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Cells
Special Issues
Cellular Mechanisms and Targeted Therapy of Acute Myeloid Leukemia
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Cellular Mechanisms and Targeted Therapy of Acute Myeloid Leukemia

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Pathology".

Deadline for manuscript submissions: 30 September 2025 | Viewed by 639

Special Issue Editor

Prof. Dr. Mookon Song

E-Mail Website
Guest Editor
Department of Hematology, Hanyang University Hanmaeum Changwon Hospital, Changwon 04763, Republic of Korea
Interests: diffuse large B-cell lymphoma; B-cell lymphoma; leukemia; non-Hodgkin lymphoma; plasmacytoma
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Acute Myeloid Leukemia (AML) is a heterogeneous hematologic malignancy characterized by the uncontrolled proliferation of myeloid progenitor cells. This Special Issue, ‘Cellular Mechanisms and Targeted Therapy of Acute Myeloid Leukemia’, aims to provide an in-depth exploration of the cellular underpinnings of AML and advancements in targeted therapies. The collection will delve into the intricate molecular pathways driving AML, including dysregulated signaling networks, epigenetic modifications, and metabolic reprogramming. We hope to explore the molecular and cellular basis of AML, providing insights into the complex interactions between leukemic cells and their microenvironment.

Moreover, this Special Issue will delve into the development and clinical application of targeted therapies, including small molecule inhibitors, monoclonal antibodies, and immunotherapies. We wish to focus on how these therapies can be tailored to target specific cellular vulnerabilities in AML, thereby enhancing efficacy and reducing toxicity.

In this Special Issue, we aim to solicit cutting-edge research that delves into the molecular mechanisms driving AML development and progression. Both original research papers and comprehensive review papers are welcome.

Prof. Dr. Mookon Song
Guest Editor

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. Cells is an international peer-reviewed open access semimonthly 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

  • Acute Myeloid Leukemia (AML)
  • molecular targets
  • gene therapy
  • drug resistance
  • targeted therapy
  • leukemia stem cells
  • oncogenic mutations
  • apoptosis
  • cell cycle regulation

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Published Papers (1 paper)

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Research

19 pages, 2523 KiB  
Article
Immunopathological Dysregulation in Acute Myeloid Leukemia: The Impact of T-bet, RORγt, and FOXP3 on Disease Dynamics
by Amira M. Mohamed Mohy El-Din, Buthayna Ahmad AlShaarawy, Eman Zaghloul Kandeel, Dalia Mahmoud AlDewi, Lobna Abdel Azeem Refaat, Borros Arneth and Hussein Sabit
Cells 2025, 14(7), 528; https://doi.org/10.3390/cells14070528 - 1 Apr 2025
Viewed by 488
Abstract
The etiology of acute myeloid leukemia (AML) is complex, including genetic and environmental abnormalities. The immune system anomalies play an essential role in the process of leukemogenesis. However, the immunopathological factors, including abnormal T helper (Th) subsets, contributing to the initiation and progression [...] Read more.
The etiology of acute myeloid leukemia (AML) is complex, including genetic and environmental abnormalities. The immune system anomalies play an essential role in the process of leukemogenesis. However, the immunopathological factors, including abnormal T helper (Th) subsets, contributing to the initiation and progression of this neoplasm, require further investigation. Considering the previously mentioned data, we decided to study the expression pattern of transcription factors T-bet, Foxp3, and RORγt that regulate Th1, Treg, and Th17, respectively, in acute myeloid leukemia with correlation to clinical and other investigation data and treatment outcomes. This study was conducted on 80 newly diagnosed patients with AML recruited from the National Cancer Institute, Cairo University, and 25 healthy control subjects. The AML patient cohort consisted of 30 females (37.5%) and 50 males (62.5%), ranging from 18 to 74 years old. The control group was 8 females (32%) and 17 males (68%), with ages ranging from 23 to 40 years old. Samples were provided from the bone marrow of donor cases for allogeneic bone marrow transplantation. The diagnosis of acute myeloid leukemia was based on morphologic and cytochemical evaluation, immunophenotyping, and complementary cytogenetics according to WHO criteria. Upshift from the normal T-bet intensity of power (MFI), RORγt+ CD4+ T lymphocyte frequency (%) with downshift from the normal FOXP3 intensity of power (MFI), may suggest a state of inflammation. In contrast, an upshift from the normal FOXP3+ CD4+ T lymphocyte frequency (%) may reflect a state of immunosuppression in the bone marrow microenvironment of AML. Combined, they constitute a sophisticated scenario of immunological disorder in AML. Co-expression of T-bet and RORγt transcription factors in CD4+ T lymphocytes in both normal and AML groups may suggest CD4+ T lymphocyte plasticity. Full article
(This article belongs to the Special Issue Cellular Mechanisms and Targeted Therapy of Acute Myeloid Leukemia)
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