
        <description><![CDATA[ObjectivesThe primary objective of this project was to explore the challenges related to the implementation of patient-reported outcome measures (PROMs) in myeloma, lymphoma and leukaemia patients undergoing chimeric antigen receptor T-cell (CAR-T) and T Cell engager bispecific antibody (BsAbs) therapies. The secondary aims focused on identifying and promoting opportunities to optimise PROM use for improved alignment, consistency, and interpretability of PROM data related to these innovative treatments.MethodsData was collected through online focus groups and interviews with patients, carers, representatives of patient organisations from myeloma, lymphoma, leukaemia communities, researchers, industry, regulatory and payer representatives. The information was transcribed for qualitative thematic analysis, using a deductive–inductive mixed approach.ResultsA total of 38 individuals participated; 14 interviews were conducted with 16 participants and two focus groups were conducted with 15 and 19 participants in each. Challenges reported included the unique complexities within trials of CAR-T and BsAbs in haematologic cancers such as the logistical challenges in the early post-infusion period for CAR-T and the wide variety of different BsAbs side-effects for patients occurring over different time periods. Further difficulties included balancing stakeholders’ expectations, and uncertainties about what to measure and when.ConclusionsCAR-T and BsAbs therapies present distinct challenges for PROM to capture treatment-related side effects and burden accurately. Use of generic and disease-specific instruments risk missing key elements of patients’ experiences and the use of ad-hoc strategies to complement these tools presents challenges for evidence synthesis. Clearer guidance, including early high-frequency assessments, systematic inclusion of patient-important domains currently under-captured, continued PRO data collection beyond clinical progression and transparent and comprehensive reporting of PRO findings will lead to substantial improvements in understanding the impact of CAR-T and BsAbs treatments.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/frhem.2026.1733719</guid>
        <link>https://www.frontiersin.org/articles/10.3389/frhem.2026.1733719</link>
        <title><![CDATA[Case Report: Pernicious anemia-associated pancytopenia responds to immunotherapy]]></title>
        <pubdate>2026-04-13T00:00:00Z</pubdate>
        <category>Case Report</category>
        <author>Alexander Krule</author><author>Carlos Murga-Zamalloa</author><author>Irum Khan</author><author>Ryan Sun</author><author>John G. Quigley</author>
        <description><![CDATA[Pancytopenia is a life-threatening condition necessitating a prompt, thorough workup to appropriately treat the underlying pathology. We describe a presentation of pancytopenia attributed to myelodysplastic syndrome (MDS)-associated immune-mediated hemolysis, which initially responded to immunotherapy, including steroids and the anti-CD20 monoclonal antibody rituximab. Cycles of relapse, followed by repeated clinical responses to immunotherapy over a two-year period, supported the diagnosis of immune-mediated cytopenias, substantially delaying identification of the true pathology. Subsequent investigations revealed pernicious anemia as the underlying diagnosis despite ostensibly normal vitamin B12 levels at presentation. This case highlights how the autoimmune features of pernicious anemia may confound the diagnostic workup of cytopenias by masking the detection of B12 deficiency, and, surprisingly, result in the sustained response of pernicious anemia to immunotherapy.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/frhem.2025.1650494</guid>
        <link>https://www.frontiersin.org/articles/10.3389/frhem.2025.1650494</link>
        <title><![CDATA[Case Report: A converging pathology: Chediak–Higashi syndrome and IEI-associated lymphoproliferative disease]]></title>
        <pubdate>2026-04-08T00:00:00Z</pubdate>
        <category>Case Report</category>
        <author>Carlos R. Varón</author><author>Santiago Andrés Suárez-Gómez</author><author>Daniela Varón</author><author>Libelly Gómez Flórez</author><author>Carolina Cortes-Urrea</author><author>Elda Graciela Vélez Colmenares</author><author>Isabella Corona</author>
        <description><![CDATA[Chediak–Higashi syndrome (CHS) is a rare autosomal recessive condition marked by lysosomal dysfunction, partial albinism, neurological impairment, and marked immunodeficiency. Patients with CHS exhibit increased susceptibility to aggressive malignancies, notably lymphoproliferative disorders. This report describes a 25-year-old man with CHS, complicated by an inborn error of immunity (IEI)-associated lymphoproliferative disorder (IEI-LPD). His initial symptoms presented were severe lower back pain, weight loss, and constitutional symptoms, alongside classic phenotypic features of CHS, including hypopigmentation, neurological abnormalities, and ocular manifestations. Laboratory findings revealed leucopenia, decreased immunoglobulins (IgA, IgM), and impaired natural killer cell function, confirming severe immune dysfunction. Imaging studies identified vertebral fractures, a retroaortic mass, and splenomegaly; histopathology confirmed IEI-LPD. Treatment comprised six cycles of dose-adjusted EPOCH chemotherapy with pegfilgrastim prophylaxis, achieving an initial complete response. Nevertheless, progressive neurological deterioration, recurrent infections, and institutional limitations contributed to this patient’s eventual demise. Genetic sequencing identified a homozygous LYST mutation variant c.9464G>A (p.R3155Q), classified as a variant of uncertain significance. This report underscores the diagnostic and therapeutic challenges in rare hematologic malignancies, emphasizing the importance of genetic characterization through next-generation sequencing and advocating for improved awareness, early diagnosis, and multidisciplinary management strategies for optimal outcomes in CHS-associated malignancies.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/frhem.2026.1749376</guid>
