Pub Date : 2026-02-03DOI: 10.1182/blood.2025029358
Ting Du, Teng Fang, Sindhu C Pillai, Arghya Ray, Minxing Wang, Xueping Wan, Kenneth Wen, Yuntong Liu, Jingyu Xu, Md Abu Musa, Xiangdong Liu, Mariateresa Fulciniti, Nikhil C Munshi, Filip Garbicz, Ruben D Carrasco, Yao Yao, Zhongkun Zhang, Yan Song, Kenneth C Anderson
We found that PSMD1, a key subunit of the 19S proteasome regulatory particle, was overexpressed and correlated with poor prognosis in multiple myeloma (MM). Genetic depletion of PSMD1 decreased cancer cell viability, induced polyubiquitinated protein accumulation, and promoted apoptosis. Proteomic analysis revealed the activation of immune-related pathways, suggesting the potential for immune modulation. Targeting PSMD1 with siRNA, delivered via lipid nanoparticles (LNPs), reduced tumor growth in MM cell lines and primary patient samples while sparing normal cells. It also overcame proteasome inhibitor resistance and the protective effects of the bone marrow milieu. In MM xenograft mouse models, PSMD1 siRNA LNPs significantly reduced tumor growth and prolonged survival. In addition, PSMD1 depletion had similar effects on other types of cancer cell lines. These findings position PSMD1 as a critical target in cancer therapy, with broad implications for overcoming drug resistance, improving therapeutic outcomes, and potentially impacting immune responses across various cancers. These findings provide a foundation for the clinical development of PSMD1-targeted therapies in myeloma and other malignancies.
{"title":"Proteasome Subunit PSMD1 is a Key Therapeutic Target in Multiple Myeloma.","authors":"Ting Du, Teng Fang, Sindhu C Pillai, Arghya Ray, Minxing Wang, Xueping Wan, Kenneth Wen, Yuntong Liu, Jingyu Xu, Md Abu Musa, Xiangdong Liu, Mariateresa Fulciniti, Nikhil C Munshi, Filip Garbicz, Ruben D Carrasco, Yao Yao, Zhongkun Zhang, Yan Song, Kenneth C Anderson","doi":"10.1182/blood.2025029358","DOIUrl":"https://doi.org/10.1182/blood.2025029358","url":null,"abstract":"<p><p>We found that PSMD1, a key subunit of the 19S proteasome regulatory particle, was overexpressed and correlated with poor prognosis in multiple myeloma (MM). Genetic depletion of PSMD1 decreased cancer cell viability, induced polyubiquitinated protein accumulation, and promoted apoptosis. Proteomic analysis revealed the activation of immune-related pathways, suggesting the potential for immune modulation. Targeting PSMD1 with siRNA, delivered via lipid nanoparticles (LNPs), reduced tumor growth in MM cell lines and primary patient samples while sparing normal cells. It also overcame proteasome inhibitor resistance and the protective effects of the bone marrow milieu. In MM xenograft mouse models, PSMD1 siRNA LNPs significantly reduced tumor growth and prolonged survival. In addition, PSMD1 depletion had similar effects on other types of cancer cell lines. These findings position PSMD1 as a critical target in cancer therapy, with broad implications for overcoming drug resistance, improving therapeutic outcomes, and potentially impacting immune responses across various cancers. These findings provide a foundation for the clinical development of PSMD1-targeted therapies in myeloma and other malignancies.</p>","PeriodicalId":9102,"journal":{"name":"Blood","volume":" ","pages":""},"PeriodicalIF":23.1,"publicationDate":"2026-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146112508","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-30DOI: 10.1182/blood.2025029985
Jonathan M Marron,Lindsay R Semler,Gregory A Abel
Caring for individuals with hematological disorders is increasingly complex, and with medical complexity often comes ethical complexity. Prognostic uncertainty, stakeholder conflicts, and myriad other ethical challenges often contribute to situations that can benefit from ethics support. Through the presentation of three vignettes focusing on ethical dilemmas arising from hematology cases, we review the four phases of clinical ethics consultation: consult triage; ethics consult intake; stakeholder meeting(s) and additional data collection; and ethics analysis and recommendations. In tandem, we review some of the most common ethical framework/approaches used to inform hematology ethics consultation support services. We conclude that ethics consult services can be a valuable resource in providing care for patients with blood disorders and are a vital resource to enhance patient care, support clinicians, and ensure that difficult choices are navigated with clarity, compassion, and integrity.
