Blood Neoplasia最新文献

{"title":"Single-cell and spatial characterization of plasmablast-like lymphoma cells in primary central nervous system lymphoma","authors":"Hiroki Kobayashi ∗ ,&nbsp;Ryota Chijimatsu ∗ ,&nbsp;Yusuke Naoi ,&nbsp;Yoshihiro Otani ,&nbsp;Ryo Mizuta ,&nbsp;Kentaro Fujii ,&nbsp;Joji Ishida ,&nbsp;Hiroyuki Murakami ,&nbsp;Hideki Ujiie ,&nbsp;Kazuhiro Ikeuchi ,&nbsp;Tomohiro Urata ,&nbsp;Keisuke Seike ,&nbsp;Hideaki Fujiwara ,&nbsp;Noboru Asada ,&nbsp;Nobuharu Fujii ,&nbsp;Ken-ichi Matsuoka ,&nbsp;Yasuharu Sato ,&nbsp;Yoshinobu Maeda ,&nbsp;Daisuke Ennishi","doi":"10.1016/j.bneo.2024.100058","DOIUrl":"10.1016/j.bneo.2024.100058","url":null,"abstract":"<div><h3>Abstract</h3><div>Primary central nervous system lymphoma (PCNSL) is a rare, aggressive type of lymphoma, most often histologically diagnosed as diffuse large B-cell lymphoma (DLBCL). Recent advancements in single-cell sequencing have elucidated that the diverse germinal center states in systemic DLBCL manifest as tumor cell diversity, intricately linked to variations in the microenvironment. However, detailed characterization of intratumoral heterogeneity reflecting B-cell states in PCNSL remains elusive. Here, we conducted single-cell and spatial multiomic analyses to elucidate the cellular and spatial heterogeneity and the microenvironment in PCNSL. We identified a distinctive lymphoma subpopulation with gene and protein expression similar to that of plasmablasts (PBLs), enriched in some patients with PCNSL. B-cell receptor (BCR) analysis revealed that BCR clonotypes of the PBL signature subpopulation were shared with other subpopulations, suggesting a common origin with other lymphoma cell subtypes. Spatial analysis additionally revealed several localization patterns of PBL signature subpopulations within the tissue, indicating spatial heterogeneity. An expansion study showed that ∼40% of patients with PCNSL had a PBL signature subpopulation, as defined by CD138 immunohistochemistry staining. Additionally, patients with a PBL signature subpopulation and low CD3⁺ cell infiltration exhibited a worse prognosis. Finally, intercellular communication analysis suggested that the PBL signature subpopulation had distinct cellular interactions with the microenvironment. In summary, our study identified a tumor subpopulation with a PBL signature in PCNSL, suggesting distinct molecular and spatial cross talk with the microenvironment. These findings provided new insights into the biological mechanisms of PCNSL.</div></div>","PeriodicalId":100189,"journal":{"name":"Blood Neoplasia","volume":"2 1","pages":"Article 100058"},"PeriodicalIF":0.0,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143149226","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":"Short-duration infusion obinutuzumab with venetoclax in chronic lymphocytic leukemia: a prospective observational study","authors":"Priyanka Pullarkat ∗ ,&nbsp;Matthew Lei ∗,† ,&nbsp;Robert Redd ,&nbsp;Ruchi Rana ,&nbsp;Uvette Lou ,&nbsp;Mark Sorial ,&nbsp;Brenna Rowen ,&nbsp;E. Bridget Kim ,&nbsp;Andrea Medrano ,&nbsp;J. Erika Haydu ,&nbsp;Jeffrey Barnes ,&nbsp;Ephraim Hochberg ,&nbsp;P. Connor Johnson ,&nbsp;Ronald Takvorian ,&nbsp;Julia Lynch ,&nbsp;Emily Patterson ,&nbsp;Katherine Thorp ,&nbsp;Maryanne Sherburne ,&nbsp;Brianne McGree ,&nbsp;Josie Ford ,&nbsp;Jacob D. Soumerai †","doi":"10.1016/j.bneo.2025.100075","DOIUrl":"10.1016/j.bneo.2025.100075","url":null,"abstract":"","PeriodicalId":100189,"journal":{"name":"Blood Neoplasia","volume":"2 2","pages":"Article 100075"},"PeriodicalIF":0.0,"publicationDate":"2025-01-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143714451","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":"Driver mutations in myeloid and lymphoid cells point to multipotent progenitor origin of diverse histiocytic neoplasms","authors":"Astrid