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Adipose tissue and adipocytes have been implicated in promoting tumour progression and hindering anti-tumour immunity. Wang et al. investigated the functional role of tumour-associated visceral adipose tissue in regulating colorectal cancer anti-tumour immunity and immunotherapy efficacy.
In a recent study published in Nature, Natarajan et al. uncover a metabolic–epigenetic circuit in which glutamine-derived itaconate functions as an oncometabolite to sustain oncogenic ZFTA–RELA expression in ependymoma. Disrupting this pathway lowers ZFTA–RELA levels and suppresses tumour growth in preclinical models, revealing a promising therapeutic vulnerability in this aggressive cancer.
In a study published in Cell, Xu et al. show that mast cells engineered with tumour-antigen specific antibodies and loaded with an oncolytic virus can be activated by antigen encounter to drive targeted tumour cell killing and amplify local anti-tumour immunity.
Mutant haematopoietic stem cells display broad fitness variation, suggesting that protective mechanisms may limit clonal expansion and malignant transformation. Now, Agarwal et al. identify a germline noncoding variant that confers resilience to clonal haematopoiesis of indeterminate potential (CHIP) by dampening expression of the RNA-binding protein MSI2.
In a recent Science Immunology paper, He et al. show that treatment with the chemotherapy carboplatin reshapes cardiac-resident macrophage populations, protecting against later heart disease.
In a study published in Nature, Lourenço et al. demonstrate that strong oncogenic driver mutations undergo negative selection unless they occur in a permissive tissue context.
By incorporating lectins that target specific tumour-associated carbohydrate antigens, Zhou et al. engineered bispecific antibodies that induce effective T cell activation and tumour regression in various cancers.
A study published in Science shows that liver zonation shapes hepatocellular carcinoma (HCC) development. In mice, HCC predominantly originates from zone 3 hepatocytes, where GSTM2 and GSTM3 drive initiation by inhibiting ferroptosis, revealing metabolic vulnerabilities in liver cancer.
A common side effect of treatment with taxane-based chemotherapy is peripheral neuropathy. Now, Fonseca et al. uncover the endoplasmic reticulum (ER) stress response in leukocytes as the effective mediator of paclitaxel-induced peripheral nerve damage.
In a recent study, Mohri et al. reveal how melanocyte stem cells integrate distinct genotoxic signals through niche-derived KITL to drive either hair greying or melanomagenesis.
Metabolic dysfunction-associated steatotic liver disease (MASLD) is an independent risk factor for developing extra-hepatic cancers. Now, Li et al. uncover an exosome-driven metabolic connection between the steatotic liver and the breast that fosters cancer progression.
In a recent study published in Nature Genetics, Kübler, Nardone et al. analysed the mechanisms underlying tamoxifen-associated uterine cancer and identified PI3K pathway activation as a key non-genetic driver.
In a study published in Nature Immunology, Fuentes et al. demonstrate that the pre-T cell receptor (TCR) is expressed in leukaemia-initiating cells in patients with T cell acute lymphoblastic leukaemia, and that targeting it can inhibit tumour progression.
In a recent study, Salomó Coll et al. demonstrate that impaired ER-phagy in Kras-mutant pancreatic acinar cells leads to the accumulation of protein aggregates and disruption of acinar cell homeostasis, thereby cooperating with oncogenic KRAS to promote cellular transformation.
Lyons et al. explored the rules of specificity and function for condensates formed by oncogenic fusion proteins, and identified a common molecular signature in these oncoproteins that compartmentalizes RNA polymerase II to confer an increase in gene activation and consequent cancer phenotypes.
In a recent study published in Nature, Liu, Wang, et al. investigate the mechanisms underlying cytarabine-induced neurotoxicity and provide a mechanistic explanation for the differing neurotoxicity profiles of other nucleoside analogues, such as gemcitabine.
In a study published in Cell, Phelps et al. find a mechanism connecting exercise, gut microbiota and anti-tumour immunity; exercise induces microbiota to produce formate, which in turn enhances CD8+ T cell functionality.
The presence of tertiary lymphoid structures (TLSs) in tumours is often linked with response to immunotherapy, however, the maturation status of the TLS can influence its immunological function. Now, Tang et al. uncover tryptophan metabolism as a factor determining TLS maturation status
Although disulfide stress in cancer cells under glucose starvation is known to trigger disulfidptosis, its role in the tumour microenvironment has remained unclear. A recent study in Nature Cell Biology reveals that in intratumoural CD8+ T cells, disulfidptosis promotes T cell exhaustion and thereby limits antitumour imunity.