        <link>https://www.frontiersin.org/articles/10.3389/frhem.2026.1749376</link>
        <title><![CDATA[Revisiting old drugs and drug combinations for polycythemia vera and related neoplasms]]></title>
        <pubdate>2026-03-31T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Gökhan Mergen</author><author>Hans C. Hasselbalch</author>
        <description><![CDATA[Polycythemia Vera (PV) and related myeloproliferative neoplasms (MPNs) require long-term management to minimize thrombotic complications, disease progression, and improve quality of life. While interferon-alpha (IFN-α) offers disease-modifying potential, disease symptoms and side effects often persist, necessitating the exploration of complementary therapeutic strategies. This review examines established drugs and lifestyle interventions for their potential to improve PV/MPN outcomes. We synthesize evidence from preclinical models, clinical trials in non-MPN populations, and observational studies in MPN patients, focusing on interventions targeting MPN-related pathways like JAK/STAT signaling, inflammation, and oxidative stress. We highlight the potential benefits of cardiovascular drugs like ACE inhibitors and statins; anti-diabetic medications such as metformin and pioglitazone; and readily available agents like colchicine, rapamycin, leukotriene modifiers, and N-acetylcysteine (NAC). Additionally, we review the evidence supporting natural compounds like green tea, curcumin, fish oil, alpha-ketoglutarate, beta-alanine, vitamin C, vitamin D3, and probiotics like Clostridium butyricum, to identify their potential for symptom management and disease control. We review evidence supporting lifestyle interventions like the Mediterranean diet, weight management, yoga and exercise. We share two case studies that highlight the potential for combination therapies. Finally, we suggest a two-pronged approach: incorporate readily applicable interventions into clinical practice based on biomarkers, while conducting rigorous research to validate emerging combination strategies. The combination therapy approach aims to improve both survival and quality of life for PV and MPNs.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/frhem.2026.1770034</guid>
        <link>https://www.frontiersin.org/articles/10.3389/frhem.2026.1770034</link>
        <title><![CDATA[Complications and treatment patterns in patients with non-transfusion-dependent α- and β-thalassemia compared with matched controls: a retrospective observational study using administrative claims data in the United States]]></title>
        <pubdate>2026-03-30T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Arielle L. Langer</author><author>Amey Rane</author><author>Keely S. Gilroy</author><author>Jing Zhao</author><author>Louise Lombard</author><author>Carolyn R. Lew</author><author>Sujit Sheth</author>
        <description><![CDATA[BackgroundNon-transfusion-dependent thalassemia (NTDT) can result in a range of clinical complications that can substantially reduce patient quality of life. To date, real-world studies on the clinical burden of the disease have focused on Europe and Asia and have been limited to β-NTDT.AimTo assess the complications and treatment patterns in patients with α- or β-NTDT vs. matched controls in the United States (US).MethodsThis retrospective observational study used data from US claims databases (January 1, 2013–June 30, 2021). Adult patients (≥18 years) with ≥1 inpatient or ≥2 outpatient claims for α- or β-thalassemia were included from Merative™ MarketScan® Commercial/Medicare and Multi-State Medicaid databases. Patients were classified as NTDT if they had <8 blood transfusions or ≥6 weeks between any two adjacent transfusions during the 12 months post-index date (date of first observed α- or β-thalassemia diagnosis code). Patients were matched with controls (1:5 ratio). Primary analysis focused on patients from the Commercial/Medicare database with mean hemoglobin <10 g/dL during follow-up, to minimize inclusion of patients with thalassemia trait. Complications and treatment patterns were assessed during ≥12 months post-index. Comparisons between patients with NTDT vs. controls were performed using Chi-square tests (categorical variables) and t-tests (continuous variables) (two-sided significance level of 0.05). Analyses for the α- and β-NTDT subgroups were also performed.ResultsIn the Commercial/Medicare database, 149 patients with NTDT and hemoglobin <10 g/dL were matched with 745 controls (mean follow-up approximately 3 years). A significantly higher percentage of patients with NTDT had complications vs. controls, including malignancy (17.4% vs. 7.1%; p < 0.001), cardiovascular disease (15.4% vs. 7.8%; p = 0.003), liver disease (6.7% vs. 0.5%; p < 0.001), and gallstones (6.7% vs. 2.1%; p = 0.002). Overall, 18.8% of patients with NTDT had ≥1 transfusion; 4.0% received oral chelators. Similar trends across outcomes were observed for NTD α- and β-thalassemia subgroups vs. controls.ConclusionsPatients with NTDT had a high disease burden and experienced a range of serious complications, with significantly higher rates compared with controls. Additional effective and well-tolerated treatments are needed to address the underlying causes of NTDT and prevent complications.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/frhem.2026.1727954</guid>
