Blood Neoplasia最新文献

{"title":"Central role of the mTORC1 pathway in glucocorticoid activity against B-ALL cells","authors":"Hiroshi Imanaga ,&nbsp;Yuichiro Semba ,&nbsp;Kensuke Sasaki ,&nbsp;Kiyoko Setoguchi ,&nbsp;Hillary Maniriho ,&nbsp;Takuji Yamauchi ,&nbsp;Tatsuya Terasaki ,&nbsp;Shigeki Hirabayashi ,&nbsp;Fumihiko Nakao ,&nbsp;Jumpei Nogami ,&nbsp;Shai Izraeli ,&nbsp;Koichi Akashi ,&nbsp;Takahiro Maeda","doi":"10.1016/j.bneo.2024.100015","DOIUrl":"https://doi.org/10.1016/j.bneo.2024.100015","url":null,"abstract":"<div><h3>Abstract</h3><p>Glucocorticoids (GCs), such as dexamethasone and prednisone, are crucial components of B-cell precursor acute lymphoblastic leukemia (B-ALL) therapies. However, the molecular basis of GC-induced cell death remains elusive. Here, we show that GC suppresses mechanistic target of rapamycin complex 1 (mTORC1) signaling and that, conversely, oncogenic activation of mTORC1 confers resistance to GCs. Our genome-wide CRISPR/CRISPR-associated protein 9 (CRISPR/Cas9) dropout screens reveal that depletion of components of either the gap activity toward Rags 1 or tuberous sclerosis complexes, both negative regulators of mTORC1 signaling, significantly attenuates B-ALL cell sensitivity to dexamethasone. Dexamethasone primarily induces B-ALL cell death by downregulating mTORC1 activity, thus promoting autophagy and impairing protein synthesis. Dexamethasone treatment failed to suppress mTORC1 activity in B-ALL cells expressing mutant GC receptors lacking DNA-binding capacity, suggesting that dexamethasone transcriptionally represses mTORC1 activity. RNA-sequencing analysis identified multiple dexamethasone target genes that negatively regulate mTORC1 activity. Our findings suggest that GC sensitivity is significantly influenced by oncogenic stimuli and/or growth factors that activate the PI3K-AKT-mTORC1 pathway. This is consistent with the frequent GC resistance found in Ph and Ph-like ALLs.</p></div>","PeriodicalId":100189,"journal":{"name":"Blood Neoplasia","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2950328024000153/pdfft?md5=ab04dd4c2a9ccc8ef49f43cf5cbbb31a&pid=1-s2.0-S2950328024000153-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141090068","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 novel application of XPO1 inhibition for the treatment of myelofibrosis","authors":"Megan Metzger ,&nbsp;Zachary M. Avigan ,&nbsp;Pankit Vachhani ,&nbsp;Julian Waksal ,&nbsp;John Mascarenhas","doi":"10.1016/j.bneo.2024.100010","DOIUrl":"10.1016/j.bneo.2024.100010","url":null,"abstract":"<div><h3>Abstract</h3><p>Myelofibrosis (MF) is a myeloproliferative neoplasm characterized by constitutional symptoms, progressive cytopenias, and splenomegaly. Activating mutations in the JAK/STAT pathway and cytokine dysregulation driving bone marrow fibrosis and extramedullary hematopoiesis underlie the pathobiology of MF. Although multiple JAK inhibitors are currently approved and provide significant symptom improvement, these agents do not possess disease course modifying potential. Additionally, outcomes are poor for patients who fail JAK inhibitors, highlighting the need for novel mechanism-based therapies and innovative combination strategies. Selinexor, a novel Exportin 1 (XPO1) inhibitor that blocks nuclear export, increases nuclear localization and activity of p53 and other tumor suppressor pathways and decreases cytoplasmic activation of multiple proliferative and profibrotic pathways. Selinexor currently has approved indications in multiple myeloma and lymphoma, with broad potential applications in other malignancies, although it can be limited by toxicity in some settings. Selinexor has shown clinical activity and tolerability in MF, both as monotherapy and, particularly, in combination with ruxolitinib. The collective, early phase trial data support a phase 3 randomized, registration study of selinexor and ruxolitinib in patients with MF naïve to JAK inhibitor therapy. Further work is needed to elucidate the role of XPO1 inhibition as a potential disease-modifying strategy to improve outcomes in MF.