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Drug-Induced Modulation and Immunotherapy of Leukemia
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Drug-Induced Modulation and Immunotherapy of Leukemia

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

Deadline for manuscript submissions: 20 February 2026 | Viewed by 3439

Special Issue Editor

Dr. Helga Maria Schmetzer

E-Mail Website
Guest Editor
Med III, Department for Hematopoetic Transplantations, Klinikum Grosshadern, Ludwig Maximilian University of Munich, Marchioninistrße 15, 81377 Munich, Germany
Interests: leukemia; dendritic cells; immunotherapy
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Although most patients with acute myeloid leukemia (AML) initially respond to induction therapy, 80% of patients suffer a relapse within the following two years, as leukemic cells hidden in the body reappear. This means that strategies are needed to not only destroy leukemic cells throughout the body, but also to modulate the cellular and soluble microenvironment into an antileukemic one that initiates and stabilizes antileukemic processes.

In this Special Issue, we focus on promising pharmacological and immunological strategies to overcome resistance, initiate antileukemic processes and stabilize remissions.

The fundamental problem with AML is that there are few neoantigens. However, several new therapeutic strategies are being developed with the aim of controlling the various forms of leukemia.

While standard stem cell transplantation immunotherapy introduces healthy donor cells into a patient’s hematopoietic system, antibody-based strategies (e.g., targeting checkpoint molecules) or cellular immunotherapies are now being tested, including the use of CAR-T or CAR-NK cells, which target myeloid or lymphatic blasts more specifically.

For several years, various pharmacological strategies have been tested that intervene in the metabolism of tumor cells, e.g., by influencing cell proliferation, apoptosis or signal transduction pathways, in order to ultimately overcome drug resistance, make malignant cells more sensitive to chemotherapy or eradicate leukemic cells more specifically.

It is also being investigated how the use of interference RNA or extracellular vesicles (exosomes) could specifically eradicate leukemic cells, e.g., by transporting signaling molecules or RNA as antileukemically directed cargo. Dendritic cells are considered to be the link between adaptive and innate immunity. Engineered DCs (loaded with leukemic antigens) have proven extremely efficient in mediating cytotoxic processes in leukemia, and are the only strategy capable of generating immunological antileukemic memory. If it is possible to generate drug-induced DCs in vivo from leukemic (residual) cells in as many leukemia subtypes as possible, this route could lead to a stabilization of remission in patients with leukemia.

Dr. Helga Maria Schmetzer
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. 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

  • leukemia
  • dendritic cells
  • immunotherapy
  • immune modulation

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Published Papers (2 papers)

