Pub Date : 2025-07-01DOI: 10.1186/s13045-025-01715-0
Néstor Tirado, Klaudyna Fidyt, María José Mansilla, Alba Garcia-Perez, Alba Martínez-Moreno, Meritxell Vinyoles, Juan Alcain, Marina García-Peydró, Heleia Roca-Ho, Narcis Fernandez-Fuentes, Mercedes Guerrero-Murillo, Aïda Falgàs, Talia Velasco-Hernandez, Clara Bueno, Patrizio Panelli, Vladimir Mulens-Arias, Apostol Apostolov, Pablo Engel, Europa Azucena González, Binje Vick, Irmela Jeremias, Aurélie Caye-Eude, André Baruchel, Hélène Cavé, Eulàlia Genescà, Jordi Ribera, Marina Díaz-Beyá, María Victoria Martínez-Sánchez, José Luis Fuster, Adela Escudero López, Jordi Minguillón, Antonio Pérez-Martínez, Manuel Ramírez-Orellana, Montserrat Torrebadell, Víctor M Díaz, María L Toribio, Diego Sánchez-Martínez, Pablo Menéndez
T cell acute lymphoblastic leukemia (T-ALL) is an aggressive malignancy characterized by high rates of induction failure and relapse, and effective targeted immunotherapies are lacking. Despite promising clinical progress with genome-edited CD7-directed CAR-T cells, which present significant logistical and regulatory issues, CAR-T cell therapy in T-ALL remains challenging due to the shared antigen expression between malignant and healthy T cells. This can result in CAR-T cell fratricide, T cell aplasia, and the potential for blast contamination during CAR-T cell manufacturing. Recently described CAR-T cells target non-pan-T antigens, absent on healthy T cells but expressed on specific T-ALL subsets. These antigens include CD1a (NCT05679895), which is expressed in cortical T-ALL, and CCR9. We show that CCR9 is expressed on >70% of T-ALL patients (132/180) and is maintained at relapse, with a safe expression profile in healthy hematopoietic and non-hematopoietic tissues. Further analyses showed that dual targeting of CCR9 and CD1a could benefit T-ALL patients with a greater blast coverage than single CAR-T cell treatments. We therefore developed, characterized, and preclinically validated a novel humanized CCR9-specific CAR with robust and specific antileukemic activity as a monotherapy in vitro and in vivo against cell lines, primary T-ALL samples, and patient-derived xenografts. Importantly, CCR9/CD1a dual-targeting CAR-T cells showed higher efficacy than single-targeting CAR-T cells, particularly in T-ALL cases with phenotypically heterogeneous leukemic populations. Dual CD1a/CCR9 CAR-T therapy may prevent T cell aplasia and obviate the need for allogeneic transplantation and regulatory-challenging genome engineering approaches in T-ALL.
{"title":"CAR-T cells targeting CCR9 and CD1a for the treatment of T cell acute lymphoblastic leukemia","authors":"Néstor Tirado, Klaudyna Fidyt, María José Mansilla, Alba Garcia-Perez, Alba Martínez-Moreno, Meritxell Vinyoles, Juan Alcain, Marina García-Peydró, Heleia Roca-Ho, Narcis Fernandez-Fuentes, Mercedes Guerrero-Murillo, Aïda Falgàs, Talia Velasco-Hernandez, Clara Bueno, Patrizio Panelli, Vladimir Mulens-Arias, Apostol Apostolov, Pablo Engel, Europa Azucena González, Binje Vick, Irmela Jeremias, Aurélie Caye-Eude, André Baruchel, Hélène Cavé, Eulàlia Genescà, Jordi Ribera, Marina Díaz-Beyá, María Victoria Martínez-Sánchez, José Luis Fuster, Adela Escudero López, Jordi Minguillón, Antonio Pérez-Martínez, Manuel Ramírez-Orellana, Montserrat Torrebadell, Víctor M Díaz, María L Toribio, Diego Sánchez-Martínez, Pablo Menéndez","doi":"10.1186/s13045-025-01715-0","DOIUrl":"https://doi.org/10.1186/s13045-025-01715-0","url":null,"abstract":"T cell acute lymphoblastic leukemia (T-ALL) is an aggressive malignancy characterized by high rates of induction failure and relapse, and effective targeted immunotherapies are lacking. Despite promising clinical progress with genome-edited CD7-directed CAR-T cells, which present significant logistical and regulatory issues, CAR-T cell therapy in T-ALL remains challenging due to the shared antigen expression between malignant and healthy T cells. This can result in CAR-T cell fratricide, T cell aplasia, and the potential for blast contamination during CAR-T cell manufacturing. Recently described CAR-T cells target non-pan-T antigens, absent on healthy T cells but expressed on specific T-ALL subsets. These antigens include CD1a (NCT05679895), which is expressed in cortical T-ALL, and CCR9. We show that CCR9 is expressed on >70% of T-ALL patients (132/180) and is maintained at relapse, with a safe expression profile in healthy hematopoietic and non-hematopoietic tissues. Further analyses showed that dual targeting of CCR9 and CD1a could benefit T-ALL patients with a greater blast coverage than single CAR-T cell treatments. We therefore developed, characterized, and preclinically validated a novel humanized CCR9-specific CAR with robust and specific antileukemic activity as a monotherapy in vitro and in vivo against cell lines, primary T-ALL samples, and patient-derived xenografts. Importantly, CCR9/CD1a dual-targeting CAR-T cells showed higher efficacy than single-targeting CAR-T cells, particularly in T-ALL cases with phenotypically heterogeneous leukemic populations. Dual CD1a/CCR9 CAR-T therapy may prevent T cell aplasia and obviate the need for allogeneic transplantation and regulatory-challenging genome engineering approaches in T-ALL.","PeriodicalId":16023,"journal":{"name":"Journal of Hematology & Oncology","volume":"27 1","pages":""},"PeriodicalIF":28.5,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144533865","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 : 2025-07-01DOI: 10.1186/s13045-025-01702-5
Allison M. Bock, Narendranath Epperla
Diffuse large B-cell lymphoma (DLBCL) is an aggressive, yet curable malignancy, that has had practice changing treatment approvals in both the frontline and relapsed setting in the last 5 years. Advent of novel therapeutic options in the recent years has added greater complexity in treatment selection and optimal sequencing given multiple treatments with the same therapeutic target or immunotherapeutic mechanism of action. Key features impacting treatment selection include the timing of relapse, eligibility for curative options in the second line setting, including chimeric antigen receptor T-cell therapy (CAR-T) and autologous stem cell transplant (auto-SCT), as well as considerations of mechanism of action and side effect profile. This article provides a comprehensive review on recently approved therapies for relapsed or refractory DLBCL, emerging cellular and non-cellular therapies, and a summary of our approach to the management of these patients.