{"title":"How I Approach Clinical Ethics Consultation in Hematology.","authors":"Jonathan M Marron,Lindsay R Semler,Gregory A Abel","doi":"10.1182/blood.2025029985","DOIUrl":"https://doi.org/10.1182/blood.2025029985","url":null,"abstract":"Caring for individuals with hematological disorders is increasingly complex, and with medical complexity often comes ethical complexity. Prognostic uncertainty, stakeholder conflicts, and myriad other ethical challenges often contribute to situations that can benefit from ethics support. Through the presentation of three vignettes focusing on ethical dilemmas arising from hematology cases, we review the four phases of clinical ethics consultation: consult triage; ethics consult intake; stakeholder meeting(s) and additional data collection; and ethics analysis and recommendations. In tandem, we review some of the most common ethical framework/approaches used to inform hematology ethics consultation support services. We conclude that ethics consult services can be a valuable resource in providing care for patients with blood disorders and are a vital resource to enhance patient care, support clinicians, and ensure that difficult choices are navigated with clarity, compassion, and integrity.","PeriodicalId":9102,"journal":{"name":"Blood","volume":"282 1","pages":""},"PeriodicalIF":20.3,"publicationDate":"2026-01-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146089067","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-29DOI: 10.1182/blood.2025032536
Niels W C J van de Donk,Pieter Sonneveld,Hermann Einsele
BCMA- or GPRC5D-directed T-cell immunotherapies have substantially improved the survival of patients with relapsed/refractory multiple myeloma (MM). Despite these advances, a subset of patients does not respond, and most patients will eventually relapse. Tumor heterogeneity, resulting in rapid selection of both antigen-negative and antigen-low cells, is a critical issue affecting response to T-cell immunotherapies targeting single tumor-associated antigens. In addition, antigen escape (due to deletions, mutations, or epigenetic alterations) is frequently observed in patients who experience disease progression after CAR T-cell infusion or during BsAb treatment. Simultaneous targeting of two tumor-associated antigens may improve efficacy by addressing heterogeneous target expression and preventing antigen escape. Various dual-targeting strategies are currently evaluated in MM, including the combination of two single-antigen targeting BsAbs. Notably, the efficacy of the combination of teclistamab and talquetamab appears to have enhanced anti-MM activity, compared to the corresponding conventional BsAbs alone in similar patient populations. Furthermore, dual-antigen targeting with T-cell redirecting trispecific antibodies (e.g., ramantamig [BCMAxGPRC5D] and ISB2001 [BCMAxCD38]) has already demonstrated promising results in heavily pretreated MM with several studies ongoing in earlier stages of the disease. Studies with limited numbers of patients have demonstrated that CAR T-cell products with specificity for more than one antigen are also effective in advanced MM, but at this time none of the dual-targeting CAR T-cell products is clearly superior to targeting BCMA alone with ciltacabtagene autoleucel (cilta-cel). Dual-targeting should eventually be compared in large phase 3 trials with the classical approach of serial treatment with mono-targeting agents with target switch.