G. S. van Halteren ∗ ,&nbsp;Paul G. Kemps ∗ ,&nbsp;Jelske Forma-Borst ,&nbsp;Yanling Xiao ,&nbsp;Maud A. J. I. van den Oetelaar ,&nbsp;Nina U. Gelineau ,&nbsp;Robert M. Verdijk ,&nbsp;Lydia E. Vos ,&nbsp;Koen D. Quint ,&nbsp;Cor van den Bos ,&nbsp;Eli L. Diamond † ,&nbsp;Jan A. M. van Laar †","doi":"10.1016/j.bneo.2025.100074","DOIUrl":"10.1016/j.bneo.2025.100074","url":null,"abstract":"<div><h3>Abstract</h3><div>Histiocytic neoplasms are rare myeloid diseases characterized by MAPK pathway–activating genetic alterations. We investigated their hematopoietic origin, with a focus on non-Langerhans cell histiocytoses. Using droplet digital polymerase chain reaction assays specific for <em>BRAF</em>, <em>MAP2K1</em>, or <em>KRAS</em> alterations detected in histiocytosis lesions, we could trace the same driver mutation to circulating blood cells in 13 of 14 patients. In 9 of 13 patients, the mutations were detected in circulating lymphoid cells, indicating that multipotent progenitors probably acquired these alterations. The 9 patients included 5 adults with single-system disease, including 3 with recurrent cutaneous xanthogranulomas. The presence of long-lived mutated progenitor cells in these 3 patients was supported by the detection of the same <em>KRAS</em> or <em>BRAF</em> mutation in xanthogranulomas that developed up to 25 years apart. As proof of concept, we traced the driver mutation to circulating CD34⁺ progenitors in 1 of the 3 patients. Distinct secondary mutations in either <em>KRAS</em>, <em>BRAF</em>, or <em>ARAF</em> were identified in separate xanthogranulomas from the same patient, indicating a 2-hit mutational process underlying the formation of these recurrent lesions. Finally, histiocytes and B cells harboring the same <em>KRAS</em> mutation were identified in the unifocal Langerhans cell sarcoma lesion of the only patient without circulating mutated cells. Together, these data point toward multipotent hematopoietic progenitors as the cell of origin of both single-system and multisystem histiocytoses.</div></div>","PeriodicalId":100189,"journal":{"name":"Blood Neoplasia","volume":"2 2","pages":"Article 100074"},"PeriodicalIF":0.0,"publicationDate":"2025-01-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143643034","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":"Clonal composition of karyotypically normal AML at diagnosis is not affected by the microenvironment","authors":"Monika M. Toma ,&nbsp;Adam Karami ,&nbsp;Margaret Nieborowska-Skorska ,&nbsp;Tomasz Skorski","doi":"10.1016/j.bneo.2025.100073","DOIUrl":"10.1016/j.bneo.2025.100073","url":null,"abstract":"","PeriodicalId":100189,"journal":{"name":"Blood Neoplasia","volume":"2 2","pages":"Article 100073"},"PeriodicalIF":0.0,"publicationDate":"2025-01-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143511362","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":"Race and age disparities in randomized trials of acute myeloid leukemia: a systematic review and meta-analysis","authors":"Nathalie Loeb ,&nbsp;Olivia Katsnelson ,&nbsp;Anshika Jain ,&nbsp;Parsa Tahvildar ,&nbsp;Daniel Teitelbaum ,&nbsp;Alejandro Garcia-Horton","doi":"10.1016/j.bneo.2025.100070","DOIUrl":"10.1016/j.bneo.2025.100070","url":null,"abstract":"<div><h3>Abstract</h3><div>There are significant racial and ethnic disparities in the incidence and survival of patients with acute myeloid leukemia (AML). Understanding the discrepancies in enrollment in randomized controlled trials (RCTs) is important for better informing access to care and clinical trial conduct. We systematically reviewed the literature on the enrollment of racial/ethnic minorities and older adults into RCTs of AML. MEDLINE was searched from inception through June 2023 for RCTs on disease-modifying therapy for AML in adults. The proportion of trials reporting