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Acute myeloid leukemia (AML) continues to pose a major hurdle in hematologic oncology, driven by its genetic complexity and tendency to resist standard therapies. Even with progress in treatment-such as high-dose chemotherapy and hematopoietic stem cell transplantation (HSCT)-outcomes remain unsatisfactory for many patients. In recent years, immunotherapy has emerged as an appealing strategy to improve survival by strengthening the body's own anti-leukemia defenses. Natural killer (NK) cells, a critical component of innate immunity, have shown strong potential for directly eliminating AML cells without prior antigen exposure. This review outlines the role of NK cells in AML immune surveillance, mechanisms by which their function becomes impaired in the disease, and the current therapeutic approaches harnessing NK cells in AML management. We also discuss key obstacles and opportunities, including strategies to boost NK cell activity, counter immune escape, and improve treatment durability. Continued investigation is essential to refine NK cell-based therapies and bring patient-tailored immunotherapeutic options into broader clinical use.

The transformation of Fanconi anemia into a hematological malignancy is consistent with the natural history of the disease. Few cases have been reported on acute myeloid leukemia, and even fewer cases involving coexistence with sickle cell anemia. Acute myeloid leukemia development is postulated to follow a multihit hypothesis where preleukaemic cells progress into leukemia through a second promotional mutation. Fever is a predominant clinical presentation, with blasts usually observed on peripheral blood smear and the immunophenotype confirmed with flow cytometry. In this case report from Tanzania, we present a case of acute myeloid leukemia with a failed induction in a patient with Sickle cell anemia andsuspected Fanconi anemia. A 6-year-old Haya boy from northern Tanzania presented to Muhimbili National Hospital with a congenital malformation of the left hand, short stature, and multiple café-au-lait spots distributed over the trunk, face, and limbs. He had experienced recurrent fever for 8 months, accompanied by headache, weight loss, and abdominal distension. Laboratory evaluation confirmed acute myeloid leukemia and sickle cell anemia with clinically suspicious features of Fanconi anemia. The patient was initiated on institutional treatment for acute myeloid leukemia. He had a failed induction and subsequently transitioned to home-based palliative care after prognostic counseling with the family. Thereafter, he had several admissions, mostly for blood product support, and eventually died 7 months post-discharge. The onset of acute myeloid leukemia in this case could be attributed to a malignant transformation from an underlying cancer predisposition syndrome. Our particular focus was on the leukemia treatment response where we observed a failed induction, prompting the need for alternative treatment approaches in this category of patients with acute myeloid leukemia in order to realize better treatment outcomes.

ABSTRACT Background Acute myeloid leukemia (AML) is a genetic disorder caused by translocations or mutations that disrupt hematopoietic function and lead to malignant transformation. In recent years, microRNA-99a and miR-100 have been found to exhibit abnormal expression in solid tumors, but their roles in AML remain unclear. This study aims to investigate the expression levels of these two microRNAs in AML and their prognostic significance. Methods We analyzed bone marrow samples from 156 newly diagnosed adult AML patients at Jiangsu Institute of Hematology (JIH) using miRNA microarray analysis. Results were validated via RT-qPCR in a non-overlapping cohort of 87 AML patients and 10 healthy controls. Results miR-99a and miR-100 expression was significantly elevated in AML compared to controls. Expression of miR-99a and miR-100 was significantly decreased in CBF-AML (core binding factor acute myeloid leukemia) patients compared to non-CBF-AML patients. In AML patients, c-KIT mutational status was associated with the downregulated expression of miR-100. Moreover, low expression of miR-99a and miR-100 is associated with lower white blood cell (WBC) counts. Increased miR-100 levels in CBF-AML (with the t(8;21) subtype included) were associated with poor overall survival (OS); notably, within CBF-AML, the t(8;21) subtype AML patients showed the same trend, where higher miR-99a and miR-100 expression correlated with adverse OS. Conclusion These findings suggest that regulated expression of miR-99a and miR-100 is common in AML and that their expression correlates with prognosis in CBF-AML.

Exploring the potential toxic mechanisms of bisphenol F exposure in acute myeloid leukemia: Insights from network toxicology, molecular docking and experimental validation.

IGF2BP3 promotes acute myeloid leukemia cell progression by regulating Semaphorin 4D stability in an m6A-dependent manner.