{"title":"Therapeutic landscape of primary refractory and relapsed diffuse large B-cell lymphoma: Recent advances and emerging therapies","authors":"Allison M. Bock, Narendranath Epperla","doi":"10.1186/s13045-025-01702-5","DOIUrl":"https://doi.org/10.1186/s13045-025-01702-5","url":null,"abstract":"Diffuse large B-cell lymphoma (DLBCL) is an aggressive, yet curable malignancy, that has had practice changing treatment approvals in both the frontline and relapsed setting in the last 5 years. Advent of novel therapeutic options in the recent years has added greater complexity in treatment selection and optimal sequencing given multiple treatments with the same therapeutic target or immunotherapeutic mechanism of action. Key features impacting treatment selection include the timing of relapse, eligibility for curative options in the second line setting, including chimeric antigen receptor T-cell therapy (CAR-T) and autologous stem cell transplant (auto-SCT), as well as considerations of mechanism of action and side effect profile. This article provides a comprehensive review on recently approved therapies for relapsed or refractory DLBCL, emerging cellular and non-cellular therapies, and a summary of our approach to the management of these patients.","PeriodicalId":16023,"journal":{"name":"Journal of Hematology & Oncology","volume":"71 1","pages":""},"PeriodicalIF":28.5,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144520889","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 : 2025-07-01DOI: 10.1186/s13045-025-01721-2
Yijin Chen, Dawei Huo, Ye Meng, Jie Zhang, Mengmeng Huang, Qian Luo, Yulin Xu, Haiqiong Zheng, Yingli Han, Xiangjun Zeng, Yanjuan Liu, Yunfei Liu, Rui Wen, Delin Kong, Ruxiu Tie, Shanshan Pei, Nan Liu, Pengxu Qian, He Huang, Meng Zhang
Terminal erythropoiesis is a complex multistep process involving coordination of gene transcription and dramatic nuclear condensation, which leads to the expulsion of nuclei to generate reticulocytes. However, we lack a comprehensive understanding of the key transcriptional and epigenetic regulators involved. We used a high-throughput small molecule screen in primary CD34+-derived human erythroblasts to identify targets that promoted terminal erythropoiesis, and further confirmed the phenotype in different differentiation systems by inhibitors and shRNAs of different BRD4 isoforms. Then we performed RNA-seq, ATAC-seq, ChIP-qPCR, Co-IP, and reanalyzed previously-published transcriptional data and mass spectrometric data to clarify how BRD4 regulates terminal erythropoiesis. We identified that inhibitors of the bromodomain protein BRD4, an epigenetic reader and transcriptional activator together with CDK9, promoted terminal erythropoiesis from hematopoietic stem/progenitor cells and embryonic stem cells, and enhanced enucleation. Combined analysis of our RNA-seq, ATAC-seq, and previously-published transcriptional data of erythroblast differentiation at different stages confirmed that BRD4 inhibition accelerates erythroblast maturation. Unexpectedly, this BRD4 function was independent of its classical CDK9 interaction and transcriptional activation. Instead, RNA-seq, ATAC-seq, and Cut&Tag upon BRD4 inhibition revealed that BRD4 regulates erythropoiesis by inhibiting the small G protein RhoB and disrupts actin reorganization. ChIP-qPCR, Co-IP, and functional studies revealed that BRD4 acts as a transcriptional repressor by interacting with the histone methyltransferase EHMT1/2. We demonstrate a non-classical role for BRD4 as a transcriptional repressor of RhoB to regulate erythroid maturation, and classical CDK9 dependent role to regulate cell proliferation of erythroblasts. Besides, we clarify RhoB’s activity and function during terminal erythropoiesis. BRD4 inhibition might be a simple method to promote in vitro blood cell production, and a candidate therapeutic target for diseases leading to dyserythropoiesis such as myelodysplastic syndromes.
