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Article

Ras oncogene-independent activation of RALB signaling is a targetable mechanism of escape from NRAS(V12) oncogene addiction in acute myeloid leukemia.

Oncogene - 8 Jun 2017

Pomeroy E J, Lee L A, Lee R D W, Schirm D K, Temiz N A, Ma J, Gruber T A, Diaz-Flores E, Moriarity B S, Downing J R, Shannon K M, Largaespada D A, Eckfeldt C E

Abstract excerpt

Somatic mutations that lead to constitutive activation of NRAS and KRAS proto-oncogenes are among the most common in human cancer and frequently occur in acute myeloid leukemia (AML). An inducible NRAS(V12)-driven AML mouse model has established a critical role for continued NRAS(V12) expression in leukemia maintenance. In this model genetic suppression of NRAS(V12) expression results in rapid leukemia remission,...

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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Source

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Identifiers

PMID: 27991934
DOI: 10.1038/onc.2016.471
PMCID: PMC5464975

Genes

NRAS
RALB
CDK5
KRAS
TBK1

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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