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Nejman et al. have comprehensively characterized the bacteria present in 1,526 human tumours and their adjacent normal tissues encompassing seven different solid tumour types. Their initial findings suggest that much like the gut microbiome, the tumour microbiome may impact many aspects of tumour biology.
Ostendorf et al. show that germline variants of human APOE play a role in melanoma that is opposite to that in Alzheimer disease, with APOE4 carrier status being associated with reduced melanoma growth in mice and improved outcome in patients with advanced melanoma.
Allen, Hiam et al. have used mass cytometry to characterize the immune landscape over time in response to tumour development, demonstrating that tumour growth dynamically alters the systemic immune landscape and that this can be reverted by tumour removal.
Baksh et al. have delineated a pathway through which serine availability is integrated with stem cell fate decisions and can control the initiation of epidermal squamous cell carcinomas.
This Review presents the evidence for the role of risk factors in breast cancer incidence and their inclusion in risk estimation tools as a step towards precision prevention to specifically target those women at increased risk for appropriate risk-reducing interventions.
This Review discusses the key role that natural killer (NK) cells play in driving an antitumour immune response throughout the progression of cancer from its initial development to its metastatic spread and eventual treatment, defined herein as the cancer–NK cell immunity cycle.
This Review discusses intra-prostatic inflammatory processes and how they are induced and perpetuated, thereby driving prostate cancer development and progression. By discussing external inflammatory cues in connection to cancer cell-intrinsic factors in prostate tumorigenesis, the authors provide insight into potential preventative and therapeutic strategies.
This Perspective explores why TP53 is the most commonly mutated gene in cancer, discussing the evolutionary conservation of the p53 pathway in the context of tissue-specific functions and underlying reasons for the order of mutations which lead to p53-related cancer.
