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Intercellular mitochondrial transfer via tunnelling nanotubes can influence cellular bioenergetics and function in tumours. A study in Cell demonstrates how this process can increase CD8+ T cell metabolic fitness and anti-tumour function.
Wang et al. demonstrate that lactate derived from glioblastoma stem cells, microglia and macrophages drives histone lactylation, activating immunosuppressive transcriptional programs and upregulating CD47, to suppress phagocytosis.
In this Journal Club, Chakrabarti discusses a method to dissect the molecular architecture of inheritable gene expression (memory) states that mark cells that transition into drug-tolerant persister cells in melanoma.
In this Comment, Ben-Aharon et al. advocate for the creation of designated OncoYoung programs to address the unique needs of individuals with early-onset cancer, as well as multinational platforms with dedicated funding to investigate the aetiology of this disease and to develop preventive measures.
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.
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.
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.
In this Comment, Connor et al. discuss how the continued poor clinical translatability of preclinical studies highlights the need to mandate well-characterized models, ideally established in the orthotopic setting and, where feasible, treated with classical standard-of-care regimens.
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.
CRISPR screens in cell cultures reveal cancer dependencies yet often miss the metabolic nuances of tissues. In this Comment, Zuber and Palm highlight how modelling tumour-specific metabolic conditions can enhance our understanding of cancer biology and improve therapeutic discovery.
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.
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.