        <link>https://www.frontiersin.org/articles/10.3389/frhem.2026.1727954</link>
        <title><![CDATA[Case Report: Burkitt’s lymphoma with concurrent HIV, CMV encephalitis, and salmonella bacteremia]]></title>
        <pubdate>2026-03-30T00:00:00Z</pubdate>
        <category>Case Report</category>
        <author>Elinor Barsh</author><author>Michele Basche</author><author>Dmitriy Scherbak</author>
        <description><![CDATA[Burkitt’s lymphoma is a highly aggressive B-cell lymphoma associated with human immunodeficiency virus (HIV) infection. Despite antiretroviral therapy (ART), Burkitt’s lymphoma remains diagnostically and therapeutically challenging, especially with concurrent infections. We describe a 50-year-old man presenting with constitutional symptoms and Salmonella bacteremia, found to have newly diagnosed HIV, stage IV Burkitt’s lymphoma with central nervous system (CNS) and marrow involvement, and cytomegalovirus (CMV) viremia. His management required coordination of ART, chemotherapy, and infection treatment, complicated by CMV encephalitis and adherence barriers. This case highlights the challenges of managing overlapping malignancy and infection, emphasizing early HIV testing and patient-centered multidisciplinary care.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/frhem.2026.1812817</guid>
        <link>https://www.frontiersin.org/articles/10.3389/frhem.2026.1812817</link>
        <title><![CDATA[Editorial: Advances and new horizons in cellular therapies for leukemia and myeloma]]></title>
        <pubdate>2026-03-27T00:00:00Z</pubdate>
        <category>Editorial</category>
        <author>Bhavana Bhatnagar</author><author>Srinivas Devarakonda</author>
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/frhem.2026.1785387</guid>
        <link>https://www.frontiersin.org/articles/10.3389/frhem.2026.1785387</link>
        <title><![CDATA[Castleman disease mimicking systemic lupus erythematosus: the importance of vigilance in diagnosing autoimmune mimickers]]></title>
        <pubdate>2026-03-26T00:00:00Z</pubdate>
        <category>Perspective</category>
        <author>Chao-Chieh Cheng</author><author>Ruo-Han Chin</author><author>Po-Cheng Shih</author><author>Su-Boon Yong</author><author>Chia-Jung Li</author>
        <description><![CDATA[Castleman disease (CD) is a rare lymphoproliferative disorder with heterogeneous clinical manifestations, particularly in its idiopathic multicentric form (iMCD), which is driven by cytokine dysregulation rather than classical autoimmunity. Owing to overlapping features such as fever, lymphadenopathy, cytopenias, renal involvement, and elevated inflammatory markers, iMCD may closely mimic systemic lupus erythematosus (SLE). This resemblance is further complicated by the presence of autoantibodies in a subset of iMCD patients, increasing the risk of misclassification and delayed diagnosis. In this Perspective, we highlight key clinical scenarios in which CD presents as a lupus-like syndrome, including cases that initially fulfill SLE classification criteria but fail to respond to conventional immunosuppressive therapy. We emphasize the limitations of serologic testing in distinguishing these entities and underscore the central role of lymph node histopathology in establishing the correct diagnosis. Recognizing Castleman disease as an important mimic of SLE has critical therapeutic implications, as iMCD requires cytokine-directed treatment rather than immune suppression alone. These observations also suggest that CD and SLE may share a cytokine-driven inflammatory spectrum in selected patients; however, distinguishing between them remains essential because their therapeutic strategies differ fundamentally. Increased awareness of this diagnostic overlap may help clinicians avoid inappropriate treatment strategies and improve outcomes in patients presenting with atypical or refractory lupus-like disease.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/frhem.2026.1802350</guid>
        <link>https://www.frontiersin.org/articles/10.3389/frhem.2026.1802350</link>
        <title><![CDATA[Single spectral flow cytometry panel for simultaneous detection of hematopoietic stem, progenitor, and mature lineages in mouse bone marrow]]></title>
        <pubdate>2026-03-18T00:00:00Z</pubdate>
        <category>Methods</category>
        <author>Léa Girondier</author><author>Manon Richaud</author><author>Julien MP Grenier</author><author>Ana Belen Pérez-Oliva</author><author>Jenny Van Asbeck-van der Wijst</author><author>Michel Aurrand-Lions</author><author>Maria De Grandis</author><author>Christophe Lachaud</author><author>Cyril Fauriat</author><author>Laura Braud</author>