{"title":"BRD4 acts as a transcriptional repressor of RhoB to inhibit terminal erythropoiesis","authors":"Yijin Chen, Dawei Huo, Ye Meng, Jie Zhang, Mengmeng Huang, Qian Luo, Yulin Xu, Haiqiong Zheng, Yingli Han, Xiangjun Zeng, Yanjuan Liu, Yunfei Liu, Rui Wen, Delin Kong, Ruxiu Tie, Shanshan Pei, Nan Liu, Pengxu Qian, He Huang, Meng Zhang","doi":"10.1186/s13045-025-01721-2","DOIUrl":"https://doi.org/10.1186/s13045-025-01721-2","url":null,"abstract":"Terminal erythropoiesis is a complex multistep process involving coordination of gene transcription and dramatic nuclear condensation, which leads to the expulsion of nuclei to generate reticulocytes. However, we lack a comprehensive understanding of the key transcriptional and epigenetic regulators involved. We used a high-throughput small molecule screen in primary CD34+-derived human erythroblasts to identify targets that promoted terminal erythropoiesis, and further confirmed the phenotype in different differentiation systems by inhibitors and shRNAs of different BRD4 isoforms. Then we performed RNA-seq, ATAC-seq, ChIP-qPCR, Co-IP, and reanalyzed previously-published transcriptional data and mass spectrometric data to clarify how BRD4 regulates terminal erythropoiesis. We identified that inhibitors of the bromodomain protein BRD4, an epigenetic reader and transcriptional activator together with CDK9, promoted terminal erythropoiesis from hematopoietic stem/progenitor cells and embryonic stem cells, and enhanced enucleation. Combined analysis of our RNA-seq, ATAC-seq, and previously-published transcriptional data of erythroblast differentiation at different stages confirmed that BRD4 inhibition accelerates erythroblast maturation. Unexpectedly, this BRD4 function was independent of its classical CDK9 interaction and transcriptional activation. Instead, RNA-seq, ATAC-seq, and Cut&Tag upon BRD4 inhibition revealed that BRD4 regulates erythropoiesis by inhibiting the small G protein RhoB and disrupts actin reorganization. ChIP-qPCR, Co-IP, and functional studies revealed that BRD4 acts as a transcriptional repressor by interacting with the histone methyltransferase EHMT1/2. We demonstrate a non-classical role for BRD4 as a transcriptional repressor of RhoB to regulate erythroid maturation, and classical CDK9 dependent role to regulate cell proliferation of erythroblasts. Besides, we clarify RhoB’s activity and function during terminal erythropoiesis. BRD4 inhibition might be a simple method to promote in vitro blood cell production, and a candidate therapeutic target for diseases leading to dyserythropoiesis such as myelodysplastic syndromes.","PeriodicalId":16023,"journal":{"name":"Journal of Hematology & Oncology","volume":"633 1","pages":""},"PeriodicalIF":28.5,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144520890","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}
BACKGROUNDCholangiocarcinoma (CCA) is a highly heterogeneous malignancy, primarily comprising intrahepatic (iCCA) and extrahepatic (eCCA) subtypes. Reconciling the variability between iCCAs and eCCAs in clinical trials remains a challenge, largely due to the inadequate understanding of their shared and subtype-specific cellular heterogeneity. We aim to address this issue using single-cell and spatially resolved transcriptomic approaches.METHODSWe performed comprehensive single-cell RNA sequencing (scRNA-seq) by profiling 109,071 single cells from 28 samples, including chronic biliary inflammatory conditions (n = 7) and CCAs from different anatomical sites (n = 21). Findings were validated using external multi-omics datasets, tissue microarray cohort, spatial RNA in situ sequencing, CCA patient-derived organoids (PDOs), and mouse models.RESULTSiCCAs and eCCAs exhibited distinct tumor ecosystems, with notable differences in cellular composition, diversity, and abundance across various cell types. Non-malignant epithelial cells displayed divergent precancer hallmarks from different biliary sites, with inflammatory extrahepatic bile ducts exhibiting early hijacking of the gastrointestinal metaplastic process. We identified seven meta-programs within cancer cells, mapped into four major subtypes. This subtyping was validated using external CCA cohorts and PDO models, distinguishing patients based on clinical outcomes and drug vulnerabilities. Specifically, iCCAs were associated with a senescent program, while eCCAs were enriched in an IFN-responsive program linked to adverse clinical outcomes and increased drug resistance. We identified a basal-like LY6D+ cancer cell subpopulation specific to eCCAs, which displayed significant stemness, drug resistance, and IFN-responsive features. This subpopulation was closely associated with an interferon-stimulated gene 15 (ISG15)-enriched mesenchymal and immune microenvironment. Functional assays demonstrated that ISG15 stimulation significantly boosted stemness, basal-like features, and drug resistance in eCCA cells, highlighting its pivotal role in sustaining the LY6D+ progenitor niches.CONCLUSIONWe present a comprehensive single-cell landscape of CCAs, uncovering the molecular heterogeneity between iCCA and eCCA subtypes. Transcriptomic subtyping of CCA cancer cells offers implications for clinical stratification and functional precision oncology. We identify basal-like epithelial progenitors and characterize their associated ISG15-enriched microenvironment in eCCAs. These findings hold significant promise for the development of novel prognostic biomarkers, therapeutic targets, and treatment strategies for CCAs.
