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Acetyl coenzyme A (acetyl-CoA) is a key metabolite in carbohydrate and lipid metabolism and plays a role in signalling through protein acetylation, and the dysregulation of these pathways is a hallmark of various cancers. In this Review, Guertin and Wellen give an overview of acetyl-CoA metabolism in health and in cancer and discuss emerging therapeutic strategies for targeting metabolic pathways involving acetyl-CoA.
To understand malignant progression, Yuan et al. delineate the complex crosstalk between cancer stem cells and their microenvironment that is initiated by oncogenic RAS.
This Review discusses the diverse ways in which cancer-associated RNA splicing dysregulation promotes tumour initiation and progression, existing and emerging approaches for targeting splicing for cancer therapy and outstanding questions and challenges in the field.
Reprogrammed metabolism is a hallmark of cancer. Here, Li, Zhang and colleagues describe how signal transducer and activator of transcription (STAT) proteins alter cancer cell metabolism by sensing and transducing signals from the tumour environment and modulating signalling pathways, transcription factors, mitochondrial proteins and enzymes.
In a study in Nature, Wang et al. describe how circadian rhythms can impact tumour suppression through their effects on dendritic cells, a finding that could help to optimize clinical trials of cancer immunotherapies.
As well-established players in the metastatic cascade, circulating tumour cells (CTCs) hold promise for improved cancer diagnosis and disease monitoring. In this Review, Ring et al. overview the current understanding of CTC biology, highlighting specific opportunities and vulnerabilities for future CTC-focused therapies.
Genes encoding DNA damage response factors are frequently mutated in cancer, causing genomic instability and presenting opportunities for therapeutic intervention. This Review discusses state-of-the-art strategies for DNA damage response inactivation using small-molecule inhibitors.
Two recent studies have demonstrated how senescent cancer cells alter their cell surface proteome to induce anti-tumour immune responses, highlighting the potential therapeutic role of inducing senescence to improve anti-tumour immunity.
Head and neck squamous cell carcinoma (HNSCC) is the sixth most common cancer worldwide and its incidence continues to rise, mostly owing to an increase in human papillomavirus (HPV)-associated oropharyngeal squamous cell carcinoma. In this Review, the authors describe HPV-positive and HPV-negative HNSCC tumour microenvironments and discuss current and novel treatment modalities.
In this study, Cao et al. identified previously undiscovered metabolites produced by human gut microbes that cause DNA damage, and analysed their implication for colorectal cancer development.
Schmitt et al. describe an adaptive mechanism employed by colorectal cancers to handle pro-apoptotic chemotherapeutic insults, which could represent a targetable vulnerability with combination therapy.
Pancreatic ductal adenocarcinomas are characterized by a robust stromal reaction. This Review discusses how the evolution of the epithelium in pancreatic cancers is coordinated with a programme of stromal progression; this comprehensive picture of tumour development might, in turn, point to new therapeutic vulnerabilities.
In this Perspective, Wahida et al. consider six riddles in precision oncology that must be solved to achieve better clinical responses to molecular targeted therapies.
This Review covers recent advances in intravital imaging of mammalian models of cancer and describes how intravital imaging can help to understand the role of the tumour microenvironment in cancer progression and metastasis, and to develop novel treatments and therapies.
Notarangelo et al. reveal that the oncometabolite d-2-hydroxyglutarate, which is released in high quantities by tumour cells, is taken up by CD8+ T cells in the tumour microenvironment and blocks their proliferation and cytotoxicity by inhibition of lactate dehydrogenase and metabolic reprogramming.
Social media has revolutionized health-care communication across medicine, particularly in the field of oncology. In this Comment, Manochakian and Dizon highlight the role of social media in promoting patient-driven cancer research to benefit all.
In two studies published concurrently, Dohlman et al. and Narunsky-Haziza et al. have found strong correlative links between the prevalence of fungal DNA and cancer.
The activation of DNA damage tolerance (DDT) pathways as part of the replication stress response to DNA damage is key for maintaining genome integrity and, as a result, these pathways are closely linked to tumorigenesis. In this Review, Cybulla and Vindigni discuss the many connections between DDT, replication stress and cancer, detail opportunities for clinical biomarker development, and outline therapeutic strategies for targeting these pathways.