Literature DB >> 17019734

Acute myeloid leukemia: epidemiology and etiology.

Barbara Deschler1, Michael Lübbert.   

Abstract

Acute myeloid leukemias (AMLs) are infrequent, yet highly malignant neoplasms responsible for a large number of cancer-related deaths. The incidence has been near stable over the last years. It continuously shows 2 peaks in occurrence in early childhood and later adulthood. With an incidence of 3.7 per 100,000 persons and an age-dependent mortality of 2.7 to nearly 18 per 100,000 persons, there is a rising awareness in the Western world of AML's special attributes resulting from an ever-aging population. To objectively describe epidemiologic data on this patient population, recent publications were evaluated to make transparent the current trends and facts. A review of the literature is presented, reflecting highlights of current research with respect to AML etiology. To estimate outcome and discuss informed treatment decisions with AML patients of different age groups and different biologic risk categories, it is mandatory to consider that the outcome results reported in clinical trials were until now heavily biased toward younger patients, whereas the overall dismal prognosis documented in population-based studies most likely reflects the exclusion of older patients from aggressive treatment. The etiology for most cases of AML is unclear, but a growing knowledge concerning leukemogenenic agents within chemotherapy regimens for other malignancies is already available. This includes specific associations of the most frequent balanced translocations in AML, including the "good-risk" abnormalities comprised by the core binding factor leukemias (i.e., AML with the translocation (8;21) and inversion of chromosome 16, and acute promyelocytic leukemia with the translocation (15;17)). In contrast to these genetic alterations, epigenetic lesions, e.g., promoter silencing by hypermethylation of the p15/INK4b and other genes, are increasingly recognized as important in the pathogenesis of AML. (c) 2006 American Cancer Society.

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Year:  2006        PMID: 17019734     DOI: 10.1002/cncr.22233

Source DB:  PubMed          Journal:  Cancer        ISSN: 0008-543X            Impact factor:   6.860


  187 in total

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4.  Design of Hydrazide-Bearing HDACIs Based on Panobinostat and Their p53 and FLT3-ITD Dependency in Antileukemia Activity.

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5.  Acute liver failure due to liver parenchymal infiltration with acute myelogenous leukaemia in a patient with myelodysplastic syndrome.

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6.  Venetoclax and BCR-ABL Tyrosine Kinase Inhibitor Combinations: Outcome in Patients with Philadelphia Chromosome-Positive Advanced Myeloid Leukemias.

Authors:  Abhishek Maiti; Miguel J Franquiz; Farhad Ravandi; Jorge E Cortes; Elias J Jabbour; Koji Sasaki; Kayleigh Marx; Naval G Daver; Tapan M Kadia; Marina Y Konopleva; Lucia Masarova; Gautam Borthakur; Courtney D DiNardo; Kiran Naqvi; Sherry Pierce; Hagop M Kantarjian; Nicholas J Short
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7.  Human acute myeloid leukemia cells express Neurokinin-1 receptor, which is involved in the antileukemic effect of Neurokinin-1 receptor antagonists.

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Journal:  Invest New Drugs       Date:  2018-05-02       Impact factor: 3.850

8.  Alleviating the progression of acute myeloid leukemia (AML) by sulforaphane through controlling miR-155 levels.

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9.  Antitumor action of CDK inhibitor LS-007 as a single agent and in combination with ABT-199 against human acute leukemia cells.

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Journal:  Acta Pharmacol Sin       Date:  2016-08-29       Impact factor: 6.150

10.  Are incidence rates of adult leukemia in the United States significantly associated with birth cohort?

Authors:  Philip S Rosenberg; Katherine L Wilson; William F Anderson
Journal:  Cancer Epidemiol Biomarkers Prev       Date:  2012-10-12       Impact factor: 4.254

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