{"title":"Deciphering cholangiocarcinoma heterogeneity and specific progenitor cell niche of extrahepatic cholangiocarcinoma at single-cell resolution.","authors":"Chunliang Liu,Xiang Wang,Erdong Liu,Yali Zong,Wenlong Yu,Youhai Jiang,Jianan Chen,Mingye Gu,Zhengyuan Meng,Jingfeng Li,Yang Liu,Yongjie Zhang,Jing Tang,Hongyang Wang,Jing Fu","doi":"10.1186/s13045-025-01716-z","DOIUrl":"https://doi.org/10.1186/s13045-025-01716-z","url":null,"abstract":"BACKGROUNDCholangiocarcinoma (CCA) is a highly heterogeneous malignancy, primarily comprising intrahepatic (iCCA) and extrahepatic (eCCA) subtypes. Reconciling the variability between iCCAs and eCCAs in clinical trials remains a challenge, largely due to the inadequate understanding of their shared and subtype-specific cellular heterogeneity. We aim to address this issue using single-cell and spatially resolved transcriptomic approaches.METHODSWe performed comprehensive single-cell RNA sequencing (scRNA-seq) by profiling 109,071 single cells from 28 samples, including chronic biliary inflammatory conditions (n = 7) and CCAs from different anatomical sites (n = 21). Findings were validated using external multi-omics datasets, tissue microarray cohort, spatial RNA in situ sequencing, CCA patient-derived organoids (PDOs), and mouse models.RESULTSiCCAs and eCCAs exhibited distinct tumor ecosystems, with notable differences in cellular composition, diversity, and abundance across various cell types. Non-malignant epithelial cells displayed divergent precancer hallmarks from different biliary sites, with inflammatory extrahepatic bile ducts exhibiting early hijacking of the gastrointestinal metaplastic process. We identified seven meta-programs within cancer cells, mapped into four major subtypes. This subtyping was validated using external CCA cohorts and PDO models, distinguishing patients based on clinical outcomes and drug vulnerabilities. Specifically, iCCAs were associated with a senescent program, while eCCAs were enriched in an IFN-responsive program linked to adverse clinical outcomes and increased drug resistance. We identified a basal-like LY6D+ cancer cell subpopulation specific to eCCAs, which displayed significant stemness, drug resistance, and IFN-responsive features. This subpopulation was closely associated with an interferon-stimulated gene 15 (ISG15)-enriched mesenchymal and immune microenvironment. Functional assays demonstrated that ISG15 stimulation significantly boosted stemness, basal-like features, and drug resistance in eCCA cells, highlighting its pivotal role in sustaining the LY6D+ progenitor niches.CONCLUSIONWe present a comprehensive single-cell landscape of CCAs, uncovering the molecular heterogeneity between iCCA and eCCA subtypes. Transcriptomic subtyping of CCA cancer cells offers implications for clinical stratification and functional precision oncology. We identify basal-like epithelial progenitors and characterize their associated ISG15-enriched microenvironment in eCCAs. These findings hold significant promise for the development of novel prognostic biomarkers, therapeutic targets, and treatment strategies for CCAs.","PeriodicalId":16023,"journal":{"name":"Journal of Hematology & Oncology","volume":"8 1","pages":"66"},"PeriodicalIF":28.5,"publicationDate":"2025-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144370199","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 : 2025-06-19DOI: 10.1186/s13045-025-01717-y
Qin Hu, Yifei Zhu, Jie Mei, Ying Liu, Guoren Zhou
The extracellular matrix (ECM), closely linked to the dynamic changes in the tumor microenvironment (TME), plays a critical role in modulating tumor immunity. The dual role of the ECM in tumor progression, encompassing both promotion and inhibition, is attributed to its components influencing immune cell activation, migration, and infiltration. This mechanism is intricately connected with the efficacy of immunotherapies. Currently, there is limited understanding of how ECM remodeling spatially and temporally coordinates with immune checkpoint inhibitors (ICIs) or adoptive cell therapies. Furthermore, strategies to selectively target pathological ECM components while preserving their homeostatic functions urgently require systematic investigation. In this review, we summarize current findings on the interplay between ECM and tumor immune regulation, with a particular focus on how key ECM components contribute to immune modulation. Furthermore, we discuss emerging strategies targeting ECM-related mechanisms to enhance the efficacy of immunotherapies, including approaches that remodel the ECM to improve immune infiltration and strategies that synergize with existing immunotherapies. By integrating these insights, we provide a perspective on leveraging ECM-targeted interventions to overcome immune evasion and optimize cancer immunotherapy outcomes.
{"title":"Extracellular matrix dynamics in tumor immunoregulation: from tumor microenvironment to immunotherapy","authors":"Qin Hu, Yifei Zhu, Jie Mei, Ying Liu, Guoren Zhou","doi":"10.1186/s13045-025-01717-y","DOIUrl":"https://doi.org/10.1186/s13045-025-01717-y","url":null,"abstract":"The extracellular matrix (ECM), closely linked to the dynamic changes in the tumor microenvironment (TME), plays a critical role in modulating tumor immunity. The dual role of the ECM in tumor progression, encompassing both promotion and inhibition, is attributed to its components influencing immune cell activation, migration, and infiltration. This mechanism is intricately connected with the efficacy of immunotherapies. Currently, there is limited understanding of how ECM remodeling spatially and temporally coordinates with immune checkpoint inhibitors (ICIs) or adoptive cell therapies. Furthermore, strategies to selectively target pathological ECM components while preserving their homeostatic functions urgently require systematic investigation. In this review, we summarize current findings on the interplay between ECM and tumor immune regulation, with a particular focus on how key ECM components contribute to immune modulation. Furthermore, we discuss emerging strategies targeting ECM-related mechanisms to enhance the efficacy of immunotherapies, including approaches that remodel the ECM to improve immune infiltration and strategies that synergize with existing immunotherapies. By integrating these insights, we provide a perspective on leveraging ECM-targeted interventions to overcome immune evasion and optimize cancer immunotherapy outcomes.","PeriodicalId":16023,"journal":{"name":"Journal of Hematology & Oncology","volume":"30 1","pages":""},"PeriodicalIF":28.5,"publicationDate":"2025-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144319753","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 : 2025-06-17DOI: 10.1186/s13045-025-01718-x
Gejia Cao, Haixiao Zhang, Shu Sun, Hong-Hu Zhu
Menin inhibitors, which target the KMT2A-menin protein-protein interaction to inhibit blasts proliferation and induce differentiation, have demonstrated potential effects on acute leukemia subtypes characterized by overexpression of HOXA gene cluster and MEIS1 (including KMT2A rearrangements, NPM1 mutations, NUP98 rearrangements and other genetic alterations). Following the promising outcomes of the two pioneering menin inhibitors, revumenib and ziftomenib, other menin inhibitors, including bleximenib, enzomenib, BN-104 and HMPL-506 are currently under investigation in clinical trials. Several trials presented their initial outcomes at the 2024 ASH Annual Meeting. This review highlights the key outcomes of these pivotal clinical trials.
