Blood Research最新文献

{"title":"Allogeneic stem cell transplantation for myelofibrosis in the modern era: Single-center outcomes with DIPSS risk stratification.","authors":"Dae-Ho Choi, Jun Ho Jang, Chul Won Jung","doi":"10.1007/s44313-026-00142-5","DOIUrl":"10.1007/s44313-026-00142-5","url":null,"abstract":"<p><strong>Purpose: </strong>To describe the post-transplant outcomes in patients with myelofibrosis stratified by the Dynamic International Prognostic Scoring System (DIPSS) risk at transplantation, and to identify clinical factors associated with overall survival (OS) after allogeneic hematopoietic stem cell transplantation (allo-HSCT).</p><p><strong>Methods: </strong>We retrospectively analyzed the data of 42 patients with myelofibrosis who underwent allo-HSCT at Samsung Medical Center between 2014 and 2023. OS was estimated using the Kaplan-Meier method and compared using the log-rank test. Exploratory Cox proportional-hazard regression analyses were performed to assess independent associations with OS.</p><p><strong>Results: </strong>At transplantation, 28 patients (66.7%) had Intermediate (Int-1/2) and 14 (33.3%) had High DIPSS risk. OS differed significantly by DIPSS risk group (log-rank P = 0.0034): the median OS was 15.2 months (95% confidence interval [CI], 7.2-NR months) in the Intermediate-risk group versus 6.4 months (95% CI, 3.3-35.1 months) in the High-risk group. All 14 patients in the High-risk group (100%) and 14 of 28 patients in the Intermediate-risk group (50%) died during follow-up. The 1-, 2-, and 3-year OS rates in the Intermediate- and High-risk groups were 57.1% vs. 28.6%, 50.0% vs. 14.3%, and 50.0% vs. 7.1%, respectively. In an exploratory multivariable analysis adjusted for hematopoietic cell transplantation-specific comorbidity index and donor type, DIPSS High-risk disease remained independently associated with inferior OS (adjusted hazard ratio [HR], 2.91; 95% CI, 1.27-6.63; P = 0.011). No other clinical variable, including age (≥ 60 vs. < 60 years; P = 0.16 by log-rank), achieved statistical significance.</p><p><strong>Conclusion: </strong>DIPSS High-risk disease at transplantation was associated with uniformly poor post-transplant survival in this single-center cohort. These hypothesis-generating findings underscore the importance of transplant timing before progression to high-risk disease, and warrant validation in larger multicenter studies.</p>","PeriodicalId":46224,"journal":{"name":"Blood Research","volume":"61 1","pages":""},"PeriodicalIF":3.7,"publicationDate":"2026-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13234046/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148151714","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Real-world experience with gilteritinib maintenance following allogeneic transplantation in relapsed/refractory AML patients harboring FLT3 mutations.","authors":"Yun-Tzu Lin, Xavier Cheng-Hong Tsai, Feng-Ming Tien, Yuan-Yeh Kuo, Mei-Hsuan Tseng, Jia-Hau Liu, Bor-Sheng Ko, Chieh-Lung Cheng, Sheng-Chieh Chou, Ming-En Lin, Chien-Chin Lin, Ming-Kai Chuang, Ming Yao, Hsin-An Hou, Wen-Chien Chou, Hwei-Fang Tien","doi":"10.1007/s44313-026-00144-3","DOIUrl":"10.1007/s44313-026-00144-3","url":null,"abstract":"<p><strong>Background: </strong>Gilteritinib is an established FLT3 inhibitor used to treat patients with relapsed or refractory (R/R) acute myeloid leukemia (AML) harboring FLT3 mutations. Prior studies have predominantly evaluated gilteritinib as a posttransplant maintenance therapy in patients who undergo allogeneic hematopoietic stem cell transplantation (allo-HSCT) in complete remission. Nonetheless, evidence remains limited for patients who receive gilteritinib as salvage therapy in a relapsed or refractory setting, proceed to allo-HSCT, and subsequently continue gilteritinib maintenance. This real-world study aimed to address this knowledge gap in an Asian cohort.