</p></div>","PeriodicalId":100189,"journal":{"name":"Blood Neoplasia","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-04-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2950328024000104/pdfft?md5=ddc40a14d238e982837d9bb17da6c825&pid=1-s2.0-S2950328024000104-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140787629","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":"Competition of dual SF3B1mt clones in MDS-RS is associated with distinct RNA mis-splicing in hematopoietic stem cells","authors":"Pedro Luis Moura ∗ ,&nbsp;Yasuhito Nannya ∗ ,&nbsp;Affaf Aliouat ∗ ,&nbsp;Isabel Juliana Hofman ∗ ,&nbsp;Teresa Mortera-Blanco ,&nbsp;Tetsuichi Yoshizato ,&nbsp;Ryunosuke Saiki ,&nbsp;Masahiro M. Nakagawa ,&nbsp;Maria Creignou ,&nbsp;Ann-Charlotte Björklund ,&nbsp;Gunilla Walldin ,&nbsp;Indira Barbosa ,&nbsp;Monika Jansson ,&nbsp;Francesca Grasso ,&nbsp;Edda M. Elvarsdottir ,&nbsp;Petter S. Woll ,&nbsp;Sten Eirik W. Jacobsen ,&nbsp;Seishi Ogawa ,&nbsp;Eva Hellström-Lindberg","doi":"10.1016/j.bneo.2024.100011","DOIUrl":"10.1016/j.bneo.2024.100011","url":null,"abstract":"","PeriodicalId":100189,"journal":{"name":"Blood Neoplasia","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-04-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2950328024000116/pdfft?md5=e1f4e294b86c0bb74441fc67727adefb&pid=1-s2.0-S2950328024000116-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140787827","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":"Saliva as a feasible alternative to blood for interrogation of somatic hematopoietic variants","authors":"Eli M. Soyfer ,&nbsp;Jianhong C. Heidmann ,&nbsp;Gajalakshmi Ramanathan ,&nbsp;Hellen Nguyen ,&nbsp;Simran Bhardwaj ,&nbsp;Jane H. Chen ,&nbsp;Yeowon Jung ,&nbsp;Eshika Arora ,&nbsp;Helen Huang ,&nbsp;Lauren Chen ,&nbsp;Aanya Amin ,&nbsp;Eduard Mas Marin ,&nbsp;W. Lucas Wadley ,&nbsp;Hew Yeng Lai ,&nbsp;Nahid Haghighi ,&nbsp;Angela G. Fleischman","doi":"10.1016/j.bneo.2024.100012","DOIUrl":"10.1016/j.bneo.2024.100012","url":null,"abstract":"","PeriodicalId":100189,"journal":{"name":"Blood Neoplasia","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-04-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2950328024000128/pdfft?md5=9011b4acd7f6d26593a3ba3c30d89418&pid=1-s2.0-S2950328024000128-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140785997","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":"Devimistat plus chemotherapy vs chemotherapy alone for older relapsed or refractory patients with AML: results of the ARMADA trial","authors":"Timothy S. Pardee ,&nbsp;Bayard L. Powell ,&nbsp;Richard A. Larson ,&nbsp;Joseph Maly ,&nbsp;Michael Keng ,&nbsp;Matthew Foster ,&nbsp;Eun-Ji Choi ,&nbsp;Heinz Sill ,&nbsp;Thomas Cluzeau ,&nbsp;Deepa Jeyakumar ,&nbsp;Olga Frankfurt ,&nbsp;Prapti Patel ,&nbsp;Michael Schuster ,&nbsp;Elisabeth Koller ,&nbsp;Regis Costello ,&nbsp;Uwe Platzbecker ,&nbsp;Pau Montesinos ,&nbsp;Susana Vives ,&nbsp;Aziz Nazha ,&nbsp;Rachel Cook ,&nbsp;Jorge Cortes","doi":"10.1016/j.bneo.2024.100009","DOIUrl":"10.1016/j.bneo.2024.100009","url":null,"abstract":"<div><h3>Abstract</h3><p>Acute myeloid leukemia (AML) is an aggressive cancer of