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Carter, Murrayet al. show that MYCN and the histone chaperone FACT are part of a positive feedback loop and that inhibition of FACT with a small molecule leads to tumour regression in a pre-clinical model of MYCN-amplified neuroblastoma.
Wanget al. report that oncogenic KRAS, but not HRAS or NRAS, promotes self-renewal properties and tumour initiation by inhibiting non-canonical WNT/Ca2+signalling.
Espositoet al. report the mechanisms of PARP inhibitor (PARPi) sensitivity in cells expressing certain leukaemia fusion oncoproteins and highlight the use of PARPis as a promising novel approach for treating acute myeloid leukaemia.
Two papers inSciencepresent evidence in mice that certain species of intestinal bacteria can drive antitumour immune responses and modulate responses to immune checkpoint blockade.
A study inNaturereports that astrocytoma cells form a multicellular network interconnected by distinct tumour microtubes that drive invasion, mediate cell–cell communication, enable self-repair and confer radioresistance.
Two studies published inNaturereport that epithelial–mesenchymal transition (EMT) is not required for metastasis in mouse tumour models of breast and pancreatic cancer; however, EMT can contribute to resistance to chemotherapy.
A paper inNature reportsthat an astrocyte exosome-derived microRNA induces the loss of PTEN expression in disseminated tumour cells in the brain, thus promoting metastasis.
Schwabet al. show that the Fanconi anaemia pathway might prevent genome instability by stabilizing replication forks when actively transcribed DNA is encountered and by removing DNA–RNA hybrids.
Why do some cancers only metastasize to certain organs? This question of organotropism is perplexing, and a team led by Lyden, Bromberg and Peinado have found that exosomes could be key.
Bestet al. describe a diagnostic platform based on platelet RNA sequencing and self-learning algorithms that discriminates patients with cancer from healthy controls, predicts the localization of the primary tumour and provides information on the molecular tumour phenotype.
Three studies demonstrate that adenosine-to-inosine RNA editing introduces transcriptome diversity in tumours from a range of cancer types and show that this diversity is both functionally important and clinically relevant.
Roger Lo and colleagues characterized the melanoma genome, transcriptome and epigenome to understand the landscape of acquired resistance to MAPK pathway inhibitors.
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.
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.
Westbrook and colleagues show that knockdown of spliceosome components causes synthetic lethality in cells with hyperactive MYC, highlighting a possible therapeutic opportunity.