</p><p><strong>Method and result: </strong>Patients with FLT3-mutated R/R AML received gilteritinib before transplantation, and those achieving engraftment without grade ≥ 2 acute graft-versus-host disease were offered posttransplant maintenance between days 30 and 90. The cohort (median age, 48 years; 92.0% FLT3-ITD) achieved a complete response (CR) rate of 76.2%. At a median follow-up of 46.2 months, gilteritinib maintenance therapy was associated with longer relapse-free and overall survival and a significantly lower 1-year cumulative incidence of relapse. Exploratory measurable residual disease (MRD) subgroup analyses suggested a numerically greater survival difference in patients without flow cytometry-detectable MRD before or after transplantation; however, the findings are limited by the small sample size and lack of FLT3-targeted next-generation sequencing-based MRD assessment.</p><p><strong>Conclusion: </strong>Gilteritinib was generally well-tolerated, with no observed increase in cytomegalovirus (CMV)-related or graft-versus-host complications. This study provides real-world evidence in a clinically relevant scenario and supports the use of gilteritinib maintenance in patients with FLT3-mutated AML who undergo transplantation during R/R disease.</p>","PeriodicalId":46224,"journal":{"name":"Blood Research","volume":"61 1","pages":""},"PeriodicalIF":3.7,"publicationDate":"2026-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13234079/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148151736","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A mitochondrial-based prognostic score for risk stratification in acute myeloid leukemia.","authors":"Isabelle C Santos, Vitória J Silva-Xavier, Amanda Moreira-Aguiar, Marcio T Reis-Silva, Lidiane P Silva, Pedro L França-Neto, Marcos A Bezerra, João A Machado-Neto, Diego A Pereira-Martins, Antonio R Lucena-Araujo, Juan L Coelho-Silva","doi":"10.1007/s44313-026-00139-0","DOIUrl":"10.1007/s44313-026-00139-0","url":null,"abstract":"","PeriodicalId":46224,"journal":{"name":"Blood Research","volume":"61 1","pages":""},"PeriodicalIF":3.7,"publicationDate":"2026-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13216444/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148036316","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The role of impaired bone marrow Tregs in hematopoietic stem cell depletion for pediatric aplastic anemia probably involves immune privilege.","authors":"Can Huang, Shanshan Li, Jingwei Yang, Yangyang Jiao, Ting Zhang, Hui Jiang, Fanyi Zeng, Shayi Jiang","doi":"10.1007/s44313-026-00141-6","DOIUrl":"10.1007/s44313-026-00141-6","url":null,"abstract":"<p><strong>Purpose: </strong>An immune-mediated pathogenesis has been postulated for aplastic anemia (AA), and impaired Tregs and other immune abnormalities have been identified in patients with AA. However, the process by which abnormal immunity specifically damages hematopoietic stem cells (HSCs) remains unclear. We conducted primary clinical studies to investigate whether the depletion of HSCs in AA could be attributed to the collapse of immune privilege (IP) afforded by regulatory T cells (Tregs).</p><p><strong>Methods: </strong>The distribution of Tregs in the bone marrow of children with AA, myelodysplastic syndrome (MDS), and control participants was separately detected by immunohistochemistry. T-helper 1 (Th1), T-helper 2 (Th2), and T-helper 17 (Th17) cells, cytokines, and HSCs in the bone marrow of the AA and control groups were examined using flow cytometry.</p><p><strong>Results: </strong>Patients with AA showed significantly lower FoxP3 + /CD4 + ratios (AA vs. normal: 18.09% ± 5.38% vs. 21.72% ± 4.21%, P = 0.014; AA vs. MDS: 18.09% ± 5.38% vs. 22.63% ± 5.98%, P = 0.030) and reduced Treg counts (AA vs. normal: 4.07 ± 1.41 vs. 5.25 ± 1.86 cells/HP, P = 0.014; AA vs. MDS: 4.07 ± 1.41 vs. 5.30 ± 1.49 cells/HP, P = 0.024) near the endosteum. The bone marrow in patients with AA exhibited Th1 dominance (AA vs. normal: 39.80% ± 5.20% vs. 22.1% ± 2.9% in controls, P < 0.001) and Th2 reduction (AA vs. normal: 59.20% ± 5.30% vs. 77.20% ± 2.60%, P < 0.001), indicating IP dysfunction. Significant elevation of tumor necrosis factor (TNF)-α, interferon (IFN)-γ, and interleukin (IL)-17 levels was observed in the bone marrow of patients with AA. Long-term (LT)-HSCs were severely depleted in patients with AA (AA vs. normal: 0.13% vs. 1.22%, P = 0.035), with moderate reduction in short-term (ST)-HSCs.