A review describes glioblastoma organoids as human systems linking molecular profiling with functional treatment tests. It identifies unresolved issues in perfusion, immune components, matrix consistency and clinical validation.
A review from researchers at Technological University Dublin and University College Dublin considers glioblastoma (GBM) organoids and related three-dimensional platforms, from explant models to bioprinted microphysiological systems. Its scope includes tumor biology, the microenvironment, therapeutic responses and clinical translation.
The authors describe patient-derived models that can preserve intertumor and intratumor heterogeneity, test treatment responses and reveal resistance pathways. Some can be generated within clinically meaningful time frames. These properties support links between molecular profiling and functional testing in precision neuro-oncology.
The review emphasizes that platforms remain unstandardized. Many lack vascular perfusion, mature immune components, reproducible extracellular matrix, matched normal-brain controls or validated clinical endpoints. Preserving selected tumor features therefore addresses only part of the translational problem.
Priorities include harmonized biobanking, integrated single-cell and spatial omics, automation, chip perfusion, vascular and immune engineering, and ethical governance. The authors call for prospective trials to test whether using organoid results to guide treatment improves patient outcomes. The review positions these models as complementary human experimental systems, with their clinical role depending on validation matched to the intended decision.
A study connects aloperine binding and VPS34 lactylation to disrupted endosomal trafficking in lung cancer cells. Patient-derived organoids provided additional evidence of a stronger response to aloperine plus cisplatin than to either agent alone.
Single-cell analysis identified conserved epithelial programs associated with survival and resistance. Patient-derived organoid experiments then shifted platinum responses through SERCA2 activation or CCDC6 inhibition.
