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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: 31 August 2025 | Viewed by 466

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 (1 paper)

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Research

11 pages, 1014 KiB  
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
Viewed by 193
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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