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Molecular Research and Pathological Mechanism of Leukemia
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Molecular Research and Pathological Mechanism of Leukemia

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 May 2025 | Viewed by 4315

Special Issue Editors

Prof. Dr. Sylwia Flis

E-Mail Website
Guest Editor
Center for Translational Medicine, Warsaw University of Life Sciences, 100 Nowoursynowska St., 02-797 Warsaw, Poland
Interests: apoptosis; cytotoxicity; molecular cell biology; cancer cells; cancer research; chronic myeloid leukemia; leukemia
Prof. Dr. Mirosława Koronkiewicz

E-Mail Website
Guest Editor
Department of Biomedical Research, National Medicines Institute, 30/34 Chelmska St., 00-725 Warsaw, Poland
Interests: protein kinase inhibitors; apoptosis; cytotoxicity; cancer biology; leukemia; molecular cell biology

Special Issue Information

Dear Colleagues,

Hematooncology is a field that dynamically uses new technologies in both diagnosis and treatment. The highest increase in the use of new therapies is observed in patients with blood cancers. The high effectiveness of targeted therapies and immunotherapy is associated with limiting the use of traditional chemotherapy. A personalized therapeutic approach in the treatment of leukemia is associated with a better cure/survival ratio, but it also has its limitations. Should traditional therapeutic approaches be abandoned? How can we improve the diagnosis and treatment efficiency of leukemia patients? How can we effectively eliminate leukemic stem cells? These and other questions will be answered in this Special Issue, which aims to present research in the field of pathophysiology, treatment strategies, and outcomes of leukemia, with a focus on the following:

  • The molecular mechanisms involved in leukemia;
  • Novel biomarkers for early leukemia diagnosis;
  • New therapeutic approaches (target therapies including drug design and development).

Prof. Dr. Sylwia Flis
Prof. Dr. Mirosława Koronkiewicz
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 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. Current Issues in Molecular Biology 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 2200 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

  • chronic leukemia
  • acute leukemia
  • T-cell prolymphocytic leukemia
  • BCR-ABL1
  • tyrosine kinase inhibitors
  • Philadelphia chromosome
  • biomarkers

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Published Papers (2 papers)

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Research

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15 pages, 5275 KiB  
Article
FLT3 and IRAK4 Inhibitor Emavusertib in Combination with BH3-Mimetics in the Treatment of Acute Myeloid Leukemia
by Katja Seipel, Harpreet Mandhair, Ulrike Bacher and Thomas Pabst
Curr. Issues Mol. Biol. 2024, 46(4), 2946-2960; https://doi.org/10.3390/cimb46040184 - 29 Mar 2024
Viewed by 2262
Abstract
Targeting the FLT3 receptor and the IL-1R associated kinase 4 as well as the anti-apoptotic proteins MCL1 and BCL2 may be a promising novel approach in the treatment of acute myeloid leukemia (AML). The FLT3 and IRAK4 inhibitor emavusertib (CA4948), the MCL1 inhibitor [...] Read more.
Targeting the FLT3 receptor and the IL-1R associated kinase 4 as well as the anti-apoptotic proteins MCL1 and BCL2 may be a promising novel approach in the treatment of acute myeloid leukemia (AML). The FLT3 and IRAK4 inhibitor emavusertib (CA4948), the MCL1 inhibitor S63845, the BCL2 inhibitor venetoclax, and the HSP90 inhibitor PU-H71 were assessed as single agents and in combination for their ability to induce apoptosis and cell death in leukemic cells in vitro. AML cells represented all major morphologic and molecular subtypes, including FLT3-ITD and NPM1 mutant AML cell lines and a variety of patient-derived AML cells. Emavusertib in combination with MCL1 inhibitor S63845 or BCL2 inhibitor venetoclax induced cell cycle arrest and apoptosis in MOLM-13 cells. In primary AML cells, the response to emavusertib was associated with the presence of the FLT3 gene mutation with an allelic ratio >0.5 and the presence of NPM1 gene mutations. S63845 was effective in all tested AML cell lines and primary AML samples. Blast cell percentage was positively associated with the response to CA4948, S63845, and venetoclax, with elevated susceptibility of primary AML with blast cell fraction >80%. Biomarkers of the response to venetoclax included the blast cell percentage and bone marrow infiltration rate, as well as the expression levels of CD11b, CD64, and CD117. Elevated susceptibility to CA4948 combination treatments with S63845 or PU-H71 was associated with FLT3-mutated AML and CD34 < 30%. The combination of CA4948 and BH3-mimetics may be effective in the treatment in FLT3-mutated AML with differential target specificity for MCL1 and BCL2 inhibitors. Moreover, the combination of CA4948 and PU-H71 may be a candidate combination treatment in FLT3-mutated AML. Full article
(This article belongs to the Special Issue Molecular Research and Pathological Mechanism of Leukemia)
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Review

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14 pages, 260 KiB  
Review
Tyrosine Kinase Inhibitor Post-Allogeneic Stem Cell Transplantation in Adult Philadelphia-Positive B-Acute Lymphoblastic Leukemia: State of the Art and Future Directions
by Martina Canichella and Paolo de Fabritiis
Curr. Issues Mol. Biol. 2025, 47(2), 129; https://doi.org/10.3390/cimb47020129 - 18 Feb 2025
Viewed by 1078
Abstract
In a scenario characterized by continuous improvement in outcomes, Philadelphia chromosome-positive (Ph+) ALL, once considered a biologically defined subtype with one of the poorest prognoses, now includes patients achieving long-term survival even without allogeneic stem cell transplantation. First-line therapy is increasingly adopting a [...] Read more.
In a scenario characterized by continuous improvement in outcomes, Philadelphia chromosome-positive (Ph+) ALL, once considered a biologically defined subtype with one of the poorest prognoses, now includes patients achieving long-term survival even without allogeneic stem cell transplantation. First-line therapy is increasingly adopting a chemo-free approach, combining tyrosine kinase inhibitors (TKIs) with immunotherapy—specifically blinatumomab—which has resulted in high rates of complete molecular responses and improved survival outcomes. Within this paradigm shift, the allocation to transplantation is becoming increasingly selective and genomically oriented, focusing on patients with particularly unfavorable prognostic and predictive factors. For patients undergoing transplantation, maintenance therapy with TKIs has emerged as one of the most important strategies to reduce the risk of relapse. However, there remains considerable uncertainty regarding which patients benefit most from this approach, the optimal TKI agents, dosing strategies, and the duration of maintenance therapy. In this review, we aim to consolidate the available evidence on this topic, analyzing it in the context of the most recent clinical experiences. Full article
(This article belongs to the Special Issue Molecular Research and Pathological Mechanism of Leukemia)
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