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A study published inCancer Cellreports that two FDA-approved drugs — an antidepressant and an anticoagulant — synergize to promote autophagy and slow glioma progression in mice.
Chi Dang and colleagues show that MYC is involved in the regulation of the circadian clock, and its deregulated expression in cancer cells leads to a loss of cellular circadian rhythm and impacts cell metabolism.
Three papers have reported new data on resistance to bromodomain and extraterminal (BET) inhibitors and how best to use these inhibitors in combination therapy.
Most cancer genomics studies have focused on identifying the most important somatic mutations ('major drivers') that promote tumour growth. However, many cancer-associated mutations might instead have relatively weak tumour-promoting effects. This Opinion article highlights the existence of these mutations (termed 'mini drivers') and the functional effects that they might have.
Two studies published inCellhave shown that reduction of glucose levels in the tumour microenvironment by highly glycolytic tumour cells reduces the ability of tumour-infiltrating lymphocytes to trigger an antitumour immune response.
MEK1 and MEK2 have key roles in tumorigenesis and, therefore, represent promising targets for cancer therapy. This Review discusses the mechanisms of action of different inhibitors of MEK1 and MEK2, the mechanisms of resistance to these inhibitors and their current clinical progress.
Westbrook and colleagues show that knockdown of spliceosome components causes synthetic lethality in cells with hyperactive MYC, highlighting a possible therapeutic opportunity.
The transcription factor MYC upregulates and downregulates distinct sets of target genes, promoting cell growth and proliferation, increased metabolic rate and RNA biogenesis. This Review discusses MYC-mediated transcriptional regulation in normal growth control, as well as in tumour development and maintenance.
Aberrations in gene expression due to an altered epigenotype that is widely distributed in normal tissues are referred to as constitutional epimutations. This Opinion article discusses the potential contribution of constitutional epimutations to the 'missing' causality and heritability of cancer.
This Review discusses the roles of members of the sirtuin (SIRT) family in cancer biology, which have dichotomous, context-dependent functions as tumour suppressors and oncogenes. Furthermore, the authors discuss the possibility of targeting the sirtuins for anticancer therapy.