</p><p><strong>Conclusions: </strong>Patients with AA showed endosteal Treg reduction, Th1 dominance, elevated proinflammatory cytokine levels, and severe LT-HSC depletion, linking bone marrow IP dysfunction to HSC damage. These findings provide a mechanistic explanation for the specific loss of HSCs in AA and highlight the IP niche as a therapeutic target.</p>","PeriodicalId":46224,"journal":{"name":"Blood Research","volume":" ","pages":""},"PeriodicalIF":3.7,"publicationDate":"2026-05-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13250033/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148018087","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A strategic approach to managing Immune Effector Cell-Associated Hematotoxicity (ICAHT) during chimeric antigen receptor T-cell therapy.","authors":"Sang Eun Yoon","doi":"10.1007/s44313-026-00143-4","DOIUrl":"10.1007/s44313-026-00143-4","url":null,"abstract":"","PeriodicalId":46224,"journal":{"name":"Blood Research","volume":"61 1","pages":""},"PeriodicalIF":3.7,"publicationDate":"2026-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13187066/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147975491","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dynamic, anthracycline-induced chromatin alterations enable ALDH1 expression as a mechanism of inducible leukemia resistance development.","authors":"Spiros A Vlahopoulos","doi":"10.1007/s44313-026-00140-7","DOIUrl":"10.1007/s44313-026-00140-7","url":null,"abstract":"<p><p>The evolution of acute myeloid leukemia (AML) cells toward developing drug resistance, which eventually leads to relapse, involves the convergence of their chromatin compaction status toward a pattern that is distinctive of \"stem-like\" cells and is conducive to increased expression of nuclear factor kappa B (NFκB). This phenomenon develops irrespective of the genetic mutations carried by the AML clones. Multiple lines of evidence therefore suggest that relapsed and refractory leukemia develops through alterations in chromatin, which perturb the normal cellular regulation of inflammatory and stress responses. In particular, during the development of acute leukemia phenotypes that resist drug treatment and give rise to relapse, malignant clones carrying different genetic alterations often converge into specific phenotypes with the apparent criterion being shared patterns of chromatin exposure. These shared patterns include genes involved in innate immune pathways that provide malignant cells with a selective advantage. Such a selective advantage is provided also by expression of cytosolic retinaldehyde dehydrogenases such as ALDH1A1, which was shown to characterize AML cells driving relapse, and which are resistant to chemotherapy.</p>","PeriodicalId":46224,"journal":{"name":"Blood Research","volume":"61 1","pages":""},"PeriodicalIF":3.7,"publicationDate":"2026-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13172156/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147934438","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exploring CD79b, LC3, and TERT expression in NON-GCB DLBCL: markers associated with Rituximab-Cyclophosphamide-Doxorubicin-Vincristin-Prednisone treatment response.","authors":"Bethy S Hernowo, Arnita Ilanur, Hasrayati Agustina, Amaylia Oehadian, Birgitta M Dewayani, Anglita Yantisetiasti, Hermin A Usman, Etis Primastari, Okky Husain, Nia Nuraeni, Nurvita Trianasari","doi":"10.1007/s44313-026-00129-2","DOIUrl":"10.1007/s44313-026-00129-2","url":null,"abstract":"<p><strong>Introduction: </strong>Diffuse large B-cell lymphoma (DLBCL) represents the most common subtype of non-Hodgkin lymphoma. The non-germinal center B-cell-like (non-GCB) subtype is associated with a poor prognosis and reduced response rates to rituximab cyclophosphamide-doxorubicin-vincristin-prednisone (R-CHOP) therapy. Resistance may involve cluster of differentiation 79B (CD79B)-driven B-cell receptor (BCR)/nuclear factor kappa B activation, microtubule-associated protein 1 light chain 3 (LC3)-mediated autophagy, and telomerase reverse transcriptase (TERT)-related survival signaling. The interrelationships between these markers and their associations with therapeutic responses remain unclear. This study evaluated the association between CD79B, LC3, and TERT expression and response to R-CHOP in non-GCB DLBCL.