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The Clinical Trials and Management of Acute Myeloid Leukemia: 2nd Edition

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Clinical Research of Cancer".

Deadline for manuscript submissions: 7 August 2026 | Viewed by 3961

Special Issue Editor

Dr. Margaret T. Kasner

E-Mail Website
Guest Editor
1. Department of Medical Oncology, Thomas Jefferson University, Philadelphia, PA 19107, USA
2. Sidney Kimmel Cancer Center Protocol, Thomas Jefferson University, Philadelphia, PA 19107, USA
Interests: acute myeloid leukemia; clinical trials; translational research; targeted therapies
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Acute myeloid leukemia (AML) has always posed a therapeutic challenge due to its molecular and cytogenetic complexity. For the first time in decades, advances in treatment through the approval of novel agents and combinations have been made. Long-term disease-free survival had plateaued at less than 30% at 5 years; however, in the last few years, a small, but steady increase has been seen thanks to the advancements in novel therapies. The exploration of novel mechanisms and immune system enhancement as therapeutic targets for the treatment of AML continues.

This Special Issue will highlight the clinical trials and advances in supportive care for acute myeloid leukemia. 

You are welcome to read the publications in the 1st edition at The Clinical Trials and Management of Acute Myeloid Leukemia (https://www.mdpi.com/journal/cancers/special_issues/ZRWMJ0J3Q4).

Dr. Margaret T. Kasner
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 communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

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. Cancers 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 2900 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
  • clinical trials
  • translational research
  • targeted therapies
  • novel agents

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Published Papers (2 papers)

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Review

23 pages, 2806 KB  
Review
Acute Myeloid Leukemias with Alterations of Lysine Methyltransferase 2A (KMT2A): Recent Therapeutic Developments
by Ugo Testa, Elvira Pelosi and Germana Castelli
Cancers 2026, 18(9), 1341; https://doi.org/10.3390/cancers18091341 - 23 Apr 2026
Viewed by 615
Abstract
Background: Chromosomal rearrangements involving lysine methyltransferase 2A (KMT2A) define a genetically distinct subset of acute myeloid leukemia (AML) in 10% of cases in adult patients; the frequency of KMT2A-r is higher in pediatric AML. Translocations involving the KMT2A locus at chromosome 11q23 [...] Read more.
Background: Chromosomal rearrangements involving lysine methyltransferase 2A (KMT2A) define a genetically distinct subset of acute myeloid leukemia (AML) in 10% of cases in adult patients; the frequency of KMT2A-r is higher in pediatric AML. Translocations involving the KMT2A locus at chromosome 11q23 result in the formation of a chimeric oncogene partner, where the N-terminal part of KMT2A is fused to a variety of translocation partners. The leukemogenic activity of KMT2A-fusion partners is related to their capacity to hyperactivate the expression of HOX-A and MEIS1 target genes, which stimulate the proliferation of hematopoietic stem cells. The oncogenic activity of KMT2A fusion proteins requires the binding with Menin, and this interaction can be targeted pharmacologically by small molecules acting as potent and selective Menin inhibitors. Methods: A search of the literature showed a marked development of experimental studies exploring the molecular pathogenesis of AML with KMT2A-r and of clinical studies evaluating new induction intensive treatments and the development of a targeted therapy based on Menin inhibitors. Results and Conclusions: In the present review article, we summarize our current understanding of the biology of KMT2A-r in AML development and the recent consistent progress made in the treatment of KMT2A-r AML through new chemotherapy regimens and targeted therapy using Menin inhibitors. However, the prognosis of older KMT2A-r AML patients remains poor and could be improved by drug combination studies including Menin inhibitors. Many encouraging observations derived from ongoing clinical trials with Menin inhibitors need to be confirmed through randomized clinical trials. Full article
(This article belongs to the Special Issue The Clinical Trials and Management of Acute Myeloid Leukemia: 2nd Edition)
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17 pages, 831 KB  
Review
Management of Acute Myeloid Leukemia: A Review
by Chetan Jeurkar, Lana King, David Baek, Lindsay Wilde, Gina Keiffer and Margaret Kasner
Cancers 2026, 18(4), 659; https://doi.org/10.3390/cancers18040659 - 18 Feb 2026
Cited by 3 | Viewed by 3005
Abstract
Background/Objectives: Acute myeloid leukemia (AML) is a heterogeneous hematologic malignancy with historically poor outcomes, particularly among older adults and patients harboring high-risk molecular features. Advances in genomic profiling have enabled the development of targeted therapies, reshaping treatment algorithms beyond conventional cytarabine-anthracycline induction and [...] Read more.
Background/Objectives: Acute myeloid leukemia (AML) is a heterogeneous hematologic malignancy with historically poor outcomes, particularly among older adults and patients harboring high-risk molecular features. Advances in genomic profiling have enabled the development of targeted therapies, reshaping treatment algorithms beyond conventional cytarabine-anthracycline induction and hypomethylating agent-based regimens. This review summarizes current evidence and emerging therapeutic strategies across four evolving areas: menin inhibition, FLT3 inhibition, IDH inhibition and treatment approaches for TP53-mutated AML. Methods: We reviewed published clinical trials, preclinical studies, and ongoing clinical trials evaluating targeted therapies in AML. Emphasis was placed on agents with regulatory approval or substantial clinical development, including menin inhibitors, FLT3 inhibitors, IDH inhibitors and novel therapies directed at TP53-mutated disease. Mechanistic data, response rates, survival outcomes, and resistance patterns were analyzed to provide an updated overview of therapeutic progress. Results: Menin inhibitors have demonstrated significant activity in NPM1-mutated and KMT2A-rearranged AML, with agents such as revumenib and ziftomenib producing meaningful remission rates and ongoing studies exploring combination strategies to mitigate resistance. FLT3 inhibitors, including midostaurin, gilteritinib, and quizartinib, have improved survival in FLT3-mutated AML, while emerging evidence supports potential benefit in selected FLT3–wild-type disease based on FLT3-like gene expression signatures. IDH inhibitors, namely ivosidenib and enasidenib, have provided increased efficacy in AML patients carrying these mutations. Questions still remain regarding their efficacy in contrast to venetoclax which has been shown to be particularly effective against this population. In contrast, TP53-mutated AML remains a therapeutic challenge: although hypomethylating-agent/venetoclax-based regimens yield improved initial responses, remissions are generally short-lived and overall survival remains poor. Early-phase therapies, including p53 reactivators and multi-kinase inhibitors, show preclinical promise but lack definitive clinical efficacy to date. Conclusions: Targeted therapies have improved outcomes in molecularly defined subsets of AML, with menin, IDH and FLT3 inhibitors representing major advances. However, TP53-mutated AML continues to carry a dismal prognosis, underscoring the need for more effective therapeutic strategies. Continued biomarker-driven research, novel drug combinations, and mechanistic insights will be essential to further refine AML treatment and improve long-term survival across disease subsets. Full article
(This article belongs to the Special Issue The Clinical Trials and Management of Acute Myeloid Leukemia: 2nd Edition)
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