Acute myeloid leukaemia

  title={Acute myeloid leukaemia},
  author={Asim Ijaz Khwaja and Magnus Bjorkholm and Rosemary E. Gale and Ross L. Levine and Craig T. Jordan and Gerhard Ehninger and Clara Derber Bloomfield and Elihu H Estey and Alan K Burnett and Jan J Cornelissen and David A. Scheinberg and Didier Bouscary and David C. Linch},
  journal={Nature Reviews Disease Primers},
Acute myeloid leukaemia (AML) is a disorder characterized by a clonal proliferation derived from primitive haematopoietic stem cells or progenitor cells. Abnormal differentiation of myeloid cells results in a high level of immature malignant cells and fewer differentiated red blood cells, platelets and white blood cells. The disease occurs at all ages, but predominantly occurs in older people (>60 years of age). AML typically presents with a rapid onset of symptoms that are attributable to bone… 

Patient with Chronic Myeloid Leukemia: A Case Study

The case of 58-year-old Asian lady experiencing generalized body weakness, pallor, left upper abdominal pain and sudden weight loss of 5 kg within three weeks and a high blood pressure is reported, indicating a myeloproliferative disorder.

Dysregulated haematopoietic stem cell behaviour in myeloid leukaemogenesis

Overall, this Review links the cellular and molecular mechanisms regulating HSC behaviour with the functional dysregulation of these mechanisms in myeloid leukaemia and discusses opportunities for targeting LSC-specific mechanisms for the prevention or cure of malignant diseases.

Clonal evolution of pre-leukemic hematopoietic stem cells precedes human acute myeloid leukemia.

  • R. Majeti
  • Biology
    Best practice & research. Clinical haematology
  • 2014

Preleukemic mutations in human acute myeloid leukemia affect epigenetic regulators and persist in remission

The identification of patterns of mutation acquisition in human AML supports a model in which mutations in “landscaping” genes, involved in global chromatin changes such as DNA methylation, histone modification, and chromatin looping, occur early in the evolution of AML, whereas mutations in "proliferative" genes occur late.

Acute Myeloid Leukemia—Genetic Alterations and Their Clinical Prognosis

This review is focused on describing the most important molecular markers with implications for clinical practice: cytogenetic markers, which are used to stratify patients in three risk categories: favorable, intermediate and unfavorable.

Reduced hematopoietic stem cell frequency predicts outcome in acute myeloid leukemia

Data suggest that decreasing numbers of hematopoietic stem cells indicate leukemic stem cell persistence and the emergence ofLeukemic relapse, and developed new mathematical models suggest that the mechanism leading to decreases in he matopoetic stem cell frequencies before leukedmic relapse must be based on expansion of leukeMic stem cells with high niche affinity and the ability to dislodge hematoietIC stem cells.

Microarray-based genomic analysis identifies germline and somatic copy number variants and loss of heterozygosity in acute myeloid leukaemia

A combined platform of CGH+SNP provides invaluable insights into the elucidation of large spectrum of genomic aberrations in AML which may have prognostic implications.

Microenvironmental remodeling as a parameter and prognostic factor of heterogeneous leukemogenesis in acute myelogenous leukemia.

It is demonstrated that remodeling of mesenchymal niche by leukemia cells is an intrinsic self-reinforcing process of leukemogenesis that can be a parameter for the heterogeneity in the clinical course of leukemia and hence serve as a potential prognostic factor.

Proteomic approaches for untangling pharmacological targets in acute myelogenous leukemia

Acute myelogenous leukemia (AML) is a highly malignant disease of the blood and bone marrow [1]. A block in differentiation in normal hematopoiesis leads to accumulation of immature cells that

Molecular and genomic landscapes in secondary & therapy related acute myeloid leukemia.

Despite significant advances in knowing the genetic aspect of secondary and therapy-related AML, its influence on the disease's pathophysiology, standard treatment prospects have not significantly evolved during the past three decades, according to this review.



Advances in Understanding the Biology and Genetics of Acute Myelocytic Leukemia

  • S. B. Mckenzie
  • Medicine, Biology
    American Society for Clinical Laboratory Science
  • 2005
The most recent understanding and research of the cellular origin of AML and associated common genetic mutations that fuel the neoplastic process are discussed and how these advances have impacted the classification, selection of therapy, and definition of complete remission in AML are discussed.

Acute myeloid leukemia ontogeny is defined by distinct somatic mutations.

Analysis of serial samples from individual patients revealed that the presence of a mutation in SRSF2, SF3B1, U2AF1, ZRSR2, ASXL1, EZH2, BCOR, or STAG2 was >95% specific for the diagnosis of s-AML and highlights a subset of patients with worse clinical outcomes, including a lower complete remission rate, more frequent reinduction, and decreased event-free survival.

Pathogenesis and management of acute myeloid leukemia that has evolved from a myeloproliferative neoplasm

Recent advances in the understanding of the molecular events that contribute to the development of leukemic transformation will need to be utilized in order to produce rational therapeutic approaches for this largely fatal disease.

The epidemiology of acute promyelocytic leukaemia.

  • D. Douer
  • Biology, Medicine
    Best practice & research. Clinical haematology
  • 2003

How I treat hyperleukocytosis in acute myeloid leukemia.

Whereas initial high blood counts and high lactate dehydrogenase as an indicator for high proliferation are part of prognostic scores guiding risk-adapted consolidation strategies, HL at initial diagnosis must be considered a hematologic emergency and requires rapid action of the admitting physician in order to prevent early death.

Human acute myeloid leukemia is organized as a hierarchy that originates from a primitive hematopoietic cell

It is demonstrated that the cell capable of initiating human AML in non-obese diabetic mice with severe combined immunodeficiency disease (NOD/SCID mice) — termed the SCID leukemia-initiating cell, or SL-IC — possesses the differentiate and proliferative capacities and the potential for self-renewal expected of a leukemic stem cell.

Chromosomal rearrangements in childhood acute myeloid leukemia and myelodysplastic syndromes.

Cytogenetic and molecular analyses may allow clinicians to more appropriately direct types of treatment and sometimes predict clinical outcome and thus also serve as prognostic parameters, which may affect the therapeutic decision.

Human acute myelogenous leukemia stem cells are rare and heterogeneous when assayed in NOD/SCID/IL2Rγc-deficient mice.

It is confirmed that human leukemic stem cells, functionally defined by us as SCID leukemia-initiating cells (SL-ICs), are rare in acute myelogenous leukemia (AML) and suggested a plasticity of the cancer stem cell phenotype that has not been previously described.

Cytogenetic heterogeneity negatively impacts outcomes in patients with acute myeloid leukemia

Clonal heterogeneity was associated with decreased response rates and inferior event-free, relapse-free and overall survival, and was confirmed as an independent predictor of poor prognosis in multivariable analysis and subgroup analysis showed that clonal heterogeneity adds prognostic information particularly in the unfavorable karyotype group.