</p><p><strong>Methods: </strong>This analytical case-control study included 58 paraffin-embedded samples from patients with non-GCB DLBCL diagnosed at the Dr. Hasan Sadikin General Hospital, Bandung, Indonesia (2017-2023). Tumor characteristics were assessed using immunohistochemical staining for CD79B, LC3, and TERT. Expression levels were evaluated semi-quantitatively based on staining intensity and the proportion of positive tumor cells. Treatment responses were categorized as response (complete/partial) or non-response (stable/progressive). Statistical analyses were performed using the chi-square test, Fisher's exact test, and binary logistic regression, with significance defined as p < 0.05.</p><p><strong>Results: </strong>TERT, CD79B, and LC3 expression was detected in 53.4%, 55.2%, and 62.1% of the cases, respectively. Among non-responsive patients, TERT and LC3 expression rates were 62.1% and 69.0% (p > 0.05), respectively. CD79B expression was significantly associated with non-response (p = 0.002). Moreover, multivariate analysis identified positive CD79B expression as an independent predictor of non-response to R-CHOP therapy (OR = 9.72).</p><p><strong>Conclusion: </strong>CD79B expression was independently associated with a poor response to R-CHOP therapy in non-GCB DLBCL. The positive association between TERT and LC3 suggests the presence of additional metabolic adaptation mechanisms supporting tumor survival.</p>","PeriodicalId":46224,"journal":{"name":"Blood Research","volume":" ","pages":""},"PeriodicalIF":3.7,"publicationDate":"2026-05-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13168377/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147870022","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Enlarged splenic volume predicts poor survival and is associated with inflammatory imbalance in patients with diffuse large B-cell lymphoma.","authors":"Zongjian Qiu, Rifeng Jiang, Shunquan Wu, Rong Zhan, Xiaomei Hu, Shaoyuan Wang","doi":"10.1007/s44313-026-00138-1","DOIUrl":"10.1007/s44313-026-00138-1","url":null,"abstract":"<p><strong>Purpose: </strong>The spleen plays a significant role in innate and adaptive immunity. We aimed to evaluate the prognostic significance of the splenic volume in patients with diffuse large B-cell lymphoma (DLBCL), research on which is limited.</p><p><strong>Methods: </strong>We retrospectively analyzed 175 patients diagnosed with DLBCL. Based on optimal thresholds, patients were stratified into small (< 185 cm³), medium (185-315 cm³), and large (≥ 315 cm³) splenic volume groups. Survival analysis was performed using Kaplan-Meier and Cox proportional hazards model.</p><p><strong>Results: </strong>A significant decrease in progression-free survival (PFS) (P < 0.0001) and overall survival (OS) (P < 0.0001) was observed in the large group that received cyclophosphamide, hydroxydaunorubicin, vincristine, and prednisone (CHOP) without or with rituximab (R-CHOP) treatment. Among the 139 patients who received R-CHOP, significant adverse effects on PFS (P < 0.0036) and OS (P < 0.0035) were observed in the large group. Univariate and multivariate analyses demonstrated that enlarged splenic volume (≥ 315 cm³) was associated with decreased PFS (P < 0.0001, P < 0.01, respectively) and OS (P < 0.001, P < 0.01, respectively). In terms of peripheral blood inflammatory markers, patients with enlarged splenic volume (≥ 315 cm³) exhibited lymphocytopenia, increased monocyte-to-lymphocyte ratio (MLR), increased neutrophil-to-lymphocyte ratio (NLR), and higher red blood cell distribution width (RDW) compared to that in those with smaller splenic volumes (P < 0.001, P < 0.001, P = 0.01, and P < 0.005, respectively).</p><p><strong>Conclusion: </strong>Splenic volume exceeding 315 cm³ is a poor prognostic factor for PFS and OS in patients with DLBCL. An enlarged splenic volume may be associated with compromised anti-cancer immune responses and aberrant inflammatory conditions.