racial and ethnic subgroups, the enrollment proportions for each race, and age ≥65 years were determined, which were stratified by year, trial phase, and geographic location. A meta-analysis of enrollment incidence ratios (EIRs), the ratio of trial proportions of members of a racial and ethnic subgroup divided by the US population–based incidence, was conducted. A total of 7759 titles and abstracts and 157 full texts were screened, yielding 90 studies. Up to 23.3% of trials reported race or ethnicity, and 28.9% reported age ≥65 years. Of the trials reporting race, 4.7% of participants were Black, 9.8% Asian/Pacific Islander, 0.5% Native American/Alaska Native, 80.8% White, and 3.4% Hispanic. Hispanic patients (EIR, 0.28), and Asian patients (EIR, 0.16) were significantly underrepresented, whereas White patients (EIR, 1.23) were significantly overrepresented. When stratifying by year, we found an increase in the proportion of trials reporting on race in the last 10 years (46.2% vs 19.5%) and an increase in the last 20 years in the proportion of racial minorities enrolled.</div></div>","PeriodicalId":100189,"journal":{"name":"Blood Neoplasia","volume":"2 2","pages":"Article 100070"},"PeriodicalIF":0.0,"publicationDate":"2025-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143619856","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 feedforward loop between ACLY and MYC supports T-ALL progression in vivo","authors":"Victoria da Silva-Diz ,&nbsp;Amartya Singh ,&nbsp;Maya Aleksandrova ,&nbsp;Oekyung Kim ,&nbsp;Christopher Thai ,&nbsp;Olga Lancho ,&nbsp;Patricia Renck Nunes ,&nbsp;Hayley Affronti ,&nbsp;Alexia Martínez de Paz ,&nbsp;Steven Z. Josefowicz ,&nbsp;Xiaoyang Su ,&nbsp;Kathryn E. Wellen ,&nbsp;Daniel Herranz","doi":"10.1016/j.bneo.2025.100069","DOIUrl":"10.1016/j.bneo.2025.100069","url":null,"abstract":"<div><h3>Abstract</h3><div>T-cell acute lymphoblastic leukemia (T-ALL) is a hematological malignancy in need of novel therapeutic approaches. Here, we identify ATP-citrate lyase (ACLY) as overexpressed in human T-ALL and as a promising therapeutic target for its treatment. To test the effects of ACLY in leukemia progression, we developed an isogenic model of NOTCH1-induced <em>Acly</em> conditional knockout leukemia. Importantly, we observed intrinsic antileukemic effects upon loss of ACLY, which further synergized with NOTCH1 inhibition in vivo. Metabolomic profiling upon ACLY loss revealed a metabolic crisis with reduced acetyl-coenzyme A (acetyl-CoA) levels and decreased oxygen consumption rate. Gene expression profiling analyses showed that the transcriptional signature of ACLY loss very significantly correlates with the signature of MYC loss in vivo. Mechanistically, the decrease in acetyl-CoA led to reduced H3K27ac levels in <em>Myc</em>, resulting in transcriptional downregulation of <em>Myc</em> and drastically reduced MYC protein levels. Moreover, pharmacological inhibition of ACLY led to reduced MYC levels and antileukemic effects in human T-ALL cell lines and patient-derived xenografts. Interestingly, our analyses also revealed a reciprocal relationship whereby <em>ACLY</em> itself is a direct transcriptional target of MYC, thus establishing a feedforward loop that is important for leukemia progression. Overall, our results identified a relevant ACLY-MYC axis and unveiled ACLY as a novel promising target for T-ALL treatment.