the myeloid lineage. Outcomes in older patients are poor, with high rates of resistant and relapsed disease. Devimistat is a lipoic acid analog that inhibits mitochondrial metabolism. Devimistat combined with high-dose cytarabine and mitoxantrone resulted in promising phase 1 and 2 response rates especially in older patients. Therefore, the phase 3 ARMADA 2000 trial was conducted in patients aged ≥50 years with relapsed or refractory AML. The study randomized patients between devimistat combined with high-dose cytarabine and mitoxantrone (CHAM) or 1 of 3 control treatment regimens without devimistat: high-dose cytarabine and mitoxantrone; mitoxantrone, etoposide, and cytarabine; or fludarabine, cytarabine, and filgrastim. Overall, 265 patients consented to participate from 56 sites across 11 countries, and 200 patients were randomized, 98 patients to the devimistat arm and 102 patients to the control arm. The safety profile was consistent with high-dose cytarabine–based salvage regimens. There were 18 (9%) deaths on study (11 on CHAM and 7 on control). The study failed to meet its primary end point, with a complete remission (CR) rate of 20.4% in the devimistat arm compared with 21.6% in the control arm (<em>P</em> = .57). Overall survival was not statistically significantly different between the study arms, with a median of 8.9 months in the CHAM arm compared with 6.2 months in the control arm (<em>P</em> = .62). In conclusion, devimistat added to chemotherapy did not improve the CR rate or survival in patients aged ≥50 years with relapsed or refractory AML. This trial was registered at <span>www.ClinicalTrials.gov</span><svg><path></path></svg> as #NCT03504410.</p></div>","PeriodicalId":100189,"journal":{"name":"Blood Neoplasia","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-03-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2950328024000098/pdfft?md5=8d5513d5e2eee809a51383d73851adc6&pid=1-s2.0-S2950328024000098-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140405002","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":"Prospective performance of the IWG-2023 criteria and IPSS-M in a phase 2 trial of guadecitabine for higher-risk MDS or CMML","authors":"Samuel Urrutia ,&nbsp;Prithviraj Bose ,&nbsp;Yesid Alvarado ,&nbsp;Gautam Borthakur ,&nbsp;Farhad Ravandi ,&nbsp;Naval Daver ,&nbsp;Naveen Pemmaraju ,&nbsp;Elias Jabbour ,&nbsp;Koichi Takahashi ,&nbsp;Tapan Kadia ,&nbsp;Courtney DiNardo ,&nbsp;Steven Kornblau ,&nbsp;Rashmi Kanagal-Shamanna ,&nbsp;Xuelin Huang ,&nbsp;Kristy Bodden ,&nbsp;Hagop Kantarjian ,&nbsp;Guillermo Garcia-Manero","doi":"10.1016/j.bneo.2024.100008","DOIUrl":"10.1016/j.bneo.2024.100008","url":null,"abstract":"<div><h3>Abstract</h3><p>Guadecitabine (SGI-110) is a dinucleotide form of decitabine that has been studied in myelodysplastic syndrome (MDS) and acute myeloid leukemia. Here, we present the results of a single-center phase 2 trial of this agent for patients with higher-risk MDS or chronic myelomonocytic leukemia (CMML). Guadecitabine was administered at a dose of 60 mg/m2 subcutaneously for 5 days. Of 100 enrolled patients, 82% had MDS. The median age was 69 years, and International Prognostic Scoring System (IPSS) was intermediate-2 in 78% and high in 14%. Thirty-eight percent had complex cytogenetics, and 32% had <em>TP53</em>^<em>mut</em>. By the International Working Group 2006 (IWG-2006) criteria, 25% achieved complete remission (CR), 30% marrow CR, and 33% no response (NR). Common grade 3 events were febrile neutropenia (32%) and infection (25%). Mortality rates at 4 and 8 weeks were 0% and 4%, respectively. The median