Latest Research
All publications from the Cancer3.AI database, newest first.
Development of a Synthetic Liver Phantom: Experimental Characterization of Tissue Mechanical Properties.
Potere F, et al
Researchers developed a synthetic liver phantom — a physical, lab-based model designed to mimic the mechanical and fluid-transport properties of real liver tissue — to support preclinical testing of injectable cancer therapies for hepatocellular carcinoma (HCC), the world's third leading cause of cancer death. Current treatments such as radiofrequency ablation and chemoembolization are limited by anatomical and clinical constraints, leaving many patients without effective options, which motivates the search for improved loco-regional therapies including emerging agents like YntraDose. The team first characterized porcine liver tissue, measuring its permeability at approximately 10⁻¹² m² and establishing compression benchmarks, then used 3D printing with controlled microstructures to fabricate phantom regions that independently replicate the stiffness of healthy parenchyma (approximately 22 kPa) and stiffer tumor tissue (approximately 185 kPa). Validation through compression testing, Darcy-based permeability experiments, and MRI imaging confirmed that injection of agents into the phantom produced reproducible diffusion patterns consistent with real tissue behavior. This research-grade model fills an important gap between oversimplified lab tests and animal studies, providing a controllable, reproducible platform to optimize injection protocols and accelerate the development of safer, more effective liver cancer therapies before clinical trials.
Annals of biomedical engineering
Source →Associations of inflammatory biomarkers with brain atrophy and clinical scores in schizophrenia patients with autistic features.
Wang J, et al
A new study published in BMC Research Notes investigated the relationship between inflammatory biomarkers, brain atrophy, and clinical symptom scores in patients diagnosed with schizophrenia who also display autistic features. The research aimed to determine whether measurable markers of inflammation in the body correspond to structural changes in the brain and to the severity of psychiatric symptoms in this overlapping patient population. Findings suggested that elevated inflammatory indicators are associated with greater degrees of brain volume loss and worse clinical outcomes, pointing to inflammation as a potential shared biological mechanism underlying both schizophrenia and autistic traits. These results are clinically significant because they may help identify a subgroup of schizophrenia patients who could benefit from anti-inflammatory treatment strategies. Understanding the biological overlap between schizophrenia and autism spectrum features may ultimately lead to more personalized and effective therapeutic approaches for affected individuals.
BMC research notes
Source →Apoptotic cell clearance triggers epithelial fate reprogramming during prostate regression.
Graham-Paquin A, et al
Researchers investigated how prostate tissue remodels itself after androgen deprivation therapy, a common treatment for prostate cancer that causes dramatic cell loss in the prostate gland. The study discovered that surviving epithelial cells actively engulf and clear the bodies of their dying neighbors through a process called efferocytosis, and that this clean-up activity directly triggers the surviving cells to revert to a stem-like progenitor state. This cellular reprogramming is driven by a metabolic shift toward lactate production, which chemically modifies histone proteins through lactylation and switches on genes associated with progenitor cell identity. When researchers experimentally blocked efferocytosis in live animals, prostate regression was impaired and the cells failed to acquire the expected progenitor characteristics, confirming the causal role of this mechanism. These findings are clinically significant because the progenitor-like state induced by efferocytosis may contribute to the development of castration-resistant prostate cancer, an aggressive form of the disease that no longer responds to hormone therapy.
Cell death & disease
Source →Mechanism and therapeutic significance of ARV-110 combined with a PDGFR inhibitor for the induction of apoptosis in castration-resistant prostate cancer cells through the ROS/JNK pathway.
Fu Y, et al
Researchers investigated a novel combination therapy strategy for castration-resistant prostate cancer (CRPC), a form of prostate cancer that no longer responds to standard hormone-blocking treatments. The study combined ARV-110, a targeted protein degrader that eliminates the androgen receptor (AR), with inhibitors of platelet-derived growth factor receptor (PDGFR), examining how these two agents interact at the molecular level. Experiments revealed that ARV-110 not only degrades AR but also unexpectedly increases the production of a growth factor called PDGFA, which can activate alternative survival pathways in cancer cells, explaining why blocking PDGFR alongside ARV-110 creates a powerful synergistic effect. The combination was found to trigger cancer cell death by activating the JNK stress-signaling pathway and causing a toxic buildup of reactive oxygen species (ROS), partly because both drugs independently suppress an antioxidant enzyme called catalase. These findings provide a detailed mechanistic rationale for combining AR-targeted and PDGFR-targeted therapies, offering a promising new treatment strategy that could benefit patients with CRPC who have limited options.
Cell death & disease
Source →Genome-wide methylome profiling of cell-free DNA enables prognostication of patients with castration-resistant prostate cancer.
Kondrup K, et al
Researchers investigated whether methylation patterns in cell-free DNA circulating in the blood could serve as a reliable biomarker for metastatic castration-resistant prostate cancer (mCRPC), a lethal form of the disease that currently lacks effective tools for guiding treatment decisions. The team developed a 48-region methylation signature called cfMeCaP using plasma samples from 27 mCRPC patients and validated it across three independent cohorts totaling over 200 prostate cancer patients. The cfMeCaP signature detected circulating tumour DNA with high sensitivity—up to 100% in the discovery cohort and around 95% in external validation—and elevated methylation levels at diagnosis were strongly linked to worse progression-free and overall survival across all cohorts. Crucially, patients in whom ctDNA remained persistently detectable during treatment experienced rapid treatment failure with a median progression-free survival of just 4.4 months, compared to 65.5 months in those where ctDNA was undetectable. These findings establish cfMeCaP as a promising non-invasive blood test that could help oncologists monitor disease progression and predict which patients are likely to respond to or fail current therapies for advanced prostate cancer.
British journal of cancer
Source →