Abstract. In the realm of nanomaterials, atomically precise quasi-molecular gold nanoclusters (AuNCs) play a prime role due to their unique, stable, and hi

Read the full paper: H3K27M enhances basal ATM signaling but is not required for radiosensitization of diffuse midline glioma via ATM inhibition with AZD1390

Background: Lung cancer is a leading cause of cancer-related mortality worldwide, underscoring the need for the development of more effective treatment strategies. Radiotherapy (RT), particularly intensity-modulated radiation therapy (IMRT), has enhanced tumor targeting while minimizing damage to healthy tissues. Nevertheless, radioresistance and challenges posed by the tumor microenvironment limit its efficacy.Objective: Selenium-curcumin-polyethylene glycol 600 nanoparticles (Se-Cur-PEG NPs) analyzed as radiosensitizers in IMRT for lung cancer treatment.Material and Methods: In this experimental study, Se-Cur-PEG NPs were synthesized and characterized for their potential as radiosensitizers.Results: The in vitro toxicity of Se-Cur-PEG NPs against A549 lung cancer cells was evaluated using MTT assays, demonstrating a dose-dependent reduction in cell viability. The combination of Se-Cur-PEG NPs (50 µg mL-1) with IMRT (4 Gy) resulted in a significant enhancement in cell death compared to either treatment alone, indicating a strong synergistic effect (CI=1.21) and a notable sensitizer enhancement ratio (SER=2.5). Intracellular ROS generation analysis confirmed that Se-Cur-PEG NPs amplified IMRT-induced oxidative stress, contributing to increased cancer cell toxicity. Conclusion: These findings suggest that Se-Cur-PEG NPs hold promise as effective radiosensitizers, potentially improving lung cancer RT outcomes.

Radiotherapy (RT), a cornerstone treatment, is fundamentally limited by tumor hypoxia-induced radioresistance and the associated need for high doses t…

Read the full paper: Engineering iron oxide nanoparticles for enhanced radiosensitization

Read the full paper: A Dual-Pronged Hafnia–Prodrug–Lipid Nanoplatform Coupling Radiosensitization and DNA Homologous Recombination Inhibition

Read the full paper: Transcriptomic analysis to uncover the mechanism of radiosensitization of AR-positive triple-negative breast cancers with AR inhibition

Read the full paper: Cell-cycle-specific lesion evolution rather than inhibition of double-strand-break repair underpins cisplatin radiosensitization

The TMPRSS2:ERG gene fusion is a truncal oncogenic event in a large subset of prostate cancers, yet its clinical relevance has remained unclear. In this issue of the JCI, Köcher et al. have demonstrated that ERG overexpression in human prostate cancer cells rewired DNA double-strand break repair toward a poly(ADP-ribose) polymerase 1–dependent (PARP1-dependent) alternative end-joining pathway without disrupting canonical repair. This repair bias created a conditional dependency on PARP1 that was exposed by radiotherapy, rendering ERG-positive tumors selectively sensitive to PARP inhibition–mediated radiosensitization. The tumor-selective cytotoxic effect of combined PARP1 inhibition and irradiation was corroborated in human-derived prostate cancer organoids. These findings establish ERG as a predictive biomarker for precision radiotherapy and highlight a tumor-selective strategy to enhance radiotherapeutic efficacy in prostate cancer.

Read the full paper: Overexpression of the ERG oncogene in prostate cancer identifies candidates for PARP inhibitor-based radiosensitization