        <description><![CDATA[Hematopoiesis occurs in the bone marrow of adult mammals and is supported by hematopoietic stem cells that sustain lifelong blood cell production. Pathological conditions can disrupt HSC differentiation, causing anemia, immunodeficiency, and other cytopenias. Therefore, precise and simultaneous identification of hematopoietic populations from stem to mature cells is essential for understanding disease mechanisms and developing targeted therapies. In order to study these alterations, flow cytometry is generally the reference technique. However, most cytometry panels are designed to study a specific population, leaving out potential discoveries on other populations from the same microenvironment. Here we present the design of a 19-marker spectral flow cytometry panel capable of simultaneously identifying HSPCs, erythroid, myeloid and lymphoid cells within a single murine bone marrow sample. This integrated approach replaces multiple conventional panels and enables comprehensive mapping of hematopoietic differentiation from a single assay. Validation confirmed accurate detection of long-term and short-term HSCs, multipotent progenitors, common myeloid and lymphoid progenitors, and erythroid populations from proerythroblasts to reticulocytes. UMAP visualization captured the continuous trajectory of differentiation. We validated our method on aged and β-thalassemic mouse models showing a clear detection of hematopoiesis and erythropoiesis alterations respectively. This panel provides a robust and flexible tool suitable for both basic research and translational studies.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/frhem.2026.1794624</guid>
        <link>https://www.frontiersin.org/articles/10.3389/frhem.2026.1794624</link>
        <title><![CDATA[Living with chronic lymphocytic leukaemia: patient perspectives from a global online cross-sectional survey on care pathways and impacts on quality of life]]></title>
        <pubdate>2026-03-16T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Kathryn Huntley</author><author>Alan J. Poots</author><author>Sarah Gunn</author><author>Jan Rynne</author><author>Nick York</author><author>Sam Salek</author>
        <description><![CDATA[BackgroundChronic Lymphocytic Leukaemia (CLL) is a slow-progressing condition often managed through active monitoring (“watch and wait”) strategies, which can lead to uncertainty for patients about prognosis, symptom management, and immunity-related risks. We studied the diagnostic and active monitoring pathway experiences of patients with CLL, and the impact of immunity-related knowledge on their quality of life (QoL).MethodsWe analysed data from 846 patients with CLL who responded to the cross-sectional 2023 Global Leukaemia Experience Survey, which included the Haematological Malignancy Specific Patient-reported Outcome (HM-PRO) instrument. Higher HM-PRO scores represent worse QoL. We used descriptive statistics and Kruskal-Wallis tests to quantify the impact on QoL.ResultsMost respondents (69%, 582/841) reported experiencing symptoms before diagnosis, although the majority (89%, 509/571) did not recognise these as signs of leukaemia. A large proportion (84%, 701/831) were placed on active monitoring, amongst whom 25% (172/689) reported being “very concerned/worried” about this approach. Fewer than half felt fully confident recognising signs of progression. QoL did not differ significantly by current active monitoring status but was associated with immunity-related knowledge: respondents unaware of their immunity status had worse QoL (median HM-PRO Part A “No”: 13 vs “Yes”: 11). Respondents who had not spoken to a healthcare professional about immunisation strategies reported higher HM-PRO Part-A scores (“No”: 13 vs “Yes, completely”: 10).ConclusionOur study highlights key challenges faced by individuals with CLL, including lack of symptom awareness, lack of association of those symptoms with cancer, inadequate understanding of active monitoring, and the impact of immunity-related education on QoL. Addressing these challenges through coordinated efforts amongst clinicians, advocacy groups, and policymakers may contribute to improved disease management and QoL for individuals living with CLL. Future research could seek to account for potential confounders to enhance the robustness of conclusions and build on these global findings by examining country-level differences.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/frhem.2026.1745884</guid>
        <link>https://www.frontiersin.org/articles/10.3389/frhem.2026.1745884</link>
        <title><![CDATA[Case Report: two cases of idiopathic plasmacytic lymphadenopathy subtype of idiopathic multicentric Castleman disease with xanthelasma palpebrum from a Canadian center]]></title>
        <pubdate>2026-02-23T00:00:00Z</pubdate>
        <category>Case Report</category>
        <author>Andrew A. Y. Chen</author><author>Vivian T. Yin</author><author>Paula Blanco</author><author>Mark Trinder</author><author>Richard I. Crawford</author><author>Ryan Henrie</author><author>Stephen Parkin</author><author>Nasreen Khalil</author><author>Mollie Carruthers</author><author>Lu Zhang</author><author>Luke Y. C. Chen</author>