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Research

24 pages, 3613 KiB  
Article
Leukemia-Derived Dendritic Cells Induce Anti-Leukemic Effects Ex Vivo in AML Independently of Patients’ Clinical and Biological Features
by Lara Kristina Klauer, Hazal Aslan Rejeski, Selda Ugur, Elias Rackl, Joudi Abdulmajid, Zuzanna Fischer, Elena Pepeldjiyska, Annalena Frischhut, Nicolas Schmieder, Antje Völker, Andreas Rank, Christoph Schmid, Jörg Schmohl, Daniel Christoph Amberger and Helga Maria Schmetzer
Int. J. Mol. Sci. 2025, 26(4), 1700; https://doi.org/10.3390/ijms26041700 - 17 Feb 2025
Viewed by 1791
Abstract
New therapies are highly needed to stabilize remission in patients with acute myeloid leukemia (AML). This study investigates the value of dendritic cells derived from leukemic blasts (DCleu) to enhance anti-leukemic immunity after T-cell-enriched mixed lymphocyte cultures (MLCs). We correlated induced [...] Read more.
New therapies are highly needed to stabilize remission in patients with acute myeloid leukemia (AML). This study investigates the value of dendritic cells derived from leukemic blasts (DCleu) to enhance anti-leukemic immunity after T-cell-enriched mixed lymphocyte cultures (MLCs). We correlated induced anti-leukemic activity with patient data, including biological, clinical and prognostic factors. Additionally, we correlated the frequencies of DC/DCleu and leukemic-specific T cells with the achieved anti-leukemic activity after MLC. We show that mature DC/DCleu can be generated using the immunomodulating Kit-M, which contains granulocyte–macrophage colony-stimulating-factor (GM-CSF) and prostaglandin E1 (PGE1), without inducing blast proliferation from leukemic whole blood (WB) samples. Activated leukemia-specific immune and memory cells increased after MLC with Kit-M-pretreated WB, leading to improved blast lysis. Enhanced anti-leukemic activity positively correlated with the frequencies of generated DC/DCleu, proliferating leukemic-specific T cells and memory T cells, but not with leukemic blast counts, hemoglobin levels or platelet counts at diagnosis. No correlation was found between improved blast lysis and patients’ prognostic data, including age, gender, ELN risk groups, disease stage and response to induction chemotherapy. These findings underscore the potential of DC/DCleu to evoke robust immune responses and potential immunological memory against AML. Overall, this innovative approach could pave the way for the development of improved immunotherapeutic strategies that function in vivo. Full article
(This article belongs to the Special Issue Drug-Induced Modulation and Immunotherapy of Leukemia)
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17 pages, 4126 KiB  
Article
In Vivo Induction of Leukemia-Specific Adaptive and Innate Immune Cells by Treatment of AML-Diseased Rats and Therapy-Refractory AML Patients with Blast Modulating Response Modifiers
by Michael Atzler, Tobias Baudrexler, Daniel Christoph Amberger, Nicole Rogers, Alexander Rabe, Joerg Schmohl, Ruixiao Wang, Andreas Rank, Olga Schutti, Klaus Hirschbühl, Marit Inngjerdingen, Diana Deen, Britta Eiz-Vesper, Christoph Schmid and Helga Maria Schmetzer
Int. J. Mol. Sci. 2024, 25(24), 13469; https://doi.org/10.3390/ijms252413469 - 16 Dec 2024
Cited by 2 | Viewed by 1090
Abstract
There is a high medical need to develop new strategies for the treatment of patients with acute myeloid leukemia (AML) refractory to conventional therapy. In vitro, the combinations of the blast-modulatory response modifiers GM-CSF + Prostaglandin E1, (summarized as Kit M) have been [...] Read more.
There is a high medical need to develop new strategies for the treatment of patients with acute myeloid leukemia (AML) refractory to conventional therapy. In vitro, the combinations of the blast-modulatory response modifiers GM-CSF + Prostaglandin E1, (summarized as Kit M) have been shown to convert myeloid leukemic blasts into antigen-presenting dendritic cells of leukemic origin (DCleu) that were able to (re-)activate the innate and adaptive immune system, direct it specifically against leukemic blasts, and induce memory cells. This study aimed to investigate the immune modulatory capacity and antileukemic efficacy of Kit M in vivo. Brown Norway rats suffering from AML were treated with Kit M (twofold application). Blasts and immune cells were monitored in peripheral blood (PB) and spleen. Upon the observation of promising immune modulatory effects in the treated animals, two patients with AML refractory to multiple lines of therapy were offered treatment with Kit M on an individualized basis. Safety, as well as immunological and clinical effects, were monitored. Samples obtained from a third patient in similar clinical conditions not receiving Kit M were used as controls for immune monitoring tests. Animal experiments: Drugs were well tolerated by the treated animals. After 9 days of treatment, DCleu and memory-like T cells increased in the peripheral blood, whereas regulatory T cells, especially blasts, decreased in treated as compared to untreated control animals. Clinical courses: No severe side effects were observed. In patient 1482, PB blasts remained under the detection threshold during 27 days of treatment, thrombocytes were normalized, and (leukemia specific) immune effector cells of the adaptive and innate immune system increased up to 800-fold compared to the start of treatment. Patient 1601 responded with a 12% reduction in blasts in PB immediately after Kit M treatment. Several subtypes of (leukemia-specific) immune effector cells in PB increased up to four-fold during the 19 days of treatment. In contrast, immune-reactive cells decreased under mild chemotherapy in the PB of control patient 1511 with comparably refractory AML. Within the limitation of low numbers in both animal experiments and clinical applications, our data suggest that Kit M treatment of AML-diseased rats and patients is feasible and may induce leukemia-specific immune reactions and clinical improvement. A larger series and a prospective clinical trial will be required to confirm our observations. Beyond optimized doses and schedules of the applied compounds, the combination with other antileukemic strategies or the application of Kit M in less proliferative stages of the myeloid diseases need to be discussed. If effects are confirmed, the concept may add to the armamentarium of treatments for highly aggressive blood cancer. Full article
(This article belongs to the Special Issue Drug-Induced Modulation and Immunotherapy of Leukemia)
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