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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.
The practice of posting preprint manuscripts on servers such as bioRxiv has become increasingly common. In this Comment, Hindle and Sever explore the utility of preprints for advancing researchers careers.
The ability of prenatal cell-free DNA sequencing to incidentally detect occult maternal malignancies was first documented over a decade ago, yet coordinated follow-up of pregnant people who receive these results is still lacking in many countries. Here we provide a call to action for oncologists to become more involved in diagnosing and managing these cases.
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.
This month, Nature Reviews Cancer launches Roadmap articles, in which we ask authors to provide a sense of direction to a field to encourage new lines of thinking and experimentation, as well as opportunities for collaboration.
In this Tools of the Trade article, Erin Brown describes the development of CytoSPACE, a computational tool that aligns single-cell transcriptomes and spatial transcriptomic data, and highlights its use in identifying spatially resolved cell states in the tumour microenvironment.
To establish microbiome-based screening for colorectal cancer, a study published in Nature Medicine tackled two key challenges: utilizing quantitative microbiome profiling and identifying covariates that might obscure the microbiota–colorectal cancer interactions.
Monteran et al. identified key interactions between granulocytes and T cells that promote an immunosuppressive bone microenvironment, enabling breast cancer metastasis.
Parreno et al. provide evidence for epigenetically initiated cancers in Drosophila and show that cancer develops after transient loss of Polycomb group proteins in the absence of recurrent mutations.
Kong et al. have now shown that Knudson’s two-hit hypothesis can be circumvented through the actions of the glycolytic metabolite methylglyoxal, which transiently inactivates the tumour-suppressive functions of BRCA2 leading to episodic mutagenesis and cancer genome evolution.
In a ‘publish or perish’ culture, some scientists may resort to questionable research practices or even fraud. Scientific paper mills and artificial intelligence increasingly threaten the pursuit of truth in science. Structural changes, including heightened scrutiny of papers and authorship and better funding, are needed to ensure scientific integrity.
Two studies published concurrently in Nature report the development and preclinical activity of RMC-7977, a multi-selective inhibitor targeting the active, GTP-bound form of RAS.
The annual American Association for Cancer Research (AACR) meeting provides a platform for scientists, clinicians and other stakeholders to share the latest advances in cancer science and medicine. Here, we outline some highlights of the 2024 meeting.
In this Tools of the Trade article, Victor Tieu describes the development of MEGA, a platform that exploits the RNA-targeting capability of CRISPR–Cas13d and demonstrates its use to improve the anti-tumour activity of CAR T cells.
In this Journal Club, Oh and Kim discuss a study demonstrating the mechanisms underlying histological transformation of lung adenocarcinoma to neuroendocrine small-cell lung cancer.
Dias et al. have shown that intentional further activation of oncogenic signalling rather than its inhibition represents an alternative strategy leading to colorectal cancer cell death with tumour suppressive acquired resistance.