{"title":"Dual-antigen-targeting T-cell immunotherapies in MM: circumventing tumor heterogeneity and preventing antigen escape.","authors":"Niels W C J van de Donk,Pieter Sonneveld,Hermann Einsele","doi":"10.1182/blood.2025032536","DOIUrl":"https://doi.org/10.1182/blood.2025032536","url":null,"abstract":"BCMA- or GPRC5D-directed T-cell immunotherapies have substantially improved the survival of patients with relapsed/refractory multiple myeloma (MM). Despite these advances, a subset of patients does not respond, and most patients will eventually relapse. Tumor heterogeneity, resulting in rapid selection of both antigen-negative and antigen-low cells, is a critical issue affecting response to T-cell immunotherapies targeting single tumor-associated antigens. In addition, antigen escape (due to deletions, mutations, or epigenetic alterations) is frequently observed in patients who experience disease progression after CAR T-cell infusion or during BsAb treatment. Simultaneous targeting of two tumor-associated antigens may improve efficacy by addressing heterogeneous target expression and preventing antigen escape. Various dual-targeting strategies are currently evaluated in MM, including the combination of two single-antigen targeting BsAbs. Notably, the efficacy of the combination of teclistamab and talquetamab appears to have enhanced anti-MM activity, compared to the corresponding conventional BsAbs alone in similar patient populations. Furthermore, dual-antigen targeting with T-cell redirecting trispecific antibodies (e.g., ramantamig [BCMAxGPRC5D] and ISB2001 [BCMAxCD38]) has already demonstrated promising results in heavily pretreated MM with several studies ongoing in earlier stages of the disease. Studies with limited numbers of patients have demonstrated that CAR T-cell products with specificity for more than one antigen are also effective in advanced MM, but at this time none of the dual-targeting CAR T-cell products is clearly superior to targeting BCMA alone with ciltacabtagene autoleucel (cilta-cel). Dual-targeting should eventually be compared in large phase 3 trials with the classical approach of serial treatment with mono-targeting agents with target switch.","PeriodicalId":9102,"journal":{"name":"Blood","volume":"281 1","pages":""},"PeriodicalIF":20.3,"publicationDate":"2026-01-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146073134","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-29DOI: 10.1182/blood.2024028300
Ofri Rabany, Sivan Ben Dror, Maram Arafat, Hadar Aharoni Levitanus, Yudit Halperin, Virginie Marchand, Nikolai Romanovski, Noga Ussishkin, Maayan Livneh Golany, Adi Reches, Judith Wexler, Nina Mayorek, Galia Monderer-Rothkoff, Sagiv Shifman, Widad Mâmmer Bouhou, Michael VanInsberghe, Cornelius Pauli, Carsten Müller-Tidow, Ola Karmi, Yoav Livneh, Alexander van Oudenaarden, Yuri Motorin, Daphna Nachmani
Abstract: Self-renewal and differentiation are at the basis of hematopoiesis. Although it is known that tight regulation of translation is vital for hematopoietic stem cells' (HSC) biology, the mechanisms underlying translation regulation across the hematopoietic system remain obscure. Here, we reveal a novel mechanism of translation regulation in the hematopoietic hierarchy, which is mediated by rRNA methylation dynamics. Using ultralow-input ribosome profiling, we characterized cell-type-specific translation capacity during erythroid differentiation. We found that translation efficiency (TE) changes progressively with differentiation and can distinguish between discrete cell populations, as well as define differentiation trajectories. To reveal the underlying mechanism, we performed comprehensive mapping of the most abundant rRNA modification, 2'-O-methyl (2'OMe). We found that, such as TE, 2'OMe dynamics followed a distinct trajectory during erythroid differentiation. Genetic perturbation of individual 2'OMe sites demonstrated their distinct roles in modulating proliferation and differentiation. By combining CRISPR screening, molecular, and functional analyses, we identified a specific methylation site, 28S-Gm4588, which is progressively lost during differentiation, as a key regulator of HSC self-renewal. We showed that low methylation at this site led to translational skewing, mediated mainly by codon frequency, which promoted differentiation. Functionally, HSC with diminished 28S-Gm4588 methylation exhibited impaired self-renewal capacity ex vivo, and loss of fitness in vivo in bone marrow transplants. Extending our findings beyond the hematopoietic system, we also found distinct dynamics of 2'OMe profiles during differentiation of non-HSC. Our findings reveal rRNA methylation dynamics as a general mechanism for cell-type-specific translation, required for cell function and differentiation.
