Current and Future Molecular Insights into Hematological Diseases: From Diagnosis to Therapy

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: 31 December 2026 | Viewed by 2359

Editors


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Guest Editor
Servicio de Hematología y Hemoterapia, Instituto Ramón y Cajal de Investigación Sanitaria (IRYCIS), Hospital Universitario Ramón y Cajal, Madrid, Spain
Interests: hematology; mastocytosis; molecular biology; myeloproliferative neoplasm

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Guest Editor
Instituto de Biomedicina y Biotecnología de Cantabria, Departamento de Biología Molecular, Universidad de Cantabria-CSIC, Albert Einstein 22, 39011 Cantabria, Spain
Interests: MYC; MNT; MXD; toncogenic transcription factors; molecular biology of lymphoma and leukemia (not clinical)

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Guest Editor
Servicio de Hematología y Hemoterapia, Instituto Ramón y Cajal de Investigación Sanitaria (IRYCIS), Hospital Universitario Ramón y Cajal, Madrid, Spain
Interests: lymphoma; immunophenotyping; flow cytometry; cytomorphology

Special Issue Information

Dear Colleagues,

We are pleased to announce a call for submissions for a Special Issue of Biomolecules entitled "Current and Future Molecular Insights into Hematological Diseases: From Diagnosis to Therapy". This issue aims to provide a comprehensive overview of the latest advancements in the diagnosis, prognosis, and treatment of hematological malignancies with a focus on molecular insights.

We invite physicians, researchers, and in-training specialists to submit both original research articles and reviews that address current challenges and innovations in the field. Topics of interest include, but are not limited to, the following:

  • Novel diagnostic strategies in hematological malignancies, with a special interest in molecular mechanisms.
  • Identification and validation of molecular prognostic and predictive markers for hematological neoplasms.
  • Targeted therapies, immunotherapy, and cellular therapy for the treatment of both myeloid and lymphoid neoplasms.

We encourage contributions that offer new perspectives or highlight emerging trends in both diagnostic and therapeutic fields.

We look forward to your valuable contributions.

Sincerely,

Dr. Miguel Piris-Villaespesa
Prof. Dr. Javier Leon
Dr. Fernando Martín-Moro
Guest Editors

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 250 words) can be sent to the Editorial Office for assessment.

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-anonymized peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biomolecules 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 2700 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

  • hematological diseases
  • diagnostic assessment
  • molecular biology
  • targeted therapies
  • lymphoid neoplasm
  • myeloid neoplasm

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Published Papers (2 papers)

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Research

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24 pages, 4606 KB  
Article
CTCF Regulates Erythroid Differentiation Through Control of Core Erythroid Transcription Factors
by Lorena García-Gaipo, Vanessa Junco, Lucía García-Gutiérrez, Verónica Torrano, Rosa Blanco, Alexandra Wiesinger, Rujula Pradeep, Jose Luis Arroyo, Ana Batlle-López, Javier León, Manuel Rosa-Garrido and M. Dolores Delgado
Biomolecules 2026, 16(4), 549; https://doi.org/10.3390/biom16040549 - 8 Apr 2026
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Abstract
Erythropoiesis is tightly regulated by lineage-specific transcription factors that govern erythroid commitment, proliferation, and differentiation. A core erythroid transcriptional network, together with non-DNA-binding cofactors, occupies regulatory regions of genes essential for erythroid development. This process is further shaped by epigenetic mechanisms, including histone [...] Read more.
Erythropoiesis is tightly regulated by lineage-specific transcription factors that govern erythroid commitment, proliferation, and differentiation. A core erythroid transcriptional network, together with non-DNA-binding cofactors, occupies regulatory regions of genes essential for erythroid development. This process is further shaped by epigenetic mechanisms, including histone post-translational modifications and long-range chromatin interactions. CCCTC-binding factor (CTCF) is a multifunctional regulator with a central role in three-dimensional chromatin organization. Although CTCF has been implicated in hematopoietic differentiation and leukemogenesis, its specific function in erythropoiesis remains poorly defined. Here, we investigated the role of CTCF during erythroid differentiation using two complementary models: pluripotent K562 leukemia cells and primary human CD34+ hematopoietic stem/progenitor cells, each induced toward the erythroid lineage by distinct stimuli. In both systems, CTCF silencing impaired erythroid differentiation by repression of key erythroid transcription factor genes, including LMO2, KLF1, MYB, and ETS1. This repression was associated with enrichment of repressive histone marks at CTCF-binding sites within their regulatory regions. Moreover, CTCF cooperated with cohesin to establish and stabilize long-range chromatin interactions at these loci. These results provide new insight into how CTCF-dependent chromatin regulation contributes to normal erythroid development and suggest that perturbation of this regulatory axis may have implications for hematopoietic disorders and malignancies. Full article
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Review

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22 pages, 1379 KB  
Review
Targeting the WNT/β-Catenin Pathway in Hematological Malignancies: From Molecular Pathogenesis to Emerging Therapeutic Strategies
by Ali Keyhani, Hamed Haddad Kashani, Khadijeh Dizaji Asl, Zeinab Mazloumi, Faride Kaikavoosnejad, Seyyede Sepide Ashraf Moosavi, Milad Verdi, Ali Rafat and Reza Nejati
Biomolecules 2026, 16(5), 653; https://doi.org/10.3390/biom16050653 - 28 Apr 2026
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Abstract
Hematological malignancies, including multiple myeloma (MM), leukemia, and lymphoma, represent a major global health burden, accounting for approximately 6.6% of all cancer cases and contributing to significant mortality. The evolutionary conserved WNT/β-catenin signaling pathway is a critical regulator of normal hematopoietic stem cell [...] Read more.
Hematological malignancies, including multiple myeloma (MM), leukemia, and lymphoma, represent a major global health burden, accounting for approximately 6.6% of all cancer cases and contributing to significant mortality. The evolutionary conserved WNT/β-catenin signaling pathway is a critical regulator of normal hematopoietic stem cell homeostasis, and its dysregulation is a hallmark of various hematological malignancies. Aberrant activation through mutations, overexpression of ligands, or disruption of the destruction complex drives uncontrolled proliferation, impaired differentiation, and therapeutic resistance to therapy in acute and chronic leukemias, lymphomas, and multiple myeloma. Therapeutic interventions targeting this pathway, such as GSK-3 inhibitors, β-catenin antagonists, and small molecules like CWP291 and salinomycin, have demonstrated promising antitumor effects. Furthermore, combining WNT/β-catenin inhibition with targeted or epigenetic therapies, such as venetoclax and chidamide, can produce synergistic antitumor effects and overcome chemoresistance. Despite this potential, clinical translation is hampered by on-target toxicities in healthy tissues, pathway complexity, and a lack of predictive biomarkers. We conclude that the future of WNT-directed therapy lies in developing biomarker-selective agents, advanced drug delivery systems to improve specificity, and exploring novel combinations with immunotherapy to harness the anti-tumor immune response. Full article
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