        <description><![CDATA[BackgroundIdiopathic plasmacytic lymphadenopathy is a newly recognized subtype of idiopathic multicentric Castleman disease (iMCD-IPL) and often mimics IgG4-related disease (IgG4-RD). We present two of the first cases of iMCD-IPL diagnosed in British Columbia, Canada. Both patients had normolipemic bilateral xanthelasma palpebrum, which has not previously been reported in iMCD-IPL.Case reportBoth patients were Asian women in the 5th decade who presented with anemia, inflammation, polyclonal hypergammaglobulinemia (PHGG), and xanthelasmas. IgG4-RD was initially suspected, but upon review of the lymph node histology and careful clinicopathological correlation, both were found to have iMCD-IPL with plasmacytic histology. Biopsies of the xanthelasmas revealed foamy macrophages consistent with common xanthelasmas. Both patients had partial clinical and biochemical response to siltuximab, but no change in xanthelasmas. We searched the literature and identified three cases of unicentric Castleman’s disease (UCD) with xanthomas, systemic inflammation and PHGG. These three patients showed marked improvement in both systemic symptoms and xanthomas after resection of the UCD.ConclusionWe report two patients with normolipemic xanthelasmas and iMCD-IPL whose xanthelasmas did not regress with siltuximab. However, the regression of xanthomas in three cases of UCD from the literature suggest a potential pathophysiological association between Castleman disease and xanthomas.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/frhem.2026.1776722</guid>
        <link>https://www.frontiersin.org/articles/10.3389/frhem.2026.1776722</link>
        <title><![CDATA[Rapid response to obinutuzumab and venetoclax in patients with nephrotic syndrome related to CLL: a report of two cases]]></title>
        <pubdate>2026-02-23T00:00:00Z</pubdate>
        <category>Case Report</category>
        <author>Emin Abdullayev</author><author>Markus Bieringer</author><author>Anna Ossami Saidy</author><author>Sefer Elezcurtaj</author><author>Wolfgang Schneider</author><author>Bertram Glaß</author><author>Snjezana Janjetovic</author>
        <description><![CDATA[IntroductionNephrotic syndrome caused by membranoproliferative glomerulonephritis (MPGN) related to chronic lymphocytic leukemia (CLL) is a rare condition. Due to the rarity, no standard of care has been established yet. The combination of rituximab, chlorambucil and fludarabin was described as an effective therapeutic regimen. However, the efficacy of the novel therapeutic options in CLL-induced nephrotic syndrome are rarely reported so far.Materials and methodsWe report two cases of patients with CLL suffering from concomitant nephrotic syndrome with significant proteinuria. The patients have consented to the evaluation and publication of their data. The patients received their initial diagnosis at our clinic and were followed for approximately 3 years.ResultsThe first patient, a 44-year old female with B-CLL, Binet A, and a low risk CLL-IPI score. Initially lupus nephritis was suspected to be associated with MPGN. However, despite the immunosuppressive treatment with mycophenolate mofetil and prednisolone no disease control was achieved. Consequently, CLL-associated nephrotic syndrome was assumed, and treatment with obinutuzumab and venetoclax was initiated. Six weeks after therapy initiation, the patient showed complete clinical resolution of nephrotic syndrome, accompanied by a marked reduction in proteinuria. The second patient, a 73-year old man, diagnosed with B-CLL, Binet C, CLL-IPI score intermediate risk presenting with concomitant MPGN. Treatment with obinutuzumab and venetoclax was initiated. Clinically, the nephrotic syndrome resolved within a few weeks after the initiation of therapy. Final assessment after completion of treatment by computed tomography and flow cytometry demonstrated complete remission of CLL. In addition, proteinuria completely resolved. At the last follow-up, the patient remains in sustained remission, with proteinuria persistently below the nephrotic range.ConclusionIn this report, we present two cases of CLL-related nephrotic syndromes, successfully treated with obinutuzumab and venetoclax. Furthermore, we emphasize the importance of awareness of this rare complication in patients with CLL.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/frhem.2026.1686097</guid>
        <link>https://www.frontiersin.org/articles/10.3389/frhem.2026.1686097</link>
        <title><![CDATA[The role of necroptosis as a possible therapeutic target in multiple myeloma: the emerging roles of necroptosis]]></title>
        <pubdate>2026-02-23T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Duygu Aydemir</author>
        <description><![CDATA[Multiple myeloma (MM) is a malignant plasma cell disorder characterized by clonal proliferation within the bone marrow, systemic organ dysfunction, and inevitable relapse due to therapeutic resistance. Despite advances in proteasome inhibitors, immunomodulatory agents, monoclonal antibodies, and autologous stem cell transplantation, MM remains incurable, primarily due to the evasion of apoptosis, which remains a central driver of relapse in multiple myeloma, necessitating alternative cytotoxic strategies. Necroptosis, a caspase-independent and immunogenic form of regulated cell death (RCD) mediated by the RIPK1–RIPK3–MLKL signaling axis, has emerged as a promising alternative mechanism to circumvent apoptotic resistance. Activation of necroptosis triggers the release of damage-associated molecular patterns (DAMPs), including high-mobility group box 1 (HMGB1), ATP, and nucleic acids, which promote dendritic cell maturation, tumor antigen presentation, and the activation of cytotoxic T cells. These features position necroptosis as both a direct cytotoxic mechanism and a driver of anti-tumor immunity. However, its dysregulated activation may foster chronic inflammation, immune suppression, and tumor progression, highlighting the need for precise therapeutic control. Recent findings reveal that necroptosis-associated genes and their polymorphisms (e.g., RIPK1, RIPK3, MAPKAPK2) influence MM pathogenesis, treatment response, and survival outcomes, suggesting potential prognostic utility. Pharmacological agents, such as SMAC mimetics, proteasome inhibitors, natural compounds, and peptidomimetics, can modulate necroptotic signaling and synergize with standard regimens to overcome drug resistance. This review integrates current evidence on necroptotic pathways to harness necroptosis in a controlled, biomarker-guided manner, offering a novel therapeutic avenue to overcome apoptosis resistance, enhance immunogenicity, and improve clinical outcomes in MM.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/frhem.2026.1709697</guid>
