Osteosarcoma

Among the validated candidates, sarsasapogenin, a compound identified from the screen, effectively suppressed CSF1R protein expression and inhibited the proliferation of both MG63 and Saos-2 cells in a dose-dependent manner. Collectively, the present findings highlight CSF1R as a clinically promising diagnostic biomarker and therapeutic target for osteosarcoma.

Additionally, three cancer cell subpopulations with distinct chemosensitivity profiles were identified; Subpopulation 2, characterized by high expression of CCNA2, UBE2C, and CENPF, demonstrated significantly reduced sensitivity to methotrexate, doxorubicin, cisplatin, ifosfamide, and etoposide. This study provides a preliminary characterization of the metabolic landscape of OS and its associated immune microenvironment. Targeting SLC7A7-deficient monocytes may represent promising strategies for enhancing the efficacy of immunotherapy in OS.

By increasing the therapeutic efficacy of the phillyrin derivative DE02 via a safe, nondestructive exosome-based delivery method, cavitation-free acoustic sensitization improves PLK4-targeted osteosarcoma therapy. For targeted osteosarcoma biotherapy, this ultrasound-enabled method provides a mechanistically defined and physiologically applicable platform.

Functionally, GAS5 overexpression suppressed inflammatory cytokine production and limited protumorigenic inflammatory remodeling, ultimately inhibiting osteosarcoma cell progression. Collectively, our findings reveal a novel GAS5/miR-93-5p/TRIM31/NLRP3 regulatory axis that connects lncRNA-mediated posttranscriptional control to inflammasome signaling in osteosarcoma, