Research Highlights

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. 

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.

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.

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.

In a recent study published in Nature, Goto et al. explore mechanisms of immune evasion in early colorectal cancers and adenomas and identify SOX17 to be crucial for immune escape through suppression of interferon-γ signalling.

In this recent study, He et al. establish that chronic stress promotes metastasis through stress-induced formation of neutrophil extracellular traps (NETs).

Sánchez-Guixé et al. investigated the possible routes to second malignancies in survivors of paediatric cancer by studying four such clinical cases.

Fu et al. provide data indicating a pathogenic role for Streptococcus anginosus in gastric cancer.

Recently published in Nature, Fan et al. demonstrate that accumulation of advanced glycation end-products in the extracellular matrix of the liver increases viscoelasticity to promote hepatocellular carcinoma growth, independent of stiffness.

Two independent studies published in Nature implicate distal cholesterol biosynthesis in the regulation of ferroptosis and show that 7-dehydrocholesterol (7-DHC) is an endogenous, anti-ferroptotic metabolite.

Mutant gain-of-function p53 is commonly found in human cancers. Huang, Cao, Qian et al. developed and validated the use of multifunctional biomimetic nanoreceptors that bind to and promote the degradation of mutant p53 as a cancer therapy.

Goddard et al. report that disseminated tumour cells evade T cell immunity due to their relative scarcity, which decreases the likelihood of T cell–tumour cell interactions.

Zhao et al. identified lymphatic endothelial-like cells in glioblastoma and demonstrated their role in promoting tumour growth through increased glioblastoma cholesterol metabolism.

In a recent Developmental Cell paper, Falvo et al. establish a role for epigenetic memory of inflammatory injury in promoting pancreatic tumorigenesis.