{"title":"Menin inhibitors from monotherapies to combination therapies: clinical trial updates from 2024 ASH annual meeting","authors":"Gejia Cao, Haixiao Zhang, Shu Sun, Hong-Hu Zhu","doi":"10.1186/s13045-025-01718-x","DOIUrl":"https://doi.org/10.1186/s13045-025-01718-x","url":null,"abstract":"Menin inhibitors, which target the KMT2A-menin protein-protein interaction to inhibit blasts proliferation and induce differentiation, have demonstrated potential effects on acute leukemia subtypes characterized by overexpression of HOXA gene cluster and MEIS1 (including KMT2A rearrangements, NPM1 mutations, NUP98 rearrangements and other genetic alterations). Following the promising outcomes of the two pioneering menin inhibitors, revumenib and ziftomenib, other menin inhibitors, including bleximenib, enzomenib, BN-104 and HMPL-506 are currently under investigation in clinical trials. Several trials presented their initial outcomes at the 2024 ASH Annual Meeting. This review highlights the key outcomes of these pivotal clinical trials.","PeriodicalId":16023,"journal":{"name":"Journal of Hematology & Oncology","volume":"7 1","pages":""},"PeriodicalIF":28.5,"publicationDate":"2025-06-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144304719","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}
Correction to: Journal of Hematology & Oncology (2018) 11:95.
https://doi.org/10.1186/s13045-018-0638-9
During figure preparation, an incorrect representative image was included in Figs. 1e, S5B, and S6C. These errors occurred during figure assembly and do not affect the results or conclusions of the study. The corrected figures have been provided.
The authors apologize for the errors and any confusion caused.
Fig. 1e
Fig. S5B
Fig. S5B/C
Author notes
Tong Shen, Ling-Dong Cai and Yu-Hong Liu contributed equally to this work.
Authors and Affiliations
Department of Pathology, Soochow University Medical School, Suzhou, 215123, People’s Republic of China
Tong Shen, Ling-Dong Cai, Shi Li, Wen-Juan Gan, Xiu-Ming Li, Jing-Ru Wang, Peng-Da Guo, Qun Zhou, Xing-Xing Lu, Li-Na Sun & Jian-Ming Li
Department of Pathology, Baoan Hospital, Southern Medical University, Shenzhen, 518101, People’s Republic of China
Yu-Hong Liu
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{"title":"Correction: Ube2v1-mediated ubiquitination and degradation of Sirt1 promotes metastasis of colorectal cancer by epigenetically suppressing autophagy","authors":"Tong Shen, Ling-Dong Cai, Yu-Hong Liu, Shi Li, Wen-Juan Gan, Xiu-Ming Li, Jing-Ru Wang, Peng-Da Guo, Qun Zhou, Xing-Xing Lu, Li-Na Sun, Jian-Ming Li","doi":"10.1186/s13045-025-01719-w","DOIUrl":"https://doi.org/10.1186/s13045-025-01719-w","url":null,"abstract":"<p><b>Correction to: Journal of Hematology & Oncology (2018) 11:95.</b></p><p><b>https://doi.org/10.1186/s13045-018-0638-9</b></p><p>During figure preparation, an incorrect representative image was included in Figs. 1e, S5B, and S6C. These errors occurred during figure assembly and do not affect the results or conclusions of the study. The corrected figures have been provided.</p><p>The authors apologize for the errors and any confusion caused.</p><p>Fig. 1e</p><figure><picture><source srcset=\"//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs13045-025-01719-w/MediaObjects/13045_2025_1719_Fig1_HTML.png?as=webp\" type=\"image/webp\"/><img alt=\"figure 1\" aria-describedby=\"Fig1\" height=\"363\" loading=\"lazy\" src=\"//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs13045-025-01719-w/MediaObjects/13045_2025_1719_Fig1_HTML.png\" width=\"685\"/></picture></figure><p>Fig. S5B</p><figure><picture><source srcset=\"//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs13045-025-01719-w/MediaObjects/13045_2025_1719_Fig2_HTML.png?as=webp\" type=\"image/webp\"/><img alt=\"figure 2\" aria-describedby=\"Fig2\" height=\"561\" loading=\"lazy\" src=\"//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs13045-025-01719-w/MediaObjects/13045_2025_1719_Fig2_HTML.png\" width=\"685\"/></picture></figure><p>Fig. S5B/C</p><figure><picture><source srcset=\"//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs13045-025-01719-w/MediaObjects/13045_2025_1719_Fig3_HTML.png?as=webp\" type=\"image/webp\"/><img alt=\"figure 3\" aria-describedby=\"Fig3\" height=\"444\" loading=\"lazy\" src=\"//media.springernature.com/lw685/springer-static/image/art%3A10.1186%2Fs13045-025-01719-w/MediaObjects/13045_2025_1719_Fig3_HTML.png\" width=\"685\"/></picture></figure><span>Author notes</span><ol><li><p>Tong Shen, Ling-Dong Cai and Yu-Hong Liu contributed equally to this work.</p></li></ol><h3>Authors and Affiliations</h3><ol><li><p>Department of Pathology, Soochow University Medical School, Suzhou, 215123, People’s Republic of China</p><p>Tong Shen, Ling-Dong Cai, Shi Li, Wen-Juan Gan, Xiu-Ming Li, Jing-Ru Wang, Peng-Da Guo, Qun Zhou, Xing-Xing Lu, Li-Na Sun & Jian-Ming Li</p></li><li><p>Department of Pathology, Baoan Hospital, Southern Medical University, Shenzhen, 518101, People’s Republic of China</p><p>Yu-Hong Liu</p></li></ol><span>Authors</span><ol><li><span>Tong Shen</span>View author publications<p><span>You can also search for this author in</span><span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Ling-Dong Cai</span>View author publications<p><span>You can also search for this author in</span><span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Yu-Hong Liu</span>View author publications<p><span>You can also search for this author in</span><span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Shi Li</span>View author publications<p><span>You can also search for this author in</sp","PeriodicalId":16023,"journal":{"name":"Journal of Hematology & Oncology","volume":"598 1","pages":""},"PeriodicalIF":28.5,"publicationDate":"2025-06-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144304702","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 : 2025-06-07DOI: 10.1186/s13045-025-01701-6
Hongzhuo Qin, Zhaokai Zhou, Run Shi, Yumiao Mai, Yudi Xu, Fu Peng, Guangyang Cheng, Pengpeng Zhang, Wenjie Chen, Yun Chen, Yajun Chen, Ran Xu, Qiong Lu
Immunotherapy has revolutionized the oncology treatment paradigm, and CAR-T cell therapy in particular represents a significant milestone in treating hematological malignancies. Nevertheless, tumor resistance due to target heterogeneity or mutation remains a Gordian knot for immunotherapy. This review elucidates molecular mechanisms and therapeutic potential of next-generation immunotherapeutic tools spanning genetically engineered immune cells, multi-specific antibodies, and cell engagers, emphasizing multi-targeting strategies to enhance personalized immunotherapy efficacy. Development of logic gate modulation-based circuits, adapter-mediated CARs, multi-specific antibodies, and cell engagers could minimize adverse effects while recognizing tumor signals. Ultimately, we highlight gene delivery, gene editing, and other technologies facilitating tailored immunotherapy, and discuss the promising prospects of artificial intelligence in gene-edited immune cells.
