Clonal evolution patterns in acute myeloid leukemia with NPM1 mutation View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2019-05-02

AUTHORS

Sibylle Cocciardi, Anna Dolnik, Silke Kapp-Schwoerer, Frank G. Rücker, Susanne Lux, Tamara J. Blätte, Sabrina Skambraks, Jan Krönke, Florian H. Heidel, Tina M. Schnöder, Andrea Corbacioglu, Verena I. Gaidzik, Peter Paschka, Veronica Teleanu, Gudrun Göhring, Felicitas Thol, Michael Heuser, Arnold Ganser, Daniela Weber, Eric Sträng, Hans A. Kestler, Hartmut Döhner, Lars Bullinger, Konstanze Döhner

ABSTRACT

Mutations in the nucleophosmin 1 (NPM1) gene are considered founder mutations in the pathogenesis of acute myeloid leukemia (AML). To characterize the genetic composition of NPM1 mutated (NPM1mut) AML, we assess mutation status of five recurrently mutated oncogenes in 129 paired NPM1mut samples obtained at diagnosis and relapse. We find a substantial shift in the genetic pattern from diagnosis to relapse including NPM1mut loss (n = 11). To better understand these NPM1mut loss cases, we perform whole exome sequencing (WES) and RNA-Seq. At the time of relapse, NPM1mut loss patients (pts) feature distinct mutational patterns that share almost no somatic mutation with the corresponding diagnosis sample and impact different signaling pathways. In contrast, profiles of pts with persistent NPM1mut are reflected by a high overlap of mutations between diagnosis and relapse. Our findings confirm that relapse often originates from persistent leukemic clones, though NPM1mut loss cases suggest a second “de novo” or treatment-associated AML (tAML) as alternative cause of relapse. More... »

PAGES

2031

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/s41467-019-09745-2

DOI

http://dx.doi.org/10.1038/s41467-019-09745-2

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1113874971

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/31048683


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