</div></div>","PeriodicalId":100189,"journal":{"name":"Blood Neoplasia","volume":"2 2","pages":"Article 100069"},"PeriodicalIF":0.0,"publicationDate":"2025-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143704102","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":"Targeting transcription-replication conflicts using G-quadruplexes stabilizers in multiple myeloma","authors":"Laure Dutrieux ,&nbsp;Sara Ovejero ,&nbsp;Antoine Guillemin ,&nbsp;Miss Leriem Zellagui ,&nbsp;Elke De Bruyne ,&nbsp;Catharina Muylaert ,&nbsp;Lien Van Hemelrijck ,&nbsp;Yea-Lih Lin ,&nbsp;Elle Loughran ,&nbsp;Armelle Choquet ,&nbsp;Talha Magat ,&nbsp;Soumya Bouchouika ,&nbsp;Caroline Bret ,&nbsp;Guilhem Requirand ,&nbsp;Nicolas Robert ,&nbsp;Laure Vincent ,&nbsp;Guillaume Cartron ,&nbsp;Charles Herbaux ,&nbsp;Raphaël Rodriguez ,&nbsp;Michel Cogné ,&nbsp;Jérôme Moreaux","doi":"10.1016/j.bneo.2025.100072","DOIUrl":"10.1016/j.bneo.2025.100072","url":null,"abstract":"<div><h3>Abstract</h3><div>Replication stress exerts an important role in fueling genomic instability characterizing multiple myeloma (MM) evolution and is a leading cause of drug resistance. Normal and malignant plasma cells (PCs) are associated with a high transcriptional stress due to the huge production of immunoglobulins. Transcription-replication conflicts (TRCs), arising from collisions between replication and transcription machineries, can promote tumor progression and represent an Achilles’ heel to cancer cells. We reported a gene signature related to TRCs management (TRC score), overexpressed in malignant vs normal PCs. High TRC score identified patients with MM with a poor prognosis who could benefit from a TRC-enhancing therapy, in independent cohorts of patients with MM treated with high-dose melphalan chemotherapy or anti-CD38 immunotherapy. Here, we investigated the therapeutic interest of increasing TRCs to target specifically malignant PCs using the G-quadruplex (G4) stabilizer pyridostatin (PDS). PDS exerted significant toxicity in MM cell lines and primary MM cells, inducing DNA damage, cell cycle arrest, and apoptosis. Importantly, primary myeloma cells are significantly more sensitive to PDS treatment than normal bone marrow cells. Moreover, PDS improved the efficacy of MM treatments such as melphalan and histone deacetylase (HDAC) or bromodomain (BRD) inhibitors. Thus, our study shows that G4 stabilizers could be used to specifically target MM cells that exhibit concomitant replication stress and a high level of transcription, through the increase of TRCs. These molecules could be used to increase the efficacy of other treatments including melphalan, HDAC inhibitors, and BRD inhibitors.</div></div>","PeriodicalId":100189,"journal":{"name":"Blood Neoplasia","volume":"2 2","pages":"Article 100072"},"PeriodicalIF":0.0,"publicationDate":"2025-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143551133","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":"Characterization of fusion transcripts in AML without recurrent genetic abnormalities unravels new putative fusion genes","authors":"Francesca Guijarro ,&nbsp;Sandra Cabezas ,&nbsp;Marc Dabad ,&nbsp;Alex Bataller ,&nbsp;Cristina López ,&nbsp;Sandra Castaño-Díez ,&nbsp;Carlos Jiménez-Vicente ,&nbsp;Albert Cortés-Bullich ,&nbsp;Marta Garrote ,&nbsp;Jose R. Álamo ,&nbsp;Miriam Prieto ,&nbsp;Aina Cardús ,&nbsp;Marta Pratcorona ,&nbsp;Maria Rozman ,&nbsp;Marta Aymerich ,&nbsp;Neus Villamor ,&nbsp;Dolors Colomer ,&nbsp;Jordi Morata ,&nbsp;Anna Esteve-Codina ,&nbsp;Sílvia Beà ,&nbsp;Jordi Esteve ∗","doi":"10.1016/j.bneo.2025.100068","DOIUrl":"10.1016/j.bneo.2025.100068","url":null,"abstract":"<div><h3>Abstract</h3><div>In the last few years, whole-transcriptome sequencing has shown a high number of low-frequency fusion transcripts (FTs) involved in acute myeloid leukemia (AML) pathogenesis. Most of them are not identifiable through conventional diagnostic techniques. In this research, using RNA sequencing, we have investigated FTs in 109 cases of AML without recurrent genetic abnormalities (as defined by the fourth edition of the World Health Organization Classification of Hematolymphoid Tumours). We identified and validated 6 well-known AML-causing FTs (Tier-1), 9 FTs in which recurrently affected genes in AML were