</p>","PeriodicalId":46224,"journal":{"name":"Blood Research","volume":" ","pages":""},"PeriodicalIF":3.7,"publicationDate":"2026-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13250030/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147844409","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Deregulation of stemness and senescence genes in bone marrow mesenchymal stem cells of multiple myeloma: implications for therapeutic approaches.","authors":"Fatemeh Soleymani, Saeideh Kavousi, Nastaran Khodakarim, Mohammad Ahmadvand","doi":"10.1007/s44313-026-00128-3","DOIUrl":"10.1007/s44313-026-00128-3","url":null,"abstract":"<p><strong>Purpose: </strong>Multiple myeloma (MM) is a hematologic malignancy associated with a poor prognosis. MM-derived mesenchymal stromal cells (MM-MSCs) contribute to disease progression by creating a supportive stromal microenvironment for malignant cells. Elucidating transcriptomic alterations in MSCs may therefore facilitate the development of novel therapeutic strategies for treatment-resistant MM.</p><p><strong>Methods: </strong>Total RNA was extracted from cultured MSCs isolated from bone marrow aspirates of patients with MM and normal donors (ND-MSCs). Expression of stemness markers (NANOG, OCT4) and senescence-associated genes (P16, P21, IL-6, IL-8) was analyzed using reverse transcription-quantitative polymerase chain reaction. Cellular senescence was assessed by senescence-associated β-galactosidase (SA-β-gal) staining.</p><p><strong>Results: </strong>Compared with ND-MSCs, MM-MSCs demonstrated a higher percentage of SA-β-gal-positive cells. Gene expression analysis showed upregulation of P21 and IL-6 in MM-MSCs, whereas NANOG and OCT4 were significantly downregulated. Notably, this downregulation was consistent with analysis of a publicly available RNA sequencing dataset, supporting the validity of our findings.</p><p><strong>Conclusions: </strong>Consistent with previous reports of increased senescence, our findings demonstrate significant downregulation of stemness-related genes (NANOG, OCT4) in MSCs from newly diagnosed, untreated patients with MM. This concurrent dysregulation of stemness and increased senescent phenotype may contribute to the pathogenicity of the tumor microenvironment and represents a potential target for therapeutic intervention.</p><p><strong>Clinical trial registration: </strong>Not applicable. This study did not involve a clinical trial.</p>","PeriodicalId":46224,"journal":{"name":"Blood Research","volume":"61 1","pages":""},"PeriodicalIF":3.7,"publicationDate":"2026-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13153312/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147844415","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Checkpoint inhibitor-induced hematologic immune-related adverse events and their association with disease recurrence in hematolymphoid malignancies: a clinical perspective.","authors":"Chokri Ben Lamine, Amr Hanbali, Ghada ElGohary, Hanan Alkhaldi, Riad El Fakih, Mahmoud Aljurf","doi":"10.1007/s44313-026-00135-4","DOIUrl":"10.1007/s44313-026-00135-4","url":null,"abstract":"<p><p>Immune checkpoint inhibitors have transformed the treatment of hematolymphoid malignancies by enhancing antitumor immunity. These agents are associated with immune-related adverse events (irAEs), including hematologic toxicities such as autoimmune hemolytic anemia, immune-related thrombocytopenia (irTCP), and neutropenia. Although rare, hematologic irAEs (hem-irAEs) may reflect systemic immune activation and could serve as biomarkers of treatment response. Emerging evidence, particularly from observational studies and meta-analyses, suggests that patients who experience hem-irAEs may have lower rates of disease recurrence and improved survival outcomes. This manuscript reviews the mechanisms, incidence, and prognostic implications of hem-irAEs in patients with hematolymphoid malignancies, emphasizing their hypothesis-generating potential as predictive markers that warrant prospective validation.</p>","PeriodicalId":46224,"journal":{"name":"Blood Research","volume":"61 1","pages":""},"PeriodicalIF":3.7,"publicationDate":"2026-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13149672/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147844392","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}