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Novel Agents and Mechanisms in Acute Leukemias 2.0
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Novel Agents and Mechanisms in Acute Leukemias 2.0

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: closed (31 July 2023) | Viewed by 3072

Special Issue Editors

Dr. Giovanni Martinelli

E-Mail Website
Guest Editor
Department of Hematology and Sciences Oncology, Institute of Haematology "L. and A. Seràgnoli" S. Orsola, University of Bologna, 40126 Bologna, Italy
Interests: leukemias; lymphomas; acute leukemia; chronic myeloid leukemia
Special Issues, Collections and Topics in MDPI journals
Dr. Claudio Cerchione

E-Mail Website
Guest Editor
Istituto Scientifico Romagnolo per lo Studio e la Cura dei Tumori, 47014 Meldola, Italy
Interests: acute lymphoblastic leukemia; acute myeloid leukemia; myelodysplastic syndromes; multiple myeloma and MGUS; non-Hodgkin and Hodgkin lymphoma
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The last 4–5 years have ushered in a new era in acute myeloid leukemia therapy, with the advent and approval of multiple targeted therapies. Additionally, an improved understanding of the immune system in patients with hematologic malignancies has resulted in major progress in the development of immune therapies for the treatment of patients with AML, including monoclonal antibodies with or without conjugated toxins (bacterial or chemical), bispecific T-cell engagers and DART antibodies, immune-checkpoint-based therapies, and CAR-T cell approaches.

At the same time, there is an increasing understanding of AML tumor biology, creating the rationale for new combinations of drugs and new therapy development.

The numerous ongoing trials evaluating these novel therapies, with well-designed correlative interrogations of the immune system in patients treated in such trials, will further enhance our understanding of immune therapies as single-agent and combination approaches for the treatment of AML.

This Special Issue aims to focus on novel agents and their combinations. Focus will be placed on the efficacy of novel therapeutics and promising combination approaches to further improve outcomes in the treatment of patients with AML. We welcome the submission of original research articles and reviews.

Dr. Giovanni Martinelli
Dr. Claudio Cerchione
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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
  • novel agents
  • target therapy

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Published Papers (1 paper)

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Research

18 pages, 5846 KiB  
Article
Targeting EZH2 Promotes Chemosensitivity of BCL-2 Inhibitor through Suppressing PI3K and c-KIT Signaling in Acute Myeloid Leukemia
by Chan Yang, Yan Gu, Zheng Ge and Chunhua Song
Int. J. Mol. Sci. 2022, 23(19), 11393; https://doi.org/10.3390/ijms231911393 - 27 Sep 2022
Cited by 4 | Viewed by 2500
Abstract
Acute myeloid leukemia (AML) is one of the most common hematological malignancies with high heterogeneity, characterized by a differentiating block at the early progenitor stage. The selective BCL-2 inhibitor, Venetoclax (Ven), has shown exciting clinical results in a certain group of AML patients. [...] Read more.
Acute myeloid leukemia (AML) is one of the most common hematological malignancies with high heterogeneity, characterized by a differentiating block at the early progenitor stage. The selective BCL-2 inhibitor, Venetoclax (Ven), has shown exciting clinical results in a certain group of AML patients. However, Ven alone is insufficient to reach an enduringly complete response, which leads to the concern of Ven resistance. Alternative combined therapies with Ven are demanded in AML. Here, we reported the synergistic effect and molecular mechanism of the enhancer of zeste homolog 2 (EZH2) inhibitor DZNeP with Ven in AML cells. Results showed that the combination of DZNeP with Ven significantly induces cell proliferation arrest compared to single-drug control in AML cells and primary samples, and CalcuSyn analysis showed their significant synergy. The combination also significantly promotes apoptosis and increases the expression of pro-apoptotic proteins. The whole transcriptome analysis showed that phosphoinositide-3-kinase-interacting protein1 (PIK3IP1), the PI3K/AKT/mTOR signaling suppressor, is upregulated upon DZNeP treatment. Moreover, EZH2 is upregulated but PIK3IP1 is downregulated in 88 newly diagnosed AML cohorts compared to 70 healthy controls, and a higher expression of EZH2 is associated with poor outcomes in AML patients. Particularly, the combination of DZNeP with Ven dramatically eliminated CD117 (c-KIT) (+) AML blasts, suggesting the effect of the combination on tumor stem cells. In summary, our data indicated that DZNeP increases the sensitivity of Ven in AML by affecting PI3K and c-KIT signaling in AML. Our results also suggested that the therapeutic targeting of both EZH2 and BCL-2 provides a novel potential combined strategy against AML. Full article
(This article belongs to the Special Issue Novel Agents and Mechanisms in Acute Leukemias 2.0)
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