overall survival (mOS) was 16.8 months. Patients who underwent transplantation (21%) had an mOS of 46.6 months. We then reanalyzed this data set using IPSS-Molecular (IPSS-M) and IWG-2023 response criteria. By IPSS-M, 60% of patients were classified as very high and 27% as high risk. By IWG-2023, overall response rate was 52%, with 30% CR, 14% CR with limited count recovery, and 42% NR. IPSS-M provided adequate risk stratification at enrollment. Patients classified as marrow CR had widely different outcomes when reclassified by IWG-2023. In conclusion, SGI-110 was active in high-risk MDS, but survival is unlikely to be superior to current hypomethylating agents. The study is registered at <span>www.ClinicalTrials.gov</span><svg><path></path></svg> as #NCT02131597.</p></div>","PeriodicalId":100189,"journal":{"name":"Blood Neoplasia","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-03-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2950328024000086/pdfft?md5=7939e3a044510c2141a1112ae93823d1&pid=1-s2.0-S2950328024000086-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140402752","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":"Long-term remission with allogeneic transplant in patients with refractory/relapsed cutaneous cytotoxic T-cell lymphoma","authors":"Wen-Kai Weng ,&nbsp;Chaitanya Iragavarapu ,&nbsp;Gavin M. Weng ,&nbsp;Richard T. Hoppe ,&nbsp;Susan Hiniker ,&nbsp;Michael S. Khodadoust ,&nbsp;Youn H. Kim","doi":"10.1016/j.bneo.2024.100007","DOIUrl":"10.1016/j.bneo.2024.100007","url":null,"abstract":"","PeriodicalId":100189,"journal":{"name":"Blood Neoplasia","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-03-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2950328024000074/pdfft?md5=2dd103e3b108c65386bc27ac3ce66988&pid=1-s2.0-S2950328024000074-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140402164","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":"Comparison of TP53 mutations in myelodysplasia and acute leukemia suggests divergent roles in initiation and progression","authors":"Ashwini Jambhekar ,&nbsp;Emily E. Ackerman ,&nbsp;Berk A. Alpay ,&nbsp;Galit Lahav ,&nbsp;Scott B. Lovitch","doi":"10.1016/j.bneo.2024.100004","DOIUrl":"https://doi.org/10.1016/j.bneo.2024.100004","url":null,"abstract":"<div><h3>Abstract</h3><p><em>TP53</em> mutation predicts adverse prognosis in many cancers, including myeloid neoplasms, but the mechanisms by which specific mutations affect disease biology, and whether they differ between disease categories, remain unknown. We analyzed <em>TP53</em> mutations in 4 myeloid neoplasm subtypes (myelodysplastic syndrome [MDS], acute myeloid leukemia [AML], AML with myelodysplasia-related changes [AML-MRC], and therapy-related AML), and identified differences in mutation types, spectrum, and hot spots between disease categories and in comparison to solid tumors. Missense mutations in the DNA-binding domain were most common across all categories, whereas inactivating mutations and mutations outside the DNA binding domain were more common in AML-MRC than in MDS. <em>TP53</em> mutations in MDS were more likely to retain transcriptional activity, and comutation profiles were distinct between disease categories and mutation types. Our findings suggest that mutated <em>TP53</em> contributes to initiation and progression of neoplasia via distinct mechanisms, and support the utility of specific identification of <em>TP53</em> mutations in myeloid malignancies.