自我更新和分化是造血的基础。虽然已知翻译的严格调控对造血干细胞（hsc）生物学至关重要，但整个造血系统翻译调控的机制仍然不清楚。在这里，我们揭示了一种新的翻译调节机制，这是由核糖体RNA （rRNA）甲基化动力学介导的。使用超低输入核糖体分析，我们表征了红细胞分化过程中细胞类型特异性翻译能力。我们发现翻译效率随着分化而逐渐变化，并且可以区分离散细胞群体以及定义分化轨迹。为了揭示潜在的机制，我们对最丰富的rRNA修饰- 2'- o -甲基（2' ome）进行了全面的定位。我们发现，像翻译效率一样，2'OMe动力学在红系分化过程中遵循着不同的轨迹。单个2'OMe位点的遗传扰动表明它们在调节增殖和分化中具有不同的作用。通过结合CRISPR筛选、分子和功能分析，我们确定了一个特定的甲基化位点28S-Gm4588，它在分化过程中逐渐丢失，是HSC自我更新的关键调节因子。我们发现，该位点的低甲基化导致翻译偏斜，主要由密码子频率介导，从而促进分化。功能上，28S-Gm4588甲基化降低的造血干细胞在体外表现出自我更新能力受损，并且在骨髓移植中体内适应性丧失。将我们的发现扩展到造血系统之外，我们还发现非造血干细胞分化过程中2'OMe谱的独特动态。我们的研究结果揭示了rRNA甲基化动力学是细胞类型特异性翻译的一般机制，是细胞功能和分化所必需的。
{"title":"Dynamic rRNA methylation regulates translation in the hematopoietic system and is essential for stem cell fitness.","authors":"Ofri Rabany, Sivan Ben Dror, Maram Arafat, Hadar Aharoni Levitanus, Yudit Halperin, Virginie Marchand, Nikolai Romanovski, Noga Ussishkin, Maayan Livneh Golany, Adi Reches, Judith Wexler, Nina Mayorek, Galia Monderer-Rothkoff, Sagiv Shifman, Widad Mâmmer Bouhou, Michael VanInsberghe, Cornelius Pauli, Carsten Müller-Tidow, Ola Karmi, Yoav Livneh, Alexander van Oudenaarden, Yuri Motorin, Daphna Nachmani","doi":"10.1182/blood.2024028300","DOIUrl":"10.1182/blood.2024028300","url":null,"abstract":"<p><strong>Abstract: </strong>Self-renewal and differentiation are at the basis of hematopoiesis. Although it is known that tight regulation of translation is vital for hematopoietic stem cells' (HSC) biology, the mechanisms underlying translation regulation across the hematopoietic system remain obscure. Here, we reveal a novel mechanism of translation regulation in the hematopoietic hierarchy, which is mediated by rRNA methylation dynamics. Using ultralow-input ribosome profiling, we characterized cell-type-specific translation capacity during erythroid differentiation. We found that translation efficiency (TE) changes progressively with differentiation and can distinguish between discrete cell populations, as well as define differentiation trajectories. To reveal the underlying mechanism, we performed comprehensive mapping of the most abundant rRNA modification, 2'-O-methyl (2'OMe). We found that, such as TE, 2'OMe dynamics followed a distinct trajectory during erythroid differentiation. Genetic perturbation of individual 2'OMe sites demonstrated their distinct roles in modulating proliferation and differentiation. By combining CRISPR screening, molecular, and functional analyses, we identified a specific methylation site, 28S-Gm4588, which is progressively lost during differentiation, as a key regulator of HSC self-renewal. We showed that low methylation at this site led to translational skewing, mediated mainly by codon frequency, which promoted differentiation. Functionally, HSC with diminished 28S-Gm4588 methylation exhibited impaired self-renewal capacity ex vivo, and loss of fitness in vivo in bone marrow transplants. Extending our findings beyond the hematopoietic system, we also found distinct dynamics of 2'OMe profiles during differentiation of non-HSC. Our findings reveal rRNA methylation dynamics as a general mechanism for cell-type-specific translation, required for cell function and differentiation.</p>","PeriodicalId":9102,"journal":{"name":"Blood","volume":" ","pages":"520-533"},"PeriodicalIF":23.1,"publicationDate":"2026-01-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145450835","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-29DOI: 10.1182/blood.2025032073
