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Molecular Insights and Therapeutic Advances in Hematological Disorders, 2nd Edition

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A special issue of Current Issues in Molecular Biology (ISSN 1467-3045). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: 31 August 2026 | Viewed by 2615

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Dr. Eleni Gavriilaki

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Second Propedeutic Department of Internal Medicine, Hippocration Hospital, Aristotle University of Thessaloniki, 54642 Thessaloniki, Greece
Interests: hematologic malignancies; thrombosis; complement; cellular therapy; lymphoma; myeloma; COVID-19
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Special Issue Information

Dear Colleagues,

In recent years, many advances have been made in the understanding of the pathophysiology behind various hematological disorders. A better understanding of the molecular biology of both benign, such as hemoglobinopathies and congenital bleeding disorders, and malignant hematological diseases has led to the development of targeted therapeutics. For example, since the discovery of the Philadelphia chromosome in patients with chronic myelogenous leukemia and the development and approval of Imatinib, a tyrosine kinase inhibitor (TKI), the management of this clinical entity has been revolutionized. Moreover, the involvement of the immune system has been recognized in the pathogenesis of many hematological diseases. Specifically, complement system activation has been described as pathogenic in various disorders, such as paroxysmal nocturnal hemoglobinuria (PNH). Immune dysregulation is also prevalent in hematological malignancies, while immune therapeutics, including chimeric antigen receptor-T (CAR-T) cells and bispecific antibodies, constitute nowadays a standard of care for patients with refractory/relapsed B-cell lymphoproliferative neoplasms and multiple myeloma. The interaction between coagulation, immunity, and vascular endothelium is an emerging issue, concerning not only hematological disorders but also the complications of hematopoietic stem cell transplantation and novel immune therapeutics. This Special Issue aims to publish cutting-edge communication, research, and review articles concerning the pathophysiology, molecular biology, and novel therapeutics of, but not limited to, the following clinical entities: acute leukemia; myeloproliferative neoplasms; lymphoma; multiple myeloma; hemoglobinopathies; and hemophilia.

Notably, we also want to thank the journal’s Topical Advisory Panel Member, Dr. Nikolaos Kotsiou, for his contribution and support to the concept proposal, collaboration promotion, Special Issue operation, and development of this Special Issue.

Dr. Eleni Gavriilaki
Guest Editor

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Keywords

acute leukemia
myeloproliferative neoplasms
lymphoma
multiple myeloma
hemoglobinopathies
hemophilia

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Published Papers (4 papers)

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Research

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23 pages, 9790 KB

Open AccessArticle

Candidate miRNA Regulators of Blood Transcriptional Signatures for Differential Diagnosis of Chronic Lymphocytic Leukemia and Multiple Myeloma: A Comprehensive In Silico Study

by Gözde Öztan, Halim İşsever and Tuğçe İşsever

Curr. Issues Mol. Biol. 2026, 48(4), 352; https://doi.org/10.3390/cimb48040352 - 27 Mar 2026

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Abstract

Chronic lymphocytic leukemia (CLL) and multiple myeloma (MM) are biologically distinct hematologic malignancies with heterogeneous clinical courses, and minimally invasive molecular biomarkers are needed to support blood-based discrimination. We performed a comprehensive in silico analysis to derive cross-cohort, direction-consistent transcriptomic programs for CLL and MM and to nominate regulatory microRNAs (miRNAs) linked to these signatures. Public gene-expression datasets from the NCBI Gene Expression Omnibus (two cohorts per disease) were processed with a reproducible workflow to define disease-biased consensus gene sets. Experimentally validated miRNA–target interactions from miRTarBase were integrated with consensus genes for miRNA target over-representation analysis, and miRNA–mRNA networks were constructed to prioritize candidate miRNAs by connectivity. A strict intersection strategy yielded a large, direction-consistent CLL consensus program, whereas a vote-based approach produced a smaller MM program due to a weaker signal in one cohort. Enrichment and network analyses identified compact regulatory modules in CLL, including a highly connected candidate miRNA linked to many CLL-up genes. This framework provides reproducible disease-biased gene programs and evidence-anchored miRNA candidates to support targeted experimental validation and the development of hypothesis-driven blood-based biomarker studies for differential diagnosis and monitoring. Full article

(This article belongs to the Special Issue Molecular Insights and Therapeutic Advances in Hematological Disorders, 2nd Edition)

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14 pages, 774 KB

Open AccessArticle

Altered Expression of Ribosome Biogenesis Regulators (TP53, C-MYC, FBL, and NCL) in Precursor B-cell Acute Lymphoblastic Leukemia and Neuroblastoma

by Michalina Horochowska, Dawid Przystupski, Marta Kamińska, Iwona Bil-Lula, Bernarda Kazanowska and Marek Ussowicz

Curr. Issues Mol. Biol. 2026, 48(1), 74; https://doi.org/10.3390/cimb48010074 - 12 Jan 2026

