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New Insights in Hematologic Malignancies: From Pathophysiologic Mechanisms to Therapeutic...
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New Insights in Hematologic Malignancies: From Pathophysiologic Mechanisms to Therapeutic Strategies

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cancer Biology and Oncology".

Deadline for manuscript submissions: 31 December 2025 | Viewed by 2936

Special Issue Editor

Dr. Yun Chen

E-Mail Website
Guest Editor
Pediatric Hematology Laboratory, Division of Hematology/Oncology, Department of Pediatrics, The Seventh Affiliated Hospital, Sun Yat-Sen University, Shenzhen 518107, China
Interests: hematopoietic malignancies; protein phosphorylation; small molecule targeted drugs; rare blood disorders

Special Issue Information

Dear Colleagues,

This Special Issue will focus on the pathogenesis, diagnosis, prognosis, and treatment of hematologic malignancies, including but not limited to leukemia, lymphoma, and myeloma. Hematologic malignancies are a diverse group of disorders arising from the abnormal proliferation and differentiation of hematopoietic cells, often driven by complex genetic, epigenetic, and microenvironmental factors. While targeted therapies and immunotherapies have improved outcomes for some patients, resistance and relapse continue to pose major challenges, emphasizing the urgency of uncovering fundamental disease mechanisms and identifying new therapeutic targets.

This Special Issue will also consider studies on emerging disease models, including organoids, 3D cultures, and patient-derived xenografts, which can help recreate the tumor microenvironment and support precision medicine. Contributions addressing novel diagnostic biomarkers, resistance mechanisms, immune evasion, treatment-related complications, and translational strategies are highly encouraged. Research exploring the interactions between malignant cells and the bone marrow or lymphoid niche, as well as the impact of systemic inflammation, immune dysregulation, and disease-associated comorbidities, will also be included.

Overall, this Special Issue aims to bring together recent insights into the biological and clinical management of hematologic malignancies, fostering interdisciplinary collaboration and facilitating translational advancements toward optimized precision medicine.

Dr. Yun Chen
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biomedicines is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • leukemia
  • hematological malignancies
  • tumor microenvironment
  • disease models
  • precision medicine
  • immunotherapy
  • targeted therapy
  • drug resistance
  • biomarkers
  • translational research

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Published Papers (4 papers)

