ID

44950

Descrizione

The implementation of targeted therapies for acute myeloid leukemia has been challenged by complex mutational patterns within and across patients as well as a dearth of pharmacologic agents for most mutational events. Here, we report initial findings from the Beat AML program on a cohort of 672 tumor specimens collected from 562 patients. We assessed these specimens using whole exome sequencing, RNA-sequencing, and ex vivo drug sensitivity analyses. Our data reveal novel mutational events not previously detected in AML. We show association of drug response with mutational status, including instances of drug sensitivity that are specific to combinatorial mutational events. Integration with RNA-sequencing also revealed gene expression signatures, which predict a role of specific gene networks in drug response. Collectively, this report offers a dataset, accessible by the Beat AML data viewer, that can be leveraged to address clinical, genomic, transcriptomic, and functional inquiries into the biology of AML. NCT 01728402 https://www.ncbi.nlm.nih.gov/projects/gap/cgi-bin/study.cgi?study_id=phs001657.v1.p1

collegamento

https://www.ncbi.nlm.nih.gov/projects/gap/cgi-bin/study.cgi?study_id=phs001657.v1.p1

Keywords

versioni (8)

1. 27/04/22 27/04/22 - Martin Dugas
2. 27/04/22 27/04/22 - Martin Dugas
3. 27/04/22 27/04/22 - Martin Dugas
4. 27/04/22 27/04/22 - Martin Dugas
5. 12/05/22 12/05/22 - Martin Dugas
6. 12/05/22 12/05/22 - Martin Dugas
7. 12/10/22 12/10/22 - Adrian Schulz
8. 22/06/23 22/06/23 - Dr. Christian Niklas

Titolare del copyright

Jeffrey W. Tyner, PhD. Oregon Health and Science University, Knight Cancer Institute, Portland, OR, USA

Caricato su

12 maggio 2022

DOI

Per favore, per richiedere un accesso.

Licenza