The incidence of early-onset cancers has increased by approximately 80% over the past three decades. These patients have unique needs. For optimal care, designated OncoYoung programs should be created. In addition, multinational platforms with dedicated funding are necessary to investigate the aetiology of early-onset cancers and develop preventive measures. In this Comment, Ben-Aharon et al. advocate

Engel et al. conducted a genetic screen in which they identified the Fanconi anaemia (FA) pathway as a driver of chromothripsis, complex genomic rearrangements and generation of extrachromosomal DNA.

The occurrence of multiple independent tumours in patients with EGFR-mutant lung cancer was unexplained. A recent study in Nature Cancer identified distinct genetic predisposition mechanisms, including developmental mosaicism and germline EGFR variants, that contribute to the formation of multiple primary tumours.

Correction to: Nature Reviews Cancer https://doi.org/10.1038/s41568-024-00704-8, published online 17 June 2024.

In this Journal Club, Chae and Chung discuss a study characterizing the differentiation and maturation of both tumour-resident and circulating B cells in patients with melanoma.

Ageing is a well-accepted risk factor for developing cancer. Yan et al. used a preclinical rat model to study the mechanisms facilitating the age-associated increase in breast tumorigenesis.

In this Tools of the Trade article, Carly Tyer describes the development of Telo-seq, a method to enrich and sequence all telomeres within a sample, and highlights its use in distinguishing between the two telomere maintenance mechanisms used in cancer cells.

In this Journal Club, Sabarinathan discusses a study suggesting immunoproteasome expression as a potential biomarker of response to immune checkpoint inhibition in melanoma.

In this Tools of the Trade article, Siyu He describes the development of Starfysh, a computational toolbox that integrates histology of complex tissues in spatial transcriptomic data analysis to characterize cell states.

In a recent study published in Cell, Chhabra et al. identify age- and sex-dependent changes in skin fibroblasts that drive melanoma aggressiveness, with aged male fibroblasts promoting a slow-cycling, invasive state and resistance to targeted therapy in melanoma cells.

Chibaya, DeMarco et al. investigated a combinatorial approach of delivering innate immune agonists and RAS pathway-targeted therapies to remodel the tumour microenvironment and improve PDAC drug response.

The precision medicine era has precipitated inherent new challenges to the preclinical tumour biology field. Overall, continued poor clinical translatability of preclinical studies highlights the need to disrupt the status quo. Well-characterized models, ideally established in the orthotopic setting and, where feasible, treated with classical standard-of-care regimens, are mandated. In this Comment

Ciwinska et al. asked whether natural tissue remodelling can drive mutant cell expansion and identified three protective mechanisms in the healthy mouse mammary gland that constrain the ability of mutant cells to transform and give rise to cancer.

In this Tools of the Trade article, Xinwen Liu describes the development of VIBRANT, a vibrational spectroscopy method for high-content phenotypic profiling, and highlights its use to predict drug mechanisms of action or identify potential drug candidates.

In this Journal Club, Kim and Jung discuss a study that demonstrates the role of CCL2 in recruiting monocytes to the metastasic site.

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.

Correction to: Nature Reviews Cancer https://doi.org/10.1038/s41568-024-00735-1, published online 16 August 2024.

Cancer screening, diagnosis and care stand to benefit greatly from advances in artificial intelligence (AI). Researchers, developers and deployers must ensure that applications of AI avoid known racial and gender biases to advance health care for all. Cancer screening, diagnosis and care can benefit greatly from advances in artificial intelligence (AI). In this Comment, Ghassemi and Gusev discuss how

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 (TH17) cells, that can initiate intestinal cancer.

Integrative medicine incorporated alongside cancer care, referred to as integrative oncology, is an evidence-informed field with established clinical guidelines. Although integrative oncology improves patient outcomes, it is inconsistently provided to patients. To align with best practices, it is necessary to increase awareness of integrative oncology, improve access to treatments, and provide consistent

In this Journal Club, Koh and Im discuss a study demonstrating the unique evolutionary trajectory of breast cancers harbouring the common driver alteration der(1;16).

Correction to: Nature Reviews Cancer https://doi.org/10.1038/s41568-022-00488-9, published online 28 June 2022.

In a recent study published in Nature, lactate has been identified as a key player in enhancing DNA repair mechanisms in gastric cancer by promoting lactylation of DNA repair proteins, leading to chemotherapy resistance.

Pregnancy involves immune system suppression to protect the fetus, making it a valuable model for understanding cancer immune tolerance. Recently in Cell, Yu et al. identified B7-H4 as a common immune tolerance checkpoint in both tumours and the placenta.

This poster explores rational combinations of immune checkpoint blockade of the PD1–PDL1 interaction with other therapies aimed at targeting effector T cells, innate immune and regulatory cells, the tumour microenvironment and cancer cells.

Leighow et al. develop a strategy called the dual-switch selection gene drive platform, which enables the evolutionary dynamics of acquired resistance to be manipulated for therapeutic ends.

In this Journal Club, Maeng and Ku discuss a study demonstrating that profiling drug responses in patient-derived organoids can identify responders to various therapies.

Lim et al. show that ASS1, silenced in many cancer types, is a metabolic checkpoint that, following DNA damage, halts cell cycle progression by restricting nucleotide synthesis and p53-related gene transcription.

In this study, Allan Balmain and colleagues used a mouse model to monitor stem cell networks at single-cell resolution during skin carcinogenesis, revealing two cancer stem cell states, rapid cycling and plasticity, between which cells can transition to drive tumour initiation, progression and therapy resistance.

Patient progression and response to immunotherapy are directly influenced by the presence and quality of tumour-infiltrating leukocytes (TILs). In a recent Cell publication, Wang, Zeng et al. demonstrate the functional role of circadian rhythms in altering TIL functionality and quantity, highlighting the therapeutic potential of leveraging this understanding.