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Research

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19 pages, 5195 KB  
Article
Key Common Genes with LTF and MMP9 Between Sepsis and Relapsed B-Cell Lineage Acute Lymphoblastic Leukemia in Children
by Ying-Ping Xiao, Yu-Cai Cheng, Chun Chen, Hong-Man Xue, Mo Yang and Chao Lin
Biomedicines 2025, 13(9), 2307; https://doi.org/10.3390/biomedicines13092307 - 20 Sep 2025
Viewed by 21
Abstract
Background: Pediatric sepsis is a life-threatening disease that is associated with the progression of acute lymphoblastic leukemia (ALL) and the recurrence of B-cell ALL (B-ALL). Although previous studies have reported a partial association between sepsis and ALL, there is limited research on the [...] Read more.
Background: Pediatric sepsis is a life-threatening disease that is associated with the progression of acute lymphoblastic leukemia (ALL) and the recurrence of B-cell ALL (B-ALL). Although previous studies have reported a partial association between sepsis and ALL, there is limited research on the shared genes between pediatric sepsis and relapsed B-ALL. This study aims to further elucidate the more comprehensive and novel common genetic factors and molecular pathways between the two diseases. Methods: Gene expression datasets pertaining to pediatric sepsis (GSE13904, GSE80496) and relapsed B-ALL (GSE3910, GSE28460) were retrieved from the Gene Expression Omnibus database for this retrospective analysis. The initial analysis identified differentially expressed genes common to both pediatric sepsis and relapsed B-ALL. Subsequent investigations employed three complementary approaches: protein–protein interaction networks, molecular complex detection (MCODE) clustering functions, and support vector machine recursive feature elimination model to separately identify the diagnostic biomarkers for each condition. Importantly, key common genes were identified by overlapping the diagnostic genes for pediatric sepsis and relapsed B-ALL. Further characterization involved comprehensive functional analysis through the Metascape platform, construction of transcription factor (TF)-mRNA-microRNA (miRNA) networks, drug prediction, and molecular docking to explore their biological significance and potential therapeutic targets. Results: Comparative analysis of pediatric sepsis-related and relapsed B-ALL-related datasets revealed two shared genetic markers, lactotransferrin (LTF) and matrix metallopeptidase 9 (MMP9), exhibiting diagnostic significance and consistent upregulation in both disease groups. Transcriptional regulatory network analysis identified specificity protein 1 (SP1) as the principal transcription factor capable of coregulating LTF and MMP9 expression. In addition, molecular docking demonstrated high-affinity interactions between curcumin and MMP9 (−7.18 kcal/mol) as well as reserpine and LTF (−5.4 kcal/mol), suggesting their potential therapeutic utility for clinical evaluation. Conclusions: These findings elucidate the molecular pathogenesis involving LTF and MMP9 in pediatric sepsis and relapsed B-ALL, providing novel insights for clinical diagnosis and therapeutic development. Full article
(This article belongs to the Special Issue New Insights in Hematologic Malignancies: From Pathophysiologic Mechanisms to Therapeutic Strategies)
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13 pages, 2606 KB  
Article
Inhibiting UNC13B Suppresses Cell Proliferation by Upregulating the Apoptotic Pathway in Multiple Myeloma
by Yuan Tao, Lihua Yuan, Yuntian Ding, Rongli Xie, Fangjie Liu, Zhongming Zhang, Xiaojun Xu and Xiaobo Wang
Biomedicines 2025, 13(9), 2086; https://doi.org/10.3390/biomedicines13092086 - 27 Aug 2025
Viewed by 522
Abstract
Background/Objectives: Multiple myeloma (MM) is the second most common hematological malignancy and remains incurable because of its complex and heterogeneous pathogenesis. UNC13B (unc-13 homolog B) encodes Munc13-2, a presynaptic protein that is involved in vesicle exocytosis. While its role has been explored in [...] Read more.
Background/Objectives: Multiple myeloma (MM) is the second most common hematological malignancy and remains incurable because of its complex and heterogeneous pathogenesis. UNC13B (unc-13 homolog B) encodes Munc13-2, a presynaptic protein that is involved in vesicle exocytosis. While its role has been explored in neurological diseases, its function in cancer biology remains largely uncharacterized. This study aimed to elucidate the role of UNC13B in regulating MM cell proliferation and apoptosis. Methods:UNC13B mRNA expression was assessed across human MM cell lines. ARD cells, which exhibited the highest UNC13B expression, were transduced with a UNC13B-specific shRNA via a lentiviral vector. Cell proliferation, apoptosis, and expression of associated proteins were evaluated by means of the Cell Counting Kit-8 (CCK-8) assay, flow cytometry, and Western blot analysis. Results: UNC13B was significantly upregulated in MM cell lines. The knockdown of UNC13B in ARD cells markedly inhibited cell proliferation and induced apoptosis. These changes were accompanied by the downregulation of proliferation-related proteins and upregulation of pro-apoptotic markers. Western blot analysis suggests that UNC13B may exert its effects by modulating key regulatory proteins, including PINK1, CDK2, AKR7A3, and Bim. Conclusions: Our findings suggest that UNC13B supports MM cell survival and proliferation, potentially through the regulation of oncogenic and apoptotic signaling pathways. UNC13B may represent a novel therapeutic target in multiple myeloma. Full article
(This article belongs to the Special Issue New Insights in Hematologic Malignancies: From Pathophysiologic Mechanisms to Therapeutic Strategies)
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18 pages, 3824 KB  
Article
Prognostic Risk Model of Megakaryocyte–Erythroid Progenitor (MEP) Signature Based on AHSP and MYB in Acute Myeloid Leukemia
by Ting Bin, Ying Wang, Jing Tang, Xiao-Jun Xu, Chao Lin and Bo Lu
Biomedicines 2025, 13(8), 1845; https://doi.org/10.3390/biomedicines13081845 - 29 Jul 2025
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Abstract
Background: Acute myeloid leukemia (AML) is a common and aggressive adults hematological malignancies. This study explored megakaryocyte–erythroid progenitors (MEPs) signature genes and constructed a prognostic model. Methods: Uniform manifold approximation and projection (UMAP) identified distinct cell types, with differential analysis between [...] Read more.
Background: Acute myeloid leukemia (AML) is a common and aggressive adults hematological malignancies. This study explored megakaryocyte–erythroid progenitors (MEPs) signature genes and constructed a prognostic model. Methods: Uniform manifold approximation and projection (UMAP) identified distinct cell types, with differential analysis between AML-MEP and normal MEP groups. Univariate and the least absolute shrinkage and selection operator (LASSO) Cox regression selected biomarkers to build a risk model and nomogram for 1-, 3-, and 5-year survival prediction. Results: Ten differentially expressed genes (DEGs) related to overall survival (OS), six (AHSP, MYB, VCL, PIM1, CDK6, as well as SNHG3) were retained post-LASSO. The model exhibited excellent efficiency (the area under the curve values: 0.788, 0.77, and 0.847). Pseudotime analysis of UMAP-defined subpopulations revealed that MYB and CDK6 exert stage-specific regulatory effects during MEP differentiation, with MYB involved in early commitment and CDK6 in terminal maturation. Finally, although VCL, PIM1, CDK6, and SNHG3 showed significant associations with AML survival and prognosis, they failed to exhibit pathological differential expression in quantitative real-time polymerase chain reaction (qRT-PCR) experimental validations. In contrast, the downregulation of AHSP and upregulation of MYB in AML samples were consistently validated by both qRT-PCR and Western blotting, showing the consistency between the transcriptional level changes and protein expression of these two genes (p < 0.05). Conclusions: In summary, the integration of single-cell/transcriptome analysis with targeted expression validation using clinical samples reveals that the combined AHSP-MYB signature effectively identifies high-risk MEP-AML patients, who may benefit from early intensive therapy or targeted interventions. Full article
(This article belongs to the Special Issue New Insights in Hematologic Malignancies: From Pathophysiologic Mechanisms to Therapeutic Strategies)
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Review