        <link>https://www.frontiersin.org/articles/10.3389/frhem.2026.1709697</link>
        <title><![CDATA[Evaluating role of TNF-α in tyrosine kinase inhibitors-treated chronic myeloid leukemia]]></title>
        <pubdate>2026-02-12T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Gratial Theres Joseph</author><author>Sandeep Kumar Swain</author><author>Himanshu Dhanda</author><author>Neetu Kushwaha</author><author>Priti Kumari</author><author>Mahek Pravin Khushalani</author><author>Rakesh Kumar</author><author>Baseer Noor</author><author>Sufian Zaheer</author><author>Aditi Jain</author><author>Ankur Jain</author><author>Sumita Chaudhry</author><author>Pranay Tanwar</author><author>Amitabh Singh</author><author>Bhavika Rishi</author><author>Aroonima Misra</author>
        <description><![CDATA[PurposeChronic Myeloid Leukemia (CML) is characterized by the BCR-ABL1 fusion gene and is effectively managed with tyrosine kinase inhibitors (TKIs). However, therapeutic resistance and the persistence of leukemic stem cells pose challenges to achieving long-term remission. Tumor Necrosis Factor-alpha (TNF-α), a pro-inflammatory cytokine, is implicated in leukemogenesis and resistance, yet its clinical relevance in Indian CML cohorts remains underexplored.ObjectiveThis study investigates the pharmacodynamic and prognostic role of serum TNF-α levels in chronic-phase CML patients receiving first-line imatinib, aiming to evaluate its utility as a biomarker for treatment response.MethodsWe conducted a prospective observational study on 40 CML patients treated at Safdarjung Hospital, New Delhi. Blood samples were taken before treatment and 5–7 months after starting imatinib. ELISA was used to quantify TNF-α levels, and qRT-PCR was used to monitor BCR-ABL1 transcripts. We analyzed clinical and hematologic parameters using appropriate statistical methods.ResultsImatinib treatment significantly reduced serum TNF-α (259.5 to 129.8 pg/mL; p < 0.0001), mirroring the observed decrease in BCR-ABL1 transcripts. Basically, if TNF-α stuck around (r = 0.87), patients responded poorly, whereas good outcomes correlated with its quicker clearance (r = 0.45).ConclusionOur data suggest that TNF-α represents a clinically relevant pharmacodynamic and prognostic biomarker for patients with chronic-phase CML receiving imatinib therapy. A decline in TNF-α levels was associated with a favorable therapeutic outcome, whereas failure of TNF-α to decline was indicative of an inferior outcome. TNF-α does not replace qRT-PCR–based monitoring of BCR-ABL1; however, it may be useful as an adjunctive prognostic marker, especially in resource-poor environments, pending appropriate prospective confirmation.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/frhem.2026.1748301</guid>
        <link>https://www.frontiersin.org/articles/10.3389/frhem.2026.1748301</link>
        <title><![CDATA[Case Report: Chronic myelomonocytic leukemia initially diagnosed as immune thrombocytopenia]]></title>
        <pubdate>2026-02-04T00:00:00Z</pubdate>
        <category>Case Report</category>
        <author>Jiaxin Wu</author><author>Hongxiang Wang</author>
        <description><![CDATA[ObjectiveTo explore the clinical characteristics, diagnosis and treatment process of a case initially diagnosed with primary immune thrombocytopenia (ITP) and finally diagnosed as chronic myeloid-monocytic leukemia (CMML).MethodsThe clinical manifestations, laboratory tests, bone marrow morphology, molecular genetic test results and treatment history of a CMML patient with thrombocytopenia as the first symptom were retrospectively analyzed.ResultsOne patient was initially diagnosed with immune thrombocytopenia (ITP). After receiving immunosuppressive treatment, the platelets temporarily rebounded, but subsequently the white blood cells increased, the proportion of monocytes increased, and typical CMML-related mutations were found in bone marrow morphology and NGS testing, and he was finally diagnosed as CMML. His condition stabilized after treatment with decitabine chemotherapy.ConclusionCMML can manifest as atypical thrombocytopenia in the early stage, which is delayed by the progression of ITP. Clinical attention should be paid to potential clonal bone marrow diseases in ITP patients who are refractory or have poor response to treatment. Early bone marrow morphological and molecular detection can help to clarify the diagnosis, guide treatment, and improve prognosis.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/frhem.2026.1733667</guid>
        <link>https://www.frontiersin.org/articles/10.3389/frhem.2026.1733667</link>
