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Kreuzaler et al. examine the spatial metabolic rewiring driven by oncogenic MYC and show that it leads to increased import of vitamin B5, which represents a metabolic vulnerability to tumour progression.
In this study, Bansaccal et al. analyse why, at some skin locations, oncogene-expressing cells rarely progress to cancer and found that a dense dermal collagen network prevents skin cancer formation.
Enzymes that produce metabolites specifically required by cancer cells have become attractive targets for therapy. Recently, Doshi et al. highlighted the potential of targeting the detoxifying enzyme UXS1 in cancer.
Maas et al. identify an inflammatory, immunosuppressive phenotype in neutrophils that accumulates in brain malignancies, and show that this tumour-promoting neutrophil activation is driven by the brain tumour microenvironment.
Wang et al. show that antibiotic targeting of anaerobic intratumoral bacteria exposes a unique repertoire of microbial neoantigens that can successfully trigger cellular immunity against colorectal cancer in mice.
Pregnancy-associated breast cancers are typically diagnosed at more advanced stages than other breast cancers. Recently, Saura et al. developed a non-invasive screening method using breast milk to diagnose patients prior to tumour detection by imaging.
In a recent study, Sanchez-Aguilera, Masmudi-Martín et al. find that a molecular program explains the cognitive impairment often seen in patients with brain metastasis, challenging the prevailing paradigm of the tumour mass being the sole cause of altered brain function.
In a recent study, Tagore et al. find that the formation of synapse-like structures that serve to transfer GABA between premalignant melanocytes and keratinocytes promotes melanoma initiation by the BRAFV600E oncogene.
Rahme et al. establish an in vivo model for low-grade glioma, and use it to demonstrate that Pdgfra insulator loss and Cdkn2a promoter silencing are epigenetic drivers of gliomagenesis.
Bland et al. show that cancer types with heterozygous somatic hotspot mutations in the spliceosome component SF3B1 are vulnerable to PARP inhibition, which causes a defective response to replication stress.
Two independent studies published together in Nature find that AT1 cells can have a role in both the initiation and suppression of lung adenocarcinoma.
Girish et al. designed a method to genetically remove extra chromosomes from human aneuploid cancer cells to show that they are important for malignant growth and not just a bystander.
Inducing ferroptosis in cancer cells has become a realistic method for promoting cancer cell death. In this study, Nakarmua et al. identify a novel ferroptosis suppressor 1 (FSP1) inhibitor that promotes FSP1 relocalization through phase separation, priming ferroptosis and ultimately impairing tumour growth.
Two independent studies published in Nature have collectively addressed the long-standing question of sex bias in cancer and implicated non-hormonal genes of the Y chromosome in aggressive features of colorectal and bladder cancers in men.
In this study, Malladi and colleagues reveal the mechanism by which mitochondrial fragmentation enables latent brain metastatic breast cancer cells to increase fatty acid oxidation to maintain cellular energetics and redox homeostasis.
Wang et al. demonstrate how tumour-derived extracellular vesicles and particles dysregulate liver function to promote fatty liver disease and diminish chemotherapeutic efficacy.