</p></div>","PeriodicalId":100189,"journal":{"name":"Blood Neoplasia","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2950328024000049/pdfft?md5=32a5eaf130b739b0f8a9549efb2c3a9f&pid=1-s2.0-S2950328024000049-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140112874","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":"Multiple myeloma–associated DIS3 gene is essential for hematopoiesis, but loss of DIS3 is insufficient for myelomagenesis","authors":"Hiroto Ohguchi ,&nbsp;Yasuyo Ohguchi ,&nbsp;Sho Kubota ,&nbsp;Kan Etoh ,&nbsp;Ai Hamashima ,&nbsp;Shingo Usuki ,&nbsp;Takako Yokomizo-Nakano ,&nbsp;Jie Bai ,&nbsp;Takeshi Masuda ,&nbsp;Yawara Kawano ,&nbsp;Takeshi Harada ,&nbsp;Mitsuyoshi Nakao ,&nbsp;Takashi Minami ,&nbsp;Teru Hideshima ,&nbsp;Kimi Araki ,&nbsp;Goro Sashida","doi":"10.1016/j.bneo.2024.100005","DOIUrl":"10.1016/j.bneo.2024.100005","url":null,"abstract":"","PeriodicalId":100189,"journal":{"name":"Blood Neoplasia","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2950328024000050/pdfft?md5=a4beda25394f8434842a1dc11102f769&pid=1-s2.0-S2950328024000050-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139874466","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":"Patients with Castleman disease report mild COVID-19 symptoms and mount a humoral response to SARS-CoV-2 vaccination","authors":"Saishravan Shyamsundar ,&nbsp;Sheila K. Pierson ,&nbsp;Caoilfhionn M. Connolly ,&nbsp;Mayan Teles ,&nbsp;Dorry L. Segev ,&nbsp;William A. Werbel ,&nbsp;Frits van Rhee ,&nbsp;Corey Casper ,&nbsp;Joshua D. Brandstadter ,&nbsp;Ariela Noy ,&nbsp;David C. Fajgenbaum","doi":"10.1016/j.bneo.2024.100002","DOIUrl":"10.1016/j.bneo.2024.100002","url":null,"abstract":"<div><h3>Abstract</h3><p>The coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection has resulted in increased morbidity and mortality in patients with impaired immunity, hematologic malignancies, and on immunosuppressive regimens. COVID-19 can cause a cytokine storm with some patients benefiting from blockade of the proinflammatory cytokine, interleukin 6 (IL-6). Because Castleman disease (CD) is an atypical lymphoproliferative disorder that can involve a cytokine storm and often requires immunosuppressive therapies, including IL-6 inhibition, we sought to evaluate outcomes after COVID-19 and SARS-CoV-2 vaccination in patients with CD. We administered a survey in April 2021 to characterize experiences with COVID-19 and SARS-CoV-2 vaccination among 300 patients enrolled in ACCELERATE, a CD natural history registry. Among 128 respondents, the prevalence of SARS-CoV-2 infection (16/95, 17%), severe disease (1/16, 6%), vaccination rates (112/128, 88%), and vaccine adverse effects after dose 1 (62/112, 55%) were comparable with that of the general US population. Although there were 2 cases of CD flares occurring shortly after SARS-CoV-2 infection (n = 1) and vaccination (n = 1), &gt;100 patients that were infected and/or vaccinated did not experience CD flares. Among patients with CD, the median antispike titer 6 months after the second vaccine dose was comparable to that of individuals with other immune-related diseases and healthy populations. Despite being on immunosuppressive therapies, patients with CD do not appear to be at increased risk of poor COVID-19 outcomes and can mount a humoral response to SARS-CoV-2 vaccination. This study was registered at <span>www.ClinicalTrials.gov</span><svg><path></path></svg> as #NCT02817997.</p></div>","PeriodicalId":100189,"journal":{"name":"Blood Neoplasia","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2950328024000025/pdfft?md5=bf82a64a1d50dd31cc6c1c8b26e2de29&pid=1-s2.0-S2950328024000025-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139826118","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}