        <title><![CDATA[Long-term outcomes of hyperbaric oxygen pretreatment in autologous hematopoietic stem cell transplantation]]></title>
        <pubdate>2026-01-30T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Vinny Lococo</author><author>Maire Okoniewski</author><author>Abdalla Shoaib</author><author>Leyla Shune</author><author>Sunil Abhyankar</author><author>Anurag Singh</author><author>Dennis Allin</author><author>Briha Ansari</author><author>Joseph McGuirk</author><author>Omar S. Aljitawi</author><author>Haitham Abdelhakim</author>
        <description><![CDATA[Autologous hematopoietic stem cell transplantation (aHSCT) is an effective treatment for hematologic malignancies. Hyperbaric oxygen (HBO) pretreatment has demonstrated safety and feasibility, improved neutrophil engraftment, and reduced mucositis in patients undergoing aHSCT. This was a retrospective review comparing 19 patients who completed HBO therapy prior to aHSCT with a 225-patient historical control cohort. Median overall survival was not reached in the HBO cohort and was 9 years in the historical control cohort (p = 0.59). Median relapse-free survival was 4.2 years in the HBO cohort and 3.7 years in the historical cohort (p = 0.34). The HBO cohort had a lower cumulative incidence of non-relapse mortality, although the difference was not statistically significant (p = 0.057). Excluding non-melanoma skin cancers, the incidence of secondary malignancy was reduced in the HBO cohort (5.26% vs. 22.07%, p = 0.074). Rates of organ damage were reduced in the HBO cohort but did not reach statistical significance (47.4% vs. 61.3%, p = 0.12). Rates of cardiac (5.3% vs. 23.9%; p = 0.046) and renal (15.8% vs. 42.8%; p = 0.016) organ damage were significantly reduced in the HBO cohort. There was less autoimmune disease observed in the HBO cohort compared with the historical control cohort (0.0% vs. 7.69%; p = 0.14). Overall, HBO therapy before aHSCT showed trends toward lower non-relapse mortality and a lower incidence of secondary malignancy. The incidence of cardiac and renal damage was significantly reduced. These findings indicate that HBO is well tolerated and may improve outcomes in patients undergoing aHSCT.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/frhem.2026.1787190</guid>
        <link>https://www.frontiersin.org/articles/10.3389/frhem.2026.1787190</link>
        <title><![CDATA[Editorial: Innovations and challenges in sickle cell disease: bridging gaps in global health]]></title>
        <pubdate>2026-01-27T00:00:00Z</pubdate>
        <category>Editorial</category>
        <author>Arturo José Martí-Carvajal</author>
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/frhem.2025.1719208</guid>
        <link>https://www.frontiersin.org/articles/10.3389/frhem.2025.1719208</link>
        <title><![CDATA[Daratumumab in severe Evans syndrome: a case report]]></title>
        <pubdate>2026-01-23T00:00:00Z</pubdate>
        <category>Case Report</category>
        <author>Stefan M. Hillmann</author><author>Hendrik Brockhoff</author><author>Sarah Loebel</author><author>Suna Hentschke</author><author>Dirk Arnold</author><author>Hans Salwender</author>
        <description><![CDATA[Evans syndrome is a rare autoimmune disorder characterized by the simultaneous or sequential occurrence of autoimmune cytopenia. The disease is chronic, relapsing, and frequently refractory to standard therapies. Typical symptoms include anemia-related fatigue, pallor, and jaundice due to hemolysis and petechiae, and purpura and mucosal bleeding due to thrombocytopenia. Treatment often involves a stepwise escalation of immunosuppressive treatments (e.g., corticosteroids, anti-CD20 monoclonal antibodies) and/or stimulants (e.g., thrombopoietin receptor agonists). However, sustained remission remains elusive in many patients. We report the case of a 69-year-old woman with a 19-year history of Evans syndrome, presenting with a life-threatening relapse marked by severe thrombocytopenia and strong hemolytic activity. The patient had previously undergone multiple treatment regimens and had developed comorbidities that both complicated disease management and treatment strategies. Despite repeated therapeutic interventions with various immunosuppressant agents, she remained transfusion-dependent and clinically unstable and experienced various treatment complications. Additionally, targeting antibody-producing plasma cells with daratumumab (anti-CD38) led to a rapid fall in transfusion dependency, clinical stabilization, and transition to outpatient care. Unfortunately, the patient later succumbed to infectious complications after a femoral fracture. This case underscores the therapeutic complexity of multirefractory Evans syndrome and the limitations of conventional therapy. The addition of daratumumab, resulting in depletion of CD38+ plasma cells, helped achieve hematologic stabilization in this refractory case.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/frhem.2025.1683981</guid>
        <link>https://www.frontiersin.org/articles/10.3389/frhem.2025.1683981</link>
        <title><![CDATA[Case Report: Durable response to PD-1 blockade after failure of ALK-targeted therapy and chemoimmunotherapy in ALK-positive large B-cell lymphoma]]></title>
        <pubdate>2026-01-23T00:00:00Z</pubdate>
        <category>Case Report</category>
        <author>Guilherme Gasparini Spiandorelo</author><author>Ahmed Alnughmush</author><author>Olivia Crum</author><author>Dragan Jevremovic</author><author>J. C. Villasboas</author>