{"title":"Insights into next-generation immunotherapy designs and tools: molecular mechanisms and therapeutic prospects","authors":"Hongzhuo Qin, Zhaokai Zhou, Run Shi, Yumiao Mai, Yudi Xu, Fu Peng, Guangyang Cheng, Pengpeng Zhang, Wenjie Chen, Yun Chen, Yajun Chen, Ran Xu, Qiong Lu","doi":"10.1186/s13045-025-01701-6","DOIUrl":"https://doi.org/10.1186/s13045-025-01701-6","url":null,"abstract":"Immunotherapy has revolutionized the oncology treatment paradigm, and CAR-T cell therapy in particular represents a significant milestone in treating hematological malignancies. Nevertheless, tumor resistance due to target heterogeneity or mutation remains a Gordian knot for immunotherapy. This review elucidates molecular mechanisms and therapeutic potential of next-generation immunotherapeutic tools spanning genetically engineered immune cells, multi-specific antibodies, and cell engagers, emphasizing multi-targeting strategies to enhance personalized immunotherapy efficacy. Development of logic gate modulation-based circuits, adapter-mediated CARs, multi-specific antibodies, and cell engagers could minimize adverse effects while recognizing tumor signals. Ultimately, we highlight gene delivery, gene editing, and other technologies facilitating tailored immunotherapy, and discuss the promising prospects of artificial intelligence in gene-edited immune cells.","PeriodicalId":16023,"journal":{"name":"Journal of Hematology & Oncology","volume":"250 1","pages":""},"PeriodicalIF":28.5,"publicationDate":"2025-06-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144237338","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 : 2025-06-06DOI: 10.1186/s13045-025-01705-2
Quchang Ouyang, Jordi Rodon, Yan Liang, Xinhong Wu, Qun Li, Lihua Song, Min Yan, Zhongsheng Tong, YunPeng Liu, Zev A. Wainberg, Ying Wang, Cuizhi Geng, Susanna V. Ulahannan, Guohua Yu, Manish R. Sharma, Xiang Wang, Judy S. Wang, Alexander Spira, Weihong Zhao, Rachel E. Sanborn, Ying Cheng, Xian Wang, Gesha Liu, Yaling Li, Junyou Ge, Elliot Chartash, Omobolaji O. Akala, Yongmei Yin
Sacituzumab tirumotecan (sac-TMT) is an antibody–drug conjugate composed of an anti-TROP2 monoclonal antibody coupled to a cytotoxic belotecan-derived topoisomerase I inhibitor (KL610023) via a novel linker. We report results from the phase 1 dose-escalation cohorts in advanced solid tumors and phase 2 expansion cohorts for metastatic triple-negative breast cancer (TNBC) from the first-in-human MK-2870-001 (KL264-01) study (NCT04152499). Patients had unresectable locally advanced/metastatic solid tumors refractory to standard therapies. In the phase 1 dose-escalation cohorts, patients had unresectable locally advanced/metastatic solid tumors refractory to standard therapies. Sac-TMT was administered by intravenous administration every 2 weeks at 2 to 12 mg/kg. In phase 2, patients with TNBC and HR+/HER2− breast cancer received sac-TMT per recommended doses for expansion (RDEs) identified in phase 1. Primary objectives were determining maximum tolerated dose (MTD) of sac-TMT and establishing RDEs (phase 1) and determining ORR per RECIST v1.1 by investigator assessment (phase 2). Adverse events were assessed per NCI-CTCAE version 5.0. Thirty patients were enrolled in phase 1 and received sac-TMT 2 mg/kg (n = 4), 4 mg/kg (n = 7), 5 mg/kg (n = 7), 5.5 mg/kg (n = 5), and 6 mg/kg (n = 7). Five patients had dose-limiting toxicities: grade 3 stomatitis at 4, 5.5, and 6 mg/kg; grade 3 rash at 5 mg/kg; and grade 3 urticaria at 6 mg/kg. MTD was 5.5 mg/kg and RDEs were 4 and 5 mg/kg. In the phase 2 dose expansion, ORR (95% CI) was 34.8% (16.4%, 57.3%) in the 4-mg/kg group (n = 23) and 38.9% (23.1%, 56.5%) in the 5-mg/kg group (n = 36) for TNBC. ORR (95% CI) was 31.7% (18.1%, 48.1%) for HR+/HER2− breast cancer (n = 41). Sac-TMT demonstrated manageable safety profile in patients with unresectable locally advanced/metastatic solid tumors and promising antitumor activity in metastatic TNBC and HR+/HER2 − breast cancer. Sac-TMT is being investigated in phase 3 studies. ClinicalTrials.gov, NCT04152499.