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Abstract

Background/Objectives: Rapid cellular proliferation, a hallmark of malignancy, requires sustained and elevated protein synthesis, which in turn requires efficient ribosome biogenesis. The aim of this study was to evaluate the expression levels of TP53, C-MYC, FBL, and NCL in pre-B ALL and neuroblastoma tissues compared to healthy bone marrow samples—factors that may carry prognostic significance in pediatric malignancies. Materials and methods: The cohort included 45 pre-B ALL patients, 19 neuroblastoma patients, and 12 healthy bone marrow donors as controls. Total RNA was extracted from bone marrow or tumor samples and cDNA synthesis was performed with the Bio-Rad iScript kit. Quantitative PCR was conducted using SYBR Green chemistry, with GAPDH as the reference gene. Primers targeted TP53, C-MYC, FBL, and NCL, and gene expression was calculated using the 2^−ΔCt method. Results: The expression of C-MYC and FBL was found to be significantly decreased in patients with pre-B ALL in comparison to the healthy control group. NCL expression was highest in healthy donors, intermediate in pre-B ALL, and lowest in neuroblastoma. In addition to intergroup comparisons, correlations between gene expression levels were assessed within each diagnostic group. In the pre-B ALL group, a positive correlation was observed between TP53 and C-MYC expression, as well as between TP53 and both FBL and NCL. Furthermore, a significant positive correlation was found between FBL and NCL. In the neuroblastoma group, a statistically significant positive correlation was identified between C-MYC and FBL expression. In the control group, TP53 expression was positively correlated with NCL, and FBL expression showed a significant positive correlation with NCL. Conclusions: This study suggests the altered expression of ribosome biogenesis-related genes in pediatric pre-B acute lymphoblastic leukemia and neuroblastoma. The reported dysregulation suggests a disease-associated disruption in nucleolar function and translational regulation and may contribute to oncogenesis through altered ribosomal assembly, protein synthesis, or proliferative signaling. Full article

(This article belongs to the Special Issue Molecular Insights and Therapeutic Advances in Hematological Disorders, 2nd Edition)

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19 pages, 695 KB

Open AccessReview

How to Change the Role of Allogeneic Hematopoietic Cell Transplantation in Adults with B-Cell Acute Lymphoblastic Leukemia

by Martina Canichella and Paolo de Fabritiis

Curr. Issues Mol. Biol. 2026, 48(4), 351; https://doi.org/10.3390/cimb48040351 - 27 Mar 2026

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Abstract

Allogeneic hematopoietic stem cell transplantation (allo-HSCT) has long constituted a cornerstone of post-remission consolidation therapy for adults with high-risk B-cell acute lymphoblastic leukemia (B-ALL), offering potent graft-versus-leukemia activity at the expense of significant treatment-related toxicity (TRT) and non-relapse mortality (NRM). Over the past two decades, however, outcomes following allo-HSCT have improved substantially. This progress has been driven primarily by a marked reduction in NRM, translating into improved overall survival (OS), as consistently documented by large cooperative group analyses and single-center series. Advances in supportive care, infectious prophylaxis, donor selection, and graft-versus-host disease (GvHD) prevention have contributed substantially to this improvement. In parallel, transplant decision-making has been profoundly reshaped by refined disease biology-based risk stratification and the systematic evaluation of measurable residual disease (MRD). Moreover, the advent of highly effective immunotherapeutic approaches—including blinatumomab, inotuzumab ozogamicin, and chimeric antigen receptor (CAR) T-cell therapies—has enabled the achievement of deeper molecular remissions prior to transplantation, both in first and subsequent complete remissions. Taken together, these developments have shifted allo-HSCT from a widely applied strategy to a more individualized, risk-adapted therapeutic approach. This review examines how the indications, timing, and objectives of allo-HSCT are evolving in the contemporary treatment landscape of adult B-ALL, with particular emphasis on Philadelphia chromosome–negative, Philadelphia-like, and Philadelphia chromosome–positive disease subsets. Full article

(This article belongs to the Special Issue Molecular Insights and Therapeutic Advances in Hematological Disorders, 2nd Edition)

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19 pages, 3865 KB

Open AccessReview

Research Progress on the KMT2A-AFF3 Fusion Gene in Childhood Acute Lymphoblastic Leukemia: Mechanisms, Clinical Implications, and Therapeutic Strategies

by Yawei Zhang and Juan Liang

Curr. Issues Mol. Biol. 2025, 47(12), 988; https://doi.org/10.3390/cimb47120988 - 26 Nov 2025

Viewed by 1147

Abstract

KMT2A-rearranged (KMT2A-r) acute lymphoblastic leukemia (ALL), particularly in infants, represents one of the most aggressive pediatric hematological malignancies with a historically dismal prognosis. While KMT2A-AFF1 (t(4;11)) is the most prevalent fusion, a diverse array of partner genes exists, each conferring distinct biological and clinical features. This review focuses on the rare but clinically significant KMT2A-AFF3 subtype, which arises from the t(2;11)(q11.2;q23) chromosomal translocation. This review summarizes the molecular pathogenesis driven by the KMT2A-AFF3 fusion oncoprotein, which functions as an aberrant transcriptional complex. This complex hijacks essential epigenetic machinery, including the recruitment of DOT1L and interaction with Menin, leading to pathogenic histone modifications (e.g., H3K79 hypermethylation) and the subsequent upregulation of critical target genes, notably the HOXA cluster and MEIS1, thereby enforcing a B-lymphoid differentiation arrest at the pro-B/pre-B stage. Clinically, KMT2A-AFF3 ALL is characterized by high-risk features, including infant onset, hyperleukocytosis, central nervous system (CNS) involvement, and a distinct CD10-negative immunophenotype. This review highlights the evidence defining its poor prognosis, which is primarily driven by profound chemoresistance to conventional therapies, including glucocorticoids. Finally, we discuss the rapidly evolving therapeutic landscape, detailing the limitations of standard intensive chemotherapy and the immense promise of novel targeted strategies, such as Menin inhibitors (e.g., Revumenib), DOT1L inhibitors, and immunotherapies (e.g., CAR-T cells, Blinatumomab), which hold the potential to revolutionize outcomes for this high-risk leukemia subtype. Full article

(This article belongs to the Special Issue Molecular Insights and Therapeutic Advances in Hematological Disorders, 2nd Edition)

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