        <description><![CDATA[BackgroundAnaplastic lymphoma kinase–positive large B-cell lymphoma (ALK+ LBCL) is an exceedingly rare and aggressive subtype of B-cell non-Hodgkin lymphoma, comprising less than 1% of all LBCL cases. These tumors often exhibit resistance to standard chemoimmunotherapy and targeted approaches, resulting in poor clinical outcomes and a median overall survival of approximately 20 months. Despite the identification of ALK rearrangements and activating mutations, effective treatment strategies remain elusive.Case presentationWe report a case of an adult diagnosed with stage IV ALK+ LBCL, confirmed via lymph node biopsy and fluorescence in situ hybridization (FISH) demonstrating ALK rearrangement in 91% of nuclei. The patient progressed through four lines of therapy, including R-CHOP, alectinib, lorlatinib with involved-field radiation, and brentuximab vedotin plus bendamustine. Comprehensive genomic profiling revealed a CLTC-ALK fusion and two ALK gain-of-function mutations (p.L1196M and p.G1202R), which are typically sensitive to lorlatinib, suggesting ALK-independent resistance mechanisms. Repeat biopsy demonstrated 20%–30% PD-L1 expression in tumor cells. With no standard options remaining, the patient elected to receive off-label nivolumab. Remarkably, despite an initial disease flare, a rapid clinical and radiological response was observed after just two cycles. As of the latest follow-up after 16 cycles, the patient remains on treatment with sustained clinical benefit and no adverse events reported.DiscussionThis case highlights the therapeutic challenges of ALK+ LBCL, including its refractoriness to both standard chemotherapy and ALK inhibitors, even in the presence of targetable mutations. The exceptional response to PD-1 blockade, possibly facilitated by acquired PD-L1 expression and an inflammatory tumor microenvironment, suggests an immunologically active tumor niche. Comparison with prior cases supports the hypothesis that PD-L1 expression, even at moderate levels, may predict responsiveness to immune checkpoint inhibitors in this rare lymphoma subtype.ConclusionThis case underscores the potential of immune checkpoint inhibition in ALK+ LBCL, particularly in patients with relapsed or refractory disease. PD-L1 testing and repeat biopsy at progression may offer critical insights for guiding therapy. Prospective studies are warranted to explore checkpoint blockade alone or in combination with targeted agents in this aggressive lymphoma.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/frhem.2025.1730554</guid>
        <link>https://www.frontiersin.org/articles/10.3389/frhem.2025.1730554</link>
        <title><![CDATA[Too soon to switch? Early TKI switching vs. continuous monotherapy: long-term outcomes in chronic myeloid leukemia]]></title>
        <pubdate>2026-01-21T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Muluken Megiso</author><author>Chidiebube Ugwu</author><author>Elvis Obomanu</author><author>Alankrita Taneja</author>
        <description><![CDATA[BackgroundEarly switching of tyrosine kinase inhibitors (TKIs) in chronic myeloid leukemia (CML), particularly within the first 3 months of initiation, may indicate intolerance or suboptimal response. However, the long-term clinical impact of such early modifications remains uncertain. This study compares outcomes between patients who switched early and those who remained on their initial TKI.MethodsWe used data from the TriNetX US Collaborative Network to compare matched cohorts of early switchers and long-term non-switchers for imatinib (n=349 vs. n=4,579), dasatinib (n=377 vs. n=2,849), and nilotinib (n=114 vs. n=1,308). Patients were followed for 3 and 5 years. Outcomes included mortality, cardiovascular complications, diabetes, thromboembolic events, hospitalizations, and ICU admissions. The analysis period began immediately after the TKI switch for switchers. To minimize bias and ensure correct outcome attribution, patients who had any of the outcomes before switching were excluded from both cohorts. Propensity matching and logistic regression were applied to estimate risk ratios (RRs) with 95% confidence intervals (CIs).ResultsEarly switch from imatinib was associated with significantly higher 5-year mortality (24.0% vs. 11.9%; RR = 2.03, 95% CI 1.43–2.87, p < 0.001). Increased rates of heart failure were observed at both 3 years (10.8% vs. 5.4%; RR = 1.99, p = 0.015) and 5 years (12.1% vs. 7.3%; RR = 1.65, p = 0.046), alongside higher hospitalization (27.9% vs. 16.5%; p = 0.019) and ICU admissions (11.9% vs. 7.0%; p = 0.033). Dasatinib early switchers had worse 5-year mortality (21.1% vs. 14.0%; RR = 1.51, p = 0.011) and more frequent heart failure at 3 years (12.1% vs. 6.7%; RR = 1.80, p = 0.020). ICU admission was also significantly elevated at both 3 years (17.3% vs. 9.2%) and 5 years (19.9% vs. 10.3%; RR = 1.88, p = 0.002). Among nilotinib users, early switching resulted in a non-significant increase in 5-year mortality (20.2% vs. 11.5%; RR = 1.75, p = 0.074) but was linked to significantly higher ICU admissions at 5 years (19.4% vs. 9.3%; RR = 2.10, p = 0.033).ConclusionsEarly switching from first-line TKI therapy in CML is consistently associated with worse survival and greater complication rates across multiple agents. These results emphasize the need for cautious decision-making and close monitoring when considering early changes to frontline therapy.]]></description>
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