{"title":"Results of a phase 1/2 study of sacituzumab tirumotecan in patients with unresectable locally advanced or metastatic solid tumors refractory to standard therapies","authors":"Quchang Ouyang, Jordi Rodon, Yan Liang, Xinhong Wu, Qun Li, Lihua Song, Min Yan, Zhongsheng Tong, YunPeng Liu, Zev A. Wainberg, Ying Wang, Cuizhi Geng, Susanna V. Ulahannan, Guohua Yu, Manish R. Sharma, Xiang Wang, Judy S. Wang, Alexander Spira, Weihong Zhao, Rachel E. Sanborn, Ying Cheng, Xian Wang, Gesha Liu, Yaling Li, Junyou Ge, Elliot Chartash, Omobolaji O. Akala, Yongmei Yin","doi":"10.1186/s13045-025-01705-2","DOIUrl":"https://doi.org/10.1186/s13045-025-01705-2","url":null,"abstract":"Sacituzumab tirumotecan (sac-TMT) is an antibody–drug conjugate composed of an anti-TROP2 monoclonal antibody coupled to a cytotoxic belotecan-derived topoisomerase I inhibitor (KL610023) via a novel linker. We report results from the phase 1 dose-escalation cohorts in advanced solid tumors and phase 2 expansion cohorts for metastatic triple-negative breast cancer (TNBC) from the first-in-human MK-2870-001 (KL264-01) study (NCT04152499). Patients had unresectable locally advanced/metastatic solid tumors refractory to standard therapies. In the phase 1 dose-escalation cohorts, patients had unresectable locally advanced/metastatic solid tumors refractory to standard therapies. Sac-TMT was administered by intravenous administration every 2 weeks at 2 to 12 mg/kg. In phase 2, patients with TNBC and HR+/HER2− breast cancer received sac-TMT per recommended doses for expansion (RDEs) identified in phase 1. Primary objectives were determining maximum tolerated dose (MTD) of sac-TMT and establishing RDEs (phase 1) and determining ORR per RECIST v1.1 by investigator assessment (phase 2). Adverse events were assessed per NCI-CTCAE version 5.0. Thirty patients were enrolled in phase 1 and received sac-TMT 2 mg/kg (n = 4), 4 mg/kg (n = 7), 5 mg/kg (n = 7), 5.5 mg/kg (n = 5), and 6 mg/kg (n = 7). Five patients had dose-limiting toxicities: grade 3 stomatitis at 4, 5.5, and 6 mg/kg; grade 3 rash at 5 mg/kg; and grade 3 urticaria at 6 mg/kg. MTD was 5.5 mg/kg and RDEs were 4 and 5 mg/kg. In the phase 2 dose expansion, ORR (95% CI) was 34.8% (16.4%, 57.3%) in the 4-mg/kg group (n = 23) and 38.9% (23.1%, 56.5%) in the 5-mg/kg group (n = 36) for TNBC. ORR (95% CI) was 31.7% (18.1%, 48.1%) for HR+/HER2− breast cancer (n = 41). Sac-TMT demonstrated manageable safety profile in patients with unresectable locally advanced/metastatic solid tumors and promising antitumor activity in metastatic TNBC and HR+/HER2 − breast cancer. Sac-TMT is being investigated in phase 3 studies. ClinicalTrials.gov, NCT04152499.","PeriodicalId":16023,"journal":{"name":"Journal of Hematology & Oncology","volume":"36 1","pages":""},"PeriodicalIF":28.5,"publicationDate":"2025-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144228900","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 : 2025-06-03DOI: 10.1186/s13045-025-01714-1
Hao Yao, Shi-hui Ren, Lin-hui Wang, Ming-qiang Ren, Jiao Cai, Dan Chen, Ying He, Si-han Lai, Bai-tao Dou, Meng-jiao Li, Yan-ling Li, Ya-li Cen, Alex H. Chang, Yi Su, Ling Qiu, Fang-yi Fan
<p><b>Journal of Hematology & Oncology (2025) 18:56</b></p><p><b>https://doi.org/10.1186/s13045-025-01713-2</b></p><p>The original article has been corrected to restore co-authors Yi Su, Ling Qiu, and Fang-yi Fan (lead contact) to co-Corresponding Authorship which was mistakenly removed by the production team which handled this article.</p><span>Author notes</span><ol><li><p>Hao Yao, Shi-hui Ren, Lin-hui Wang and Ming-qiang Ren contributed equally to this work.</p></li></ol><h3>Authors and Affiliations</h3><ol><li><p>Department of Hematology, Chinese People’s Liberation Army The General Hospital of Western Theater Command, Chengdu, 610083, Sichuan, China</p><p>Hao Yao, Shi-hui Ren, Jiao Cai, Dan Chen, Ying He, Si-han Lai, Bai-tao Dou, Meng-jiao Li, Yan-ling Li, Ya-li Cen, Yi Su, Ling Qiu & Fang-yi Fan</p></li><li><p>Branch of National Clinical Research Center for Hematological Disease, Chengdu, 610083, Sichuan, China</p><p>Hao Yao, Shi-hui Ren, Jiao Cai, Dan Chen, Ying He, Si-han Lai, Bai-tao Dou, Meng-jiao Li, Yan-ling Li, Ya-li Cen, Yi Su, Ling Qiu & Fang-yi Fan</p></li><li><p>Sichuan Clinical Research Center for Hematological Disease, Chengdu, 610083, China</p><p>Hao Yao, Shi-hui Ren, Jiao Cai, Dan Chen, Ying He, Si-han Lai, Bai-tao Dou, Meng-jiao Li, Yan-ling Li, Ya-li Cen, Yi Su, Ling Qiu & Fang-yi Fan</p></li><li><p>Department of Clinical Medicine, North Sichuan Medical College, Nanchong, 637000, Sichuan, China</p><p>Bai-tao Dou, Meng-jiao Li, Yan-ling Li & Fang-yi Fan</p></li><li><p>Institute of Basic Medicine, North Sichuan Medical College, Nanchong, 637000, Sichuan, China</p><p>Hao Yao</p></li><li><p>Department of Hematology, The People’s Hospital of Guizhou Province, Guiyang, 550002, Guizhou, China</p><p>Lin-hui