Judith López,Konstantinos Tzelepis
{"title":"Ribosomal RNA methylation in HSCs: it's so \"good for you\".","authors":"Judith López,Konstantinos Tzelepis","doi":"10.1182/blood.2025032073","DOIUrl":"https://doi.org/10.1182/blood.2025032073","url":null,"abstract":"","PeriodicalId":9102,"journal":{"name":"Blood","volume":"72 1","pages":"476-478"},"PeriodicalIF":20.3,"publicationDate":"2026-01-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146073085","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-29DOI: 10.1182/blood.2025031546
Mary L Clarke
{"title":"Targeting proteostasis addiction in AML.","authors":"Mary L Clarke","doi":"10.1182/blood.2025031546","DOIUrl":"https://doi.org/10.1182/blood.2025031546","url":null,"abstract":"","PeriodicalId":9102,"journal":{"name":"Blood","volume":"147 5","pages":"479-480"},"PeriodicalIF":23.1,"publicationDate":"2026-01-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146084032","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-29DOI: 10.1182/blood.2025031744
Aintzane Zabaleta,Luis-Esteban Tamariz-Amador,Ioannis V Kostopoulos,Romanos Sklavenitis Pistofidis,Febe Smits,Paula Rodriguez-Otero,Carmen Roncal,Michelle P Aranha,David Žihala,Michaela Machu,Nikolaos Tsakirakis,Panagiotis Bakouros,Ourania Tsitsilonis,Irene Solia,Cristina Moreno,Catarina Maia,Esperanza Martin-Sanchez,José Juan Pérez,Cristina Encinas,Rafael Ríos-Tamayo,Albert Oriol,María-Jesús Blanchard,Felipe de Arriba,Esther González-García,Sunil Lakhwani,Anna Sureda,Valentín Cabañas,Fernando Escalante,Estrella Carrillo-Cruz,Albert Pérez-Montaña,Enrique María M Ocio,Joan Bargay,Alberto Orfao,Tomas Jelínek,Irene M Ghobrial,Tuna Mutis,Sonja Zweegman,Evangelos Terpos,Efstathios Kastritis,Joaquín Martínez-López,Juan-Jose Lahuerta,Carlos Fernández de Larrea,Laura Rosiñol,Joan Bladé,Maria-Victoria Mateos,Jesús F San-Miguel,Maria Teresa Cedena,Noemi Puig,Bruno Paiva
Infection remains a leading cause of morbidity in multiple myeloma. Preventing infections is paramount and immune profiling could reflect the cumulative effect of host, tumor and treatment-related immunosuppression. However, current understanding of immune dysfunction and its association with infection is limited. To address this gap in knowledge and identify immune biomarkers of increased infection risk, we performed immune profiling using next-generation flow cytometry in bone marrow and peripheral blood samples from 1,786 patients at various disease stages and treatment scenarios. Patients developing infection had significantly lower percentages of CD27+ B cells and CD27- NK cells, as well as increased CD27-/CD27+ T-cell ratio in bone marrow. These immune risk factors were validated in three independent datasets. An immune score was developed to stratify patients with ≤1 vs ≥2 of the aforementioned risk factors, which was associated with higher infection incidence (35% vs 60%, P <.001). The immune score (odds ratio: 2.31, P <.001), disease stage and CD38, BCMA or GPRC5D targeted therapy were independently associated with infection incidence. All cell types detectable in bone marrow and peripheral blood were significantly correlated, suggesting that immune biomarkers of increased infection risk could be monitored using minimally-invasive methods that are available in routine laboratories.
