Although p53 was once considered undruggable, in this Review, Peuget et al. discuss the progress made in targeting p53 as a form of cancer therapy with approaches ranging from restoration of mutant p53 function to inhibition of the negative regulator of p53, MDM2, as well as newer strategies, including p53-based mRNA vaccines and antibodies.

In this Review, de Souza et al. discuss how advances in the ability to image protein markers at high-plex, at single-cell and even subcellular resolution, are expanding our understanding of tumour biology and clinical outcomes, and outline the future promise of combining such multiplex protein imaging methods with other forms of spatial omics.

The World Trade Center (WTC) disaster exposed individuals to carcinogens, leading to elevated cancer rates. Responders who received care through the WTC Health Program have higher survival rates. Twenty-three years post-disaster, we summarize cancer incidence and outcome studies in this population and highlight the importance of a dedicated health programme response.

In a recent Nature paper, Ruggero and colleagues found that fasting and ketogenic diets induce metabolic rewiring through a translational mechanism involving MNK-mediated phosphorylation of eIF4E, which enhances ketogenesis. This process creates a metabolic vulnerability in pancreatic cancer that could be therapeutically exploited.

In this Tools of the Trade article, Radhika Mathur describes the development of a novel 3D whole-tumour sampling approach for glioblastoma, which can be used to elucidate tumour heterogeneity.

Pan et al. performed a large-scale, cluster-randomized controlled trial to assess whether eradicating Helicobacter pylori in asymptomatic individuals would be beneficial in preventing gastric cancer.

Cancer screening, diagnosis and care can benefit greatly from advances in artificial intelligence (AI). In this Comment, Ghassemi and Gusev discuss how AI applications must address and avoid known racial and gender biases to improve health care for all.

Inflammation is well established as a risk factor for cancer development in the gut. In this study, Fesneau et al. identify a specific immune cell population, derived from T helper 17 (T_H17) cells, that can initiate intestinal cancer.