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Hematologic Malignancies: From Molecular Pathology to Novel Therapeutics

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Oncology".

Deadline for manuscript submissions: 20 May 2026 | Viewed by 3766

Special Issue Editor


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Guest Editor
Instituto Nacional de Cancerología, Mexico City, Mexico
Interests: lymphoma; non-Hodgkin lymphoma; B cell lymphoma
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Hematological malignancies comprise a heterogeneous group of diseases, in whom the knowledge of implicated pathways in pathogenesis has allowed advances in classification and targeted therapy.

In recent years, numerous genomic sequencing studies have primarily targeted recurrent mutations in individual genes, elucidating underlying oncogenic mechanisms. Moreover, molecular classifications have deepened our understanding of hematological diseases. Therefore, deeper and more detailed analyses using genomic, transcriptome, and epigenetic data have been performed by different research groups in order to refine the disease classification into clusters related to the disease impact and clinical outcomes.

This Special Issue will include reviews and research studies regarding the role of genomes, epigenetic regulation, genes implicated in cell cycle control, proliferation, apoptosis, biological processes participating in the pathogenesis, and the impact on treatment of patients.

I look forward to your submissions.

Dr. Myrna Gloria Candelaria
Guest Editor

Manuscript Submission Information

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Keywords

  • pathogenesis
  • B-cell lymphoma regulation
  • epigenetics and hematology
  • bispecific antibodies in hematology
  • hematologic malignancies

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Published Papers (3 papers)

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Research

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11 pages, 1014 KB  
Article
Clonal Hematopoiesis and Outcomes After High-Dose Chemotherapy and Autologous Stem Cell Transplantation in Patients with AML, Myeloma, and Lymphoma
by Corinne Natalie Schmid, Katharina Sponagel, Ulrike Bacher, Katja Seipel, Naomi Porret, Gertrud Wiedemann, Michèle Hoffmann, Michael Daskalakis and Thomas Pabst
Int. J. Mol. Sci. 2025, 26(16), 8021; https://doi.org/10.3390/ijms26168021 - 19 Aug 2025
Cited by 1 | Viewed by 1619
Abstract
Autologous stem cell transplantation (ASCT) after high-dose chemo-therapy (HDCT) is an option of consolidation therapy in patients with AML, lymphoma, or myeloma. Clonal hematopoiesis (CH) is a premalignant state, associated with an increased risk of hematological cancer. The incidence of CH in patients [...] Read more.
Autologous stem cell transplantation (ASCT) after high-dose chemo-therapy (HDCT) is an option of consolidation therapy in patients with AML, lymphoma, or myeloma. Clonal hematopoiesis (CH) is a premalignant state, associated with an increased risk of hematological cancer. The incidence of CH in patients with AML, myeloma, and lymphoma and its effect on the outcome after HDCT/ASCT remain poorly studied. Here we screened 142 patients treated with HDCT/ASCT between 2002 and 2021 at Bern University Hospital for somatic gene mutations in ASXL1, DNMT3A, JAK2, TET2, and TP53. CH-associated somatic gene mutations were detected in 14/31 AML patients (45%), 13/64 myeloma patients (20%), and 9/47 lymphoma patients (19%). Clinical characteristics, treatment modalities, and responses to treatment were similar in patients with and without CH. Patients with CH-associated gene mutations had higher relapse rates and reduced progression free survival, most evident in lymphoma patients (p = 0.007). Overall survival tended to be shorter in lymphoma patients with CH-associated mutations (p = 0.078), whereas this was not observed in AML and myeloma patients. Survival in lymphoma patients with CH was inferior, which may have an impact on post-transplant surveillance strategies in the future. In contrast, survival outcomes were not associated significantly with CH in AML and myeloma patients in our study. Longer follow-ups and larger cohorts will be needed to validate our observations. Full article
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Review

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20 pages, 997 KB  
Review
Decoding NOTCH1: From T-Cell Development Guardian to Driver of Pediatric T-Cell Lymphoblastic Lymphoma
by Fran Leijnen and Tim Lammens
Int. J. Mol. Sci. 2026, 27(4), 2083; https://doi.org/10.3390/ijms27042083 - 23 Feb 2026
Viewed by 824
Abstract
T-cell lymphoblastic lymphoma (T-LBL) is an aggressive malignancy of immature T-cells accounting for a substantial proportion of pediatric non-Hodgkin lymphoma cases. Current chemotherapeutic regimens achieve five-year event-free survival rates of 80–90%, yet relapse occurs in approximately 20% of patients and remains a major [...] Read more.
T-cell lymphoblastic lymphoma (T-LBL) is an aggressive malignancy of immature T-cells accounting for a substantial proportion of pediatric non-Hodgkin lymphoma cases. Current chemotherapeutic regimens achieve five-year event-free survival rates of 80–90%, yet relapse occurs in approximately 20% of patients and remains a major therapeutic challenge. This underscores the need for improved, molecularly informed treatment strategies. Recent genomic profiling has highlighted the central role of NOTCH1 signaling in T-LBL pathogenesis. NOTCH1, a transmembrane receptor critical for T-cell differentiation and maturation, requires tightly regulated activation during normal thymocyte development. Dysregulated signaling disrupts this balance, driving aberrant proliferation and impaired differentiation, characteristics of malignant transformation. While activating mutations have long been recognized as key oncogenic events, the recent identification of recurrent NOTCH1 translocations, associated with adverse outcomes, reveals an additional mechanism of pathway activation. These findings reinforce NOTCH1 as a pivotal oncogenic hub in T-cell malignancies and a compelling target for therapeutic intervention. This review synthesizes current insights into the molecular landscape of pediatric T-LBL, with a focus on the biological and clinical implications of NOTCH1 mutations and translocations. Furthermore, we examine emerging approaches to therapeutically exploit aberrant NOTCH1 signaling for the more precise and effective treatment of this disease and formulate outstanding research questions. Full article
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17 pages, 1398 KB  
Review
Pathways of Resistance: Modern Multiple Myeloma Therapies and Overcoming Reliance on Genomic Integrity
by Iulianna Taritsa and Eric Fossel
Int. J. Mol. Sci. 2026, 27(3), 1439; https://doi.org/10.3390/ijms27031439 - 31 Jan 2026
Viewed by 736
Abstract
Multiple myeloma (MM) is the second most common hematological malignancy in the US and Europe—comprising approximately 10% of all hematologic cancer cases—and its incidence has increased over the last three decades by approximately 120% due to an aging world population. It remains an [...] Read more.
Multiple myeloma (MM) is the second most common hematological malignancy in the US and Europe—comprising approximately 10% of all hematologic cancer cases—and its incidence has increased over the last three decades by approximately 120% due to an aging world population. It remains an incurable cancer among diseases in modern medicine. This review outlines the relevant cancer biology of MM, with a special emphasis on the role of tumor protein p53. We provide the most up-to-date summary of the current drugs in clinical or pre-clinical trials targeting weaknesses in the MM apoptotic mechanism. In addition, we highlight the potential for new routes to strike and kill myeloma cells, possibly creating a vaccine-like effect that prevents relapse, using the principles of immunogenic cell death (ICD). Full article
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