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29 pages, 1395 KB  
Review
Advances and Challenges in Targeted Therapy and Its Combination Strategies for Leukemia
by Zhiyuan Zhong, Ran Yao, Yifei Duan, Cheng Ouyang, Zefan Du, Lindi Li, Hailin Zou, Yong Liu, Hongman Xue, Liang Li and Chun Chen
Biomedicines 2025, 13(7), 1652; https://doi.org/10.3390/biomedicines13071652 - 7 Jul 2025
Viewed by 1554
Abstract
Leukemia is a group of hematological malignancies with a complex pathogenesis and diverse clinical manifestations. Although traditional treatments such as chemotherapy, radiotherapy, and hematopoietic stem cell transplantation have improved patient outcomes, their efficacy is often limited by non-specificity, drug resistance, and relapse. In [...] Read more.
Leukemia is a group of hematological malignancies with a complex pathogenesis and diverse clinical manifestations. Although traditional treatments such as chemotherapy, radiotherapy, and hematopoietic stem cell transplantation have improved patient outcomes, their efficacy is often limited by non-specificity, drug resistance, and relapse. In recent years, targeted therapy has emerged as a major breakthrough, offering new opportunities for precision medicine in leukemia. The development of molecularly targeted agents has significantly advanced our ability to treat specific leukemia subtypes. However, challenges such as resistance to targeted drugs, adverse effects, and tumor heterogeneity remain significant obstacles. As a result, treatment strategies are shifting from single-agent chemotherapy toward combination therapies that integrate targeted agents, aiming to enhance therapeutic efficacy and reduce the likelihood of resistance. This review summarizes the current research landscape, clinical applications, and limitations of targeted therapies in leukemia, with a focus on recent progress in combination treatment strategies and ongoing clinical trials. Full article
(This article belongs to the Special Issue New Insights in Hematologic Malignancies: From Pathophysiologic Mechanisms to Therapeutic Strategies)
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