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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.
In this Journal Club, Oh and Kim discuss a study demonstrating the mechanisms underlying histological transformation of lung adenocarcinoma to neuroendocrine small-cell lung cancer.
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.