Acute Myeloid Leukemia in Adults

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

Deadline for manuscript submissions: 30 April 2025 | Viewed by 2048

Special Issue Editor


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Guest Editor
Department of Oncology, Johns Hopkins University, Baltimore, MD 21218, USA
Interests: acute myeloid leukemia; myelodysplastic syndrome; myeloproliferative neoplasms; inflammatory signaling; targeted therapies
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Special Issue Information

Dear Colleagues,

Acute myeloid leukemia is the most common type of leukemia in adults and is caused by the acquisition of somatic mutations in hematopoietic stem and progenitor cells mediating their transformation to malignant cells that dominate the bone marrow. Despite the extensive investigation of the molecular biology of AML and the introduction of numerous novel agents and combinational approaches for the treatment of this disease, the outcomes of AML patients and particularly older individuals and those with antecedent myeloid neoplasms remain poor overall. A deeper and better understanding of the molecular pathways mediating the growth and resistance of AML blasts is required to introduce new therapies especially for resistant and relapsed forms of AML. This can be achieved by collaborative approaches in AML research and better comprehension of the resistant patterns to the current therapeutic approaches.

This Special Issue discusses the recent discoveries related to the biology of AML, the current therapeutic landscape and possible mechanisms of resistance to the current treatments. This covers studies at the basic and translational level but also clinical studies with an emphasis on studies focusing on the characteristics of relapsed and treatment-resistant AMLs.

Dr. Theodoros Karantanos
Guest Editor

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Keywords

  • acute myeloid leukemia
  • molecular biology
  • treatment landscape
  • resistance mechanisms

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Published Papers (2 papers)

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Research

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12 pages, 843 KiB  
Article
Patients with TP53-Mutated Acute Myeloid Leukemia Receiving Intensive Induction Therapy Have Superior Outcomes Due to a Higher Rate of Salvage Therapy: A Single Institution, Retrospective Study
by Nuttavut Sumransub, Gabriel K. Steinwand, Keith Cordner, Yoonkyu Lee, Qing Cao, Jeremy Allred, Veronika Bachanova, Mark Juckett, Craig Eckfeldt, Joseph E. Maakaron, Sean I. Tracy, Vidhyalakshmi Ramesh, Andrew C. Nelson, Sophia Yohe and Zohar Sachs
Cancers 2024, 16(16), 2784; https://doi.org/10.3390/cancers16162784 - 7 Aug 2024
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Abstract
Background: TP53 mutations (TP53m) define the most treatment-refractory acute myeloid leukemia (AML) subtype. Optimal treatment approaches have not been established in this setting. We reviewed our institutional experience to identify therapy sequencing, treatment response, and survival patterns in these patients. Methods: [...] Read more.
Background: TP53 mutations (TP53m) define the most treatment-refractory acute myeloid leukemia (AML) subtype. Optimal treatment approaches have not been established in this setting. We reviewed our institutional experience to identify therapy sequencing, treatment response, and survival patterns in these patients. Methods: This study was a single-center, retrospective cohort analysis. Results: Our cohort includes 86 TP53m and 337 TP53 wild-type (TP53wt) adult AML patients. TP53m AML patients presented with lower bone marrow and peripheral blasts; none presented with hyperleukocytosis. Patients who received intensive treatment up front demonstrated superior overall survival (OS) over those receiving first-line non-intensive therapy (2-year OS 22% versus 7%; p = 0.02). However, the complete remission (CR) rates among the first-line intensive and non-intensive therapy groups were comparable (21.9% and 29.4%, respectively, p = 0.49). The improved OS is therefore attributed to superior cumulative CR in the intensive group. First-line intensively treated patients were more likely to receive and respond to salvage, leading to a cumulative CR rate of 65.7% (versus 29.4%, p = 0.003). Achieving CR at any point is strongly associated with superior survival outcomes with 2-year OS of 31% versus 0% for those not achieving CR ever (p < 0.01). Conclusions: We find that TP53m AML rarely presents with oncological emergencies, suggesting that clinical trial enrollment is feasible in this group. Additionally, in our cohort, intensive induction therapies lead to superior survival outcomes attributed to successful salvage therapy. These data suggest that strategic therapy sequencing and salvage therapy may be important in optimizing outcomes for TP53m AML patients. Full article
(This article belongs to the Special Issue Acute Myeloid Leukemia in Adults)
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Review

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22 pages, 350 KiB  
Review
An Overview of Myeloid Blast-Phase Chronic Myeloid Leukemia
by Gulsum E. Pamuk and Lori A. Ehrlich
Cancers 2024, 16(21), 3615; https://doi.org/10.3390/cancers16213615 - 26 Oct 2024
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Abstract
Myeloid blast-phase chronic myeloid leukemia (MBP-CML) is a rare disease with a dismal prognosis. It is twice as common as lymphoid blast-phase CML, and its prognosis is poorer. Despite the success with tyrosine kinase inhibitors in the treatment of chronic-phase CML, the same [...] Read more.
Myeloid blast-phase chronic myeloid leukemia (MBP-CML) is a rare disease with a dismal prognosis. It is twice as common as lymphoid blast-phase CML, and its prognosis is poorer. Despite the success with tyrosine kinase inhibitors in the treatment of chronic-phase CML, the same does not hold true for MBP-CML. In addition to the Philadelphia chromosome, other chromosomal and molecular changes characterize rapid progression. Although some progress in elucidating the biology of MBP-CML has been made, there is need to discover more in order to develop more satisfactory treatment options. Currently, most common treatment options include tyrosine kinase inhibitors (TKIs) as monotherapy or in combination with acute myeloid leukemia-based intensive chemotherapy regimens. Some patients may develop resistance to TKIs via BCR-ABL1-dependent or BCR-ABL1-independent mechanisms. In this paper, we provide an overview of the biology of MBP-CML, the current treatment approaches, and mechanisms of resistance to TKIs. In order to improve treatment responses in these patients, more emphasis should be placed on understanding the biology of myeloid blastic transformation in CML and mechanisms of resistance to TKIs. Although patient numbers are small, randomized clinical trials should be considered. Full article
(This article belongs to the Special Issue Acute Myeloid Leukemia in Adults)
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