Acute myeloid leukaemia genomics
JournalArticle (Originalarbeit in einer wissenschaftlichen Zeitschrift)
ID 4499908
Author(s) Medinger, Michael; Passweg, Jakob R.
Author(s) at UniBasel Medinger, Michael
Year 2017
Title Acute myeloid leukaemia genomics
Journal British Journal of Haematology
Volume 179
Number 4
Pages / Article-Number 530-542
Mesh terms Carcinogenesis, genetics; Epigenesis, Genetic, genetics; Genes, ras, genetics; Genomics, methods; Humans; Leukemia, Myeloid, Acute, diagnosis, drug therapy, genetics; Molecular Targeted Therapy; Mutation; Mutation Accumulation; Nuclear Proteins, genetics; Prognosis; fms-Like Tyrosine Kinase 3, genetics
Abstract Acute myeloid leukaemia (AML) is a biologically complex, molecularly and clinically heterogeneous disease. Despite major advances in understanding the genetic landscape of AML and its impact on the pathophysiology and biology of the disease, standard treatment options have not significantly changed during the past three decades. AML is characterized by multiple somatically acquired mutations that affect genes of different functional categories. Mutations in genes encoding epigenetic modifiers, such as DNMT3A, ASXL1, TET2, IDH1, and IDH2, are commonly acquired early and are present in the founding clone. By contrast, mutations involving NPM1 or signalling molecules (e.g., FLT3, RAS gene family) are typically secondary events that occur later during leukaemogenesis. This review aims to provide an overview of advances in new prognostic markers, including targetable mutations that will probably guide the development and use of novel molecularly targeted therapies.
ISSN/ISBN 1365-2141
Full Text on edoc No
Digital Object Identifier DOI 10.1111/bjh.14823
PubMed ID
Document type (ISI) Journal Article, Review

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