{"title":"Immune biomarkers of increased infection risk in multiple myeloma.","authors":"Aintzane Zabaleta,Luis-Esteban Tamariz-Amador,Ioannis V Kostopoulos,Romanos Sklavenitis Pistofidis,Febe Smits,Paula Rodriguez-Otero,Carmen Roncal,Michelle P Aranha,David Žihala,Michaela Machu,Nikolaos Tsakirakis,Panagiotis Bakouros,Ourania Tsitsilonis,Irene Solia,Cristina Moreno,Catarina Maia,Esperanza Martin-Sanchez,José Juan Pérez,Cristina Encinas,Rafael Ríos-Tamayo,Albert Oriol,María-Jesús Blanchard,Felipe de Arriba,Esther González-García,Sunil Lakhwani,Anna Sureda,Valentín Cabañas,Fernando Escalante,Estrella Carrillo-Cruz,Albert Pérez-Montaña,Enrique María M Ocio,Joan Bargay,Alberto Orfao,Tomas Jelínek,Irene M Ghobrial,Tuna Mutis,Sonja Zweegman,Evangelos Terpos,Efstathios Kastritis,Joaquín Martínez-López,Juan-Jose Lahuerta,Carlos Fernández de Larrea,Laura Rosiñol,Joan Bladé,Maria-Victoria Mateos,Jesús F San-Miguel,Maria Teresa Cedena,Noemi Puig,Bruno Paiva","doi":"10.1182/blood.2025031744","DOIUrl":"https://doi.org/10.1182/blood.2025031744","url":null,"abstract":"Infection remains a leading cause of morbidity in multiple myeloma. Preventing infections is paramount and immune profiling could reflect the cumulative effect of host, tumor and treatment-related immunosuppression. However, current understanding of immune dysfunction and its association with infection is limited. To address this gap in knowledge and identify immune biomarkers of increased infection risk, we performed immune profiling using next-generation flow cytometry in bone marrow and peripheral blood samples from 1,786 patients at various disease stages and treatment scenarios. Patients developing infection had significantly lower percentages of CD27+ B cells and CD27- NK cells, as well as increased CD27-/CD27+ T-cell ratio in bone marrow. These immune risk factors were validated in three independent datasets. An immune score was developed to stratify patients with ≤1 vs ≥2 of the aforementioned risk factors, which was associated with higher infection incidence (35% vs 60%, P <.001). The immune score (odds ratio: 2.31, P <.001), disease stage and CD38, BCMA or GPRC5D targeted therapy were independently associated with infection incidence. All cell types detectable in bone marrow and peripheral blood were significantly correlated, suggesting that immune biomarkers of increased infection risk could be monitored using minimally-invasive methods that are available in routine laboratories.","PeriodicalId":9102,"journal":{"name":"Blood","volume":"31 1","pages":""},"PeriodicalIF":20.3,"publicationDate":"2026-01-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146073082","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2026-01-29DOI: 10.1182/blood.2025031975
Ronjon Chakraverty
{"title":"Menin inhibitors: a 2-in-1 defense versus AML immune evasion.","authors":"Ronjon Chakraverty","doi":"10.1182/blood.2025031975","DOIUrl":"https://doi.org/10.1182/blood.2025031975","url":null,"abstract":"","PeriodicalId":9102,"journal":{"name":"Blood","volume":"43 1","pages":"482-483"},"PeriodicalIF":20.3,"publicationDate":"2026-01-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146073084","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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