Oncogenes articles from across Nature Portfolio

In this Review, Cichowski and colleagues provide an overview of combinatorial strategies designed to treat RAS-driven cancers that are based on four concepts that include vertical pathway inhibition, co-targeting RAS and adaptive survival pathways, co-targeting downstream or converging pathways and capitalizing on other cancer-associated vulnerabilities.

We show that in addition to promoter activation, MYC drives cancer progression by activating transcriptional enhancers via a distinct mechanism. MYC cooperates with several other proteins at these cis-regulatory regions to change the epigenome and promote recruitment of RNA polymerase II and enhancer transcription.

Kreuzaler et al. examine the spatial metabolic rewiring driven by oncogenic MYC and show that it leads to increased import of vitamin B5, which represents a metabolic vulnerability to tumour progression.

Previous studies reported an effect of N⁶-methyladenosine (m⁶A) of super-enhancer RNAs (seRNAs) on chromatin accessibility and gene transcription. We investigated seRNA m⁶A levels in pancreatic ductal adenocarcinoma (PDAC) and found that aberrantly increased m⁶A methylation promoted local chromatin accessibility, resulting in increased transcription of oncogenes acting in PDAC progression.

We present an analysis that shows that although nearly half of the human genome comprises repetitive sequences, recombination between homologous repeats has a minor role in cancer chromosomal evolution.

In this Journal Club, Hajj discusses a study demonstrating that oncogene activation modulates immune control through both transcription and translation.

Many precision cancer therapies function by inhibiting oncogenic signaling pathways. A new study describes the counterintuitive finding that forced hyperactivation of the same pathways can also enable selective tumor targeting.