involved (Tier-2), and 4 Tier-3 FTs, along with other FTs found in healthy tissue databases (Tier-4). We highlighted 2 previously unknown FTs (<em>ARHGAP11A</em>::<em>NUTM1</em> and <em>RAP1B</em>::<em>GPC3</em>) that constitute putative driver fusion genes in AML after performing a thorough analysis of their intrinsic properties, expression pattern, and clinical data correlation. Altogether, 15 patients from our cohort (14%) presented at least 1 validated FT, half of which had diagnostic and/or therapeutic implications. Furthermore, we were able to monitor 8 FTs during disease evolution, finding a good correlation with tumor burden. Nevertheless, the significance of many FTs remains unknown, which makes it necessary to enlarge curated FT databases to implement whole-transcriptome sequencing in clinical practice.</div></div>","PeriodicalId":100189,"journal":{"name":"Blood Neoplasia","volume":"2 2","pages":"Article 100068"},"PeriodicalIF":0.0,"publicationDate":"2025-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143619857","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":"New leads to enhance tagraxofusp efficacy in pDC-AML","authors":"Morgane Boichut ∗ ,&nbsp;Margaux Poussard ∗ ,&nbsp;Xavier Roussel ,&nbsp;Imane Belakri ,&nbsp;Sabeha Biichlé ,&nbsp;Maxime Fredon ,&nbsp;Florian Renosi ,&nbsp;Romain Boidot ,&nbsp;Olivier Adotevi ,&nbsp;Christopher Brooks ,&nbsp;Francine Garnache-Ottou ,&nbsp;Fanny Angelot Delettre","doi":"10.1016/j.bneo.2025.100066","DOIUrl":"10.1016/j.bneo.2025.100066","url":null,"abstract":"","PeriodicalId":100189,"journal":{"name":"Blood Neoplasia","volume":"2 2","pages":"Article 100066"},"PeriodicalIF":0.0,"publicationDate":"2025-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143551136","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":"Clinical correlation and prognostic impact of cytogenetic clone size for myelodysplastic syndromes/neoplasm","authors":"Zhuoer Xie ,&nbsp;Najla Al Ali ,&nbsp;Ling Zhang ,&nbsp;Peter Papenhausen ,&nbsp;Virginia Olivia Volpe ,&nbsp;Onyee Chan ,&nbsp;Andrew Kuykendall ,&nbsp;Seongseok Yun ,&nbsp;Alison Walker ,&nbsp;Kendra Sweet ,&nbsp;Jeffrey E. Lancet ,&nbsp;Eric Padron ,&nbsp;David A. Sallman ∗ ,&nbsp;Rami S. Komrokji ∗","doi":"10.1016/j.bneo.2024.100062","DOIUrl":"10.1016/j.bneo.2024.100062","url":null,"abstract":"<div><h3>Abstract</h3><div>Most myelodysplastic syndromes/neoplasms (MDS) risk stratification models dichotomize conventional cytogenetic abnormalities into present or absent, neglecting the prognostic impact of clone size (percentage of the total cells/metaphases harboring the chromosome abnormality). We investigated the prognostic value of clone size in 1001 patients with MDS using G-banding and fluorescence in situ hybridization. Clone size correlated with anemia severity and thrombocytosis in del(5q) cases, and with anemia and blast percentage in complex karyotypes. <em>TP53</em> mutation prevalence was significantly elevated in patients with clone size of ≥25% compared with those with &lt;25% (34.2% vs 3%; <em>P</em> = .07). Complex karyotypes with clone size of ≥75% demonstrated superior response to hypomethylating agents (20.8% vs 10%; <em>P</em> = .03). Crucially, clone size of ≥25% independently predicted overall survival and leukemia-free survival, regardless of revised International Prognostic Scoring System (IPSS) or molecular IPSS. Our findings establish clone size as a robust prognostic factor in MDS, warranting its integration into clinical practice and potential incorporation into risk stratification models.</div></div>","PeriodicalId":100189,"journal":{"name":"Blood Neoplasia","volume":"2 2","pages":"Article 100062"},"PeriodicalIF":0.0,"publicationDate":"2024-12-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143551135","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}