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Mutations in RAS pathway induce synthetic lethality of MEK inhibition with mitochondrial oxidative metabolism in acute myeloid leukemia

ABSTRACT: Bulk RNAseq of primary AML samples at diagnosis

INSTRUMENT(S): Illumina HiSeq 4000

ORGANISM(S): Homo sapiens

SUBMITTER: Jerome Tamburini 

PROVIDER: E-MTAB-10048 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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RAS activation induces synthetic lethality of MEK inhibition with mitochondrial oxidative metabolism in acute myeloid leukemia.

Decroocq Justine J   Birsen Rudy R   Montersino Camille C   Chaskar Prasad P   Mano Jordi J   Poulain Laury L   Friedrich Chloe C   Alary Anne-Sophie AS   Guermouche Helene H   Sahal Ambrine A   Fouquet Guillemette G   Gotanègre Mathilde M   Simonetta Federico F   Mouche Sarah S   Gestraud Pierre P   Lescure Auriane A   Del Nery Elaine E   Bosc Claudie C   Grenier Adrien A   Mazed Fetta F   Mondesir Johanna J   Chapuis Nicolas N   Ho Liza L   Boughalem Aicha A   Lelorc'h Marc M   Gobeaux Camille C   Fontenay Michaela M   Recher Christian C   Vey Norbert N   Guillé Arnaud A   Birnbaum Daniel D   Hermine Olivier O   Radford-Weiss Isabelle I   Tsantoulis Petros P   Collette Yves Y   Castellano Rémy R   Sarry Jean-Emmanuel JE   Pasmant Eric E   Bouscary Didier D   Kosmider Olivier O   Tamburini Jerome J  

Leukemia 20220330 5

Despite recent advances in acute myeloid leukemia (AML) molecular characterization and targeted therapies, a majority of AML cases still lack therapeutically actionable targets. In 127 AML cases with unmet therapeutic needs, as defined by the exclusion of ELN favorable cases and of FLT3-ITD mutations, we identified 51 (40%) cases with alterations in RAS pathway genes (RAS+, mostly NF1, NRAS, KRAS, and PTPN11 genes). In 79 homogeneously treated AML patients from this cohort, RAS+ status were asso  ...[more]

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