Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain
the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in
Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles
and JavaScript.
Little is known about how mutations in genes encoding tumor suppressors influence metastatic site selection and whether sustained inactivation of such genes influences tumor maintenance at these sites. A new study shows that restoration of Smad4 expression in extant pancreatic metastases has anti-tumor effects in the liver but pro-tumor effects in the lungs.
Bidirectional signaling between the brain and peripheral tumors plays a major part in cancer biology but is poorly understood. Stress-sensitive neurons in the lateral septum connect with the enteric nervous system via a polysynaptic circuit. Subsequently, these activated enteric cholinergic neurons promote tumor growth in colorectal cancer models.
The ESMO Targeted Anticancer Therapies Asia Congress took place in Hong Kong from 18–20 July 2025. Focusing on innovation, early clinical trials, and regulatory insights, the meeting advanced key discussions shaping the future of cancer research and treatment in the region.
Neri and colleagues discuss the development of drug conjugates for cancer therapy, focusing on current and future opportunities to improve tumor-targeting efficacy with small molecule–drug conjugates and combination therapies.
We developed paclitaxome-2, an optimized version of the sphingomyelin-derived paclitaxel nanovesicle paclitaxome. Leveraging the cationization-enabled transcytosis machinery boosted tumor penetration, and incorporating CD47 ‘self’ peptide masking minimized phagocytosis. Co-delivery of gemcitabine or carboplatin improved therapeutic outcomes in advanced pancreatic cancer and post-surgical triple-negative breast cancer in mouse models.
Prostate MRI has emerged as a way to improve accuracy in prostate cancer diagnostics. However, the subjectivity of assessments remains a challenge. New research shows that AI can help in this task and serve as a tool to improve MRI-based prediction of prostate cancer aggressiveness.
We integrated multi-omics data to construct a dynamic epigenomic atlas of colorectal cancer, identifying functional cis-regulatory elements through CRISPR interference screening. Furthermore, we developed a functionally informed polygenic risk score based on cis-regulatory element variants for risk prediction and revealed an epigenetic mechanism that drives colorectal cancer progression.
Cancer-associated fibroblasts represent a functionally diverse and heterogeneous entity within the solid tumor microenvironment. Mitochondrial transfer from cancer cells to fibroblasts is now shown to act as a reprogramming stimulus, driving metabolic and functional differentiation of fibroblasts to support tumor growth.
Ubellacker and Dixon summarize the latest discoveries on ferroptosis in cancer, covering the molecular and cellular pathways underlying sensitivity and resistance to this type of cell death, as well as potential translational applications in cancer therapeutics.
Kim and colleagues provide an overview of the current state of the art of nanomaterials and their application in immuno-oncology, discussing preclinical development and the clinical landscape.
In metastatic, immunologically ‘cold’ non-small cell lung cancer, the combination of radiation therapy and immune checkpoint inhibition (ICI) demonstrates heightened anti-tumor immune responses at non-irradiated sites and improved clinical responses compared with ICI alone. Radio-immunotherapy holds promise for patients with ICI-refractory lung cancer.
Dotti and colleagues review chimeric antigen receptor (CAR)-engineered cell-based cancer therapy and overview its transition for solid tumors from CAR T to CAR-engineered innate immune cells, discussing strengths and limitations for clinical application.
Trowbridge and colleagues provide a comprehensive review of clonal hematopoiesis in diverse cancer settings, from myeloid malignancies to solid tumors, covering underlying molecular and cellular mechanisms and exploring therapy-related approaches.
Glioblastoma (GBM) is highly invasive, but the crosstalk between GBM cells and glia at the invasion front is unclear. A study now analyzes the invasive region and shows that GBM cells induce plexin-B2 expression in macrophages and microglia to guide extracellular matrix remodeling and facilitate a shift from bulk to infiltrative GBM growth.
The 2025 American Society of Clinical Oncology (ASCO) Annual Meeting convened a global community of oncology professionals in Chicago, USA, to share groundbreaking clinical research, foster cross-sector collaboration, and shape the future of cancer treatment.
Muscle atrophy in cachexia drives weight loss and represents a major complication for patients with cancer. The tumor-derived cytokine activin A is now shown to decrease endothelial cell viability in skeletal muscle, leading to loss of muscle mass and function and inducing cachexia in multiple preclinical cancer models.
B cell leukemias are heterogeneous cancers believed to develop from pro-B lymphoid progenitors. Single-cell transcriptomics of patients and donors now reveal a map of B cell leukemia cell states and suggest that the cell of origin may be more dedifferentiated than previously assumed, thus influencing our understanding of the disease.
We investigated the early-stages of prostate cancer initiation. Deletion of Pten from epithelial basal cells in mice leads to cell plasticity, lineage infidelity and tumor formation, which are orchestrated by the activation of innate immunity and NF-κB signaling in prostate basal stem cells. Our findings have implications for human prostate cancer.
Extracellular DNA within neutrophil extracellular traps contributes to doxorubicin cardiotoxicity by interacting with CCDC25, a transmembrane DNA sensor on cardiomyocytes. This interaction promotes the generation of reactive oxygen species and activates autophagy, subsequently impairing cardiac function. Targeting CCDC25 mitigates cardiac damage and enhances the anti-tumor efficacy of doxorubicin, revealing a dual therapeutic strategy.