Wang</p></li><li><p>Department of Hematology, Affiliated Hospital of Zunyi Medical University, Zunyi, 563000, Guizhou Province, China</p><p>Ming-qiang Ren</p></li><li><p>Engineering Research Center of Gene Technology, Ministry of Education, Institute of Genetics, School of Life Sciences, Fudan University, Shanghai, 200438, China</p><p>Alex H. Chang</p></li><li><p>Shanghai YaKe Biotechnology Ltd., Yangpu District, Shanghai, 200090, China</p><p>Alex H. Chang</p></li></ol><span>Authors</span><ol><li><span>Hao Yao</span>View author publications<p><span>You can also search for this author in</span><span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Shi-hui Ren</span>View author publications<p><span>You can also search for this author in</span><span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Lin-hui Wang</span>View author publications<p><span>You can also search for this author in</span><span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Ming-qiang Ren</span>View author publications<p><span>You can also search for this author in</span><span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Jiao Cai</span>View author publications<p><span>You can also search for
{"title":"Correction: BCMA/GPRC5D bispecific CAR T-cell therapy for relapsed/refractory multiple myeloma with extramedullary disease: a single-center, single-arm, phase 1 trial","authors":"Hao Yao, Shi-hui Ren, Lin-hui Wang, Ming-qiang Ren, Jiao Cai, Dan Chen, Ying He, Si-han Lai, Bai-tao Dou, Meng-jiao Li, Yan-ling Li, Ya-li Cen, Alex H. Chang, Yi Su, Ling Qiu, Fang-yi Fan","doi":"10.1186/s13045-025-01714-1","DOIUrl":"https://doi.org/10.1186/s13045-025-01714-1","url":null,"abstract":"<p><b>Journal of Hematology & Oncology (2025) 18:56</b></p><p><b>https://doi.org/10.1186/s13045-025-01713-2</b></p><p>The original article has been corrected to restore co-authors Yi Su, Ling Qiu, and Fang-yi Fan (lead contact) to co-Corresponding Authorship which was mistakenly removed by the production team which handled this article.</p><span>Author notes</span><ol><li><p>Hao Yao, Shi-hui Ren, Lin-hui Wang and Ming-qiang Ren contributed equally to this work.</p></li></ol><h3>Authors and Affiliations</h3><ol><li><p>Department of Hematology, Chinese People’s Liberation Army The General Hospital of Western Theater Command, Chengdu, 610083, Sichuan, China</p><p>Hao Yao, Shi-hui Ren, Jiao Cai, Dan Chen, Ying He, Si-han Lai, Bai-tao Dou, Meng-jiao Li, Yan-ling Li, Ya-li Cen, Yi Su, Ling Qiu & Fang-yi Fan</p></li><li><p>Branch of National Clinical Research Center for Hematological Disease, Chengdu, 610083, Sichuan, China</p><p>Hao Yao, Shi-hui Ren, Jiao Cai, Dan Chen, Ying He, Si-han Lai, Bai-tao Dou, Meng-jiao Li, Yan-ling Li, Ya-li Cen, Yi Su, Ling Qiu & Fang-yi Fan</p></li><li><p>Sichuan Clinical Research Center for Hematological Disease, Chengdu, 610083, China</p><p>Hao Yao, Shi-hui Ren, Jiao Cai, Dan Chen, Ying He, Si-han Lai, Bai-tao Dou, Meng-jiao Li, Yan-ling Li, Ya-li Cen, Yi Su, Ling Qiu & Fang-yi Fan</p></li><li><p>Department of Clinical Medicine, North Sichuan Medical College, Nanchong, 637000, Sichuan, China</p><p>Bai-tao Dou, Meng-jiao Li, Yan-ling Li & Fang-yi Fan</p></li><li><p>Institute of Basic Medicine, North Sichuan Medical College, Nanchong, 637000, Sichuan, China</p><p>Hao Yao</p></li><li><p>Department of Hematology, The People’s Hospital of Guizhou Province, Guiyang, 550002, Guizhou, China</p><p>Lin-hui Wang</p></li><li><p>Department of Hematology, Affiliated Hospital of Zunyi Medical University, Zunyi, 563000, Guizhou Province, China</p><p>Ming-qiang Ren</p></li><li><p>Engineering Research Center of Gene Technology, Ministry of Education, Institute of Genetics, School of Life Sciences, Fudan University, Shanghai, 200438, China</p><p>Alex H. Chang</p></li><li><p>Shanghai YaKe Biotechnology Ltd., Yangpu District, Shanghai, 200090, China</p><p>Alex H. Chang</p></li></ol><span>Authors</span><ol><li><span>Hao Yao</span>View author publications<p><span>You can also search for this author in</span><span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Shi-hui Ren</span>View author publications<p><span>You can also search for this author in</span><span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Lin-hui Wang</span>View author publications<p><span>You can also search for this author in</span><span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Ming-qiang Ren</span>View author publications<p><span>You can also search for this author in</span><span>PubMed<span> </span>Google Scholar</span></p></li><li><span>Jiao Cai</span>View author publications<p><span>You can also search for ","PeriodicalId":16023,"journal":{"name":"Journal of Hematology & Oncology","volume":"102 1","pages":""},"PeriodicalIF":28.5,"publicationDate":"2025-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144211126","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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