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CCAAT enhancer binding protein alpha (CEBPA) biallelic acute myeloid leukaemia: cooperating lesions, molecular mechanisms and clinical relevance

Publikation: Bidrag til tidsskriftReviewpeer review

DOI

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Vis graf over relationer

Recent advances in sequencing technologies have allowed for the identification of recurrent mutations in acute myeloid leukaemia (AML). The transcription factor CCAAT enhancer binding protein alpha (CEBPA) is frequently mutated in AML, and biallelic CEBPA-mutant AML was recognised as a separate disease entity in the recent World Health Organization classification. However, CEBPA mutations are co-occurring with other aberrations in AML, and together these lesions form the clonal hierarchy that comprises the leukaemia in the patient. Here, we aim to review the current understanding of co-occurring mutations in CEBPA-mutated AML and their implications for disease biology and clinical outcome. We will put emphasis on patterns of cooperation, how these lesions cooperate with CEBPA mutations and the underlying potential molecular mechanisms. Finally, we will relate this to patient outcome and future options for personalised medicine.

OriginalsprogEngelsk
TidsskriftBritish Journal of Haematology
Vol/bind190
Udgave nummer4
Sider (fra-til)495-507
ISSN0007-1048
DOI
StatusUdgivet - 1 aug. 2020

Bibliografisk note

© 2020 The Authors. British Journal of Haematology published by British Society for Haematology and John Wiley & Sons Ltd.

ID: 59691377