Exosomal miR-140-3p produced by bone marrow stromal cells affects acute myeloid leukemia cell growth and apoptosis by targeting SUZ12.

Relapsed or refractory cases of pediatric acute myeloid leukemia (AML) have poor outcomes despite advancements in chemotherapy and hematopoietic stem cell transplantation (HSCT). While a second HSCT is often a salvage option, its outcomes vary widely, and prognostic factors remain unclear. This study aimed to evaluate outcomes and identify prognostic factors in pediatric patients with AML who underwent multiple HSCTs. We conducted a retrospective, multicenter study of 49 pediatric patients with AML who underwent two or more HSCTs at 18 Japan Association of Childhood Leukemia Study institutions during 2000-2019. Clinical data on patient demographics, disease status, transplant characteristics, and complications were collected. The primary endpoint was 5-year overall survival (OS) after the second HSCT. Kaplan-Meier and multivariate Cox regression analyses were performed. Of the 49 patients, three and 46 underwent three and two HSCTs, respectively. Among these 46 patients, 5-year OS after the second HSCT was 28.3%. Achieving hematological complete remission (CR) before the second HSCT was associated with significantly better outcomes (5-year OS: 45.0% vs. 0%, p < 0.01). Severe sinusoidal obstruction syndrome (SOS) after the second HSCT was a strong predictor of transplant-related mortality (5-year OS: 0% in severe SOS cases, p < 0.01). Patient age, donor type, conditioning regimen, and acute/chronic graft-versus-host disease were not significantly associated with survival in multivariate analysis. Achieving CR before the second HSCT is critical for long-term survival, while severe SOS significantly worsens prognosis. Optimized pre-transplant strategies to reduce SOS risk are essential to improve outcomes of pediatric patients with AML who undergo multiple HSCTs.

MRC2 expression modulates metabolism in acute myeloid leukemia stem cells.

In situ generation of anti-leukemia vaccine by immunogenic dual-drug nanomedicine and polymersomal CpG nanoadjuvant.

Association between sociodemographic and clinical factors and utilization of hematopoietic cell transplant in acute myeloid leukemia from 2004 to 2020.

Acute myeloid leukemia (AML) is a highly heterogeneous hematologic malignancy, characterized by complex molecular features and mechanisms of treatment resistance, which lead to a poor prognosis and high relapse rates. The complexity of multi‑pathway interactions and the dysregulated dynamics of tumor cell death pathways may contribute to the wide range of clinical outcomes observed despite advancements in current therapies. Most current research focuses on a single form of cell death, neglecting the mechanisms of other death pathways and their synergistic interactions, which hinders the development of novel therapeutic approaches. The present review systematically integrates and compares the molecular features of key cell death modalities in AML, including autophagy, apoptosis, pyroptosis, necroptosis, ferroptosis and cuproptosis. The present review analyzes their specific triggers, signaling hubs and regulatory networks within the metabolic microenvironment, and discusses the dynamic crosstalk among these pathways. A key focus is the therapeutic potential of exploiting this crosstalk to design synergistic combination therapies. To overcome the limitations of conventional treatments and improve patient outcomes, it is essential to further investigate the transition mechanisms of various cell death modes in AML progression, drug resistance and relapse. Additionally, establishing a theoretical foundation for the development of innovative therapies that synergistically regulate multiple death pathways is crucial.

Regorafenib promotes ferroptosis in acute myeloid leukemia by upregulating NOX4.

The role of interim bone marrow assessments in acute myeloid leukemia - A systematic review and meta-analysis.

Heterogeneity of acute myeloid leukemia patients explored through single-cell and single-sample gene regulatory networks.

Multicenter retrospective analysis of the short-term efficacy and safety of the VAH regimen in the treatment of acute myeloid leukemia.

Harnessing the E3 ligase SPOP for targeted degradation of the NUP98::KDM5A fusion oncoprotein.

Design, synthesis, and biological evaluation of a bioavailable EZH2 PROTAC with a 2,8-diazaspiro[4.5]decane linker.

Spinal Cord Compression Secondary to Spinal Extradural Myeloid Sarcoma in Acute Myeloid Leukaemia: A Case Report and Literature Review

Association between childhood cancer and prenatal exposure to ambient PM2.5 and NO2: a population-based cohort study in Canada.