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An oncogene is a gene that will transform a cell in culture. Oncogenes were initially identified in cancer-causing retroviruses. Genes involved in the regulation of cell division, movement and signalling for example can function as oncogenes under specific conditions.
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.
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.
In this study, Insco et al. find patient-specific CDK13 mutations to impede RNA surveillance, leading to the accumulation and translation of prematurely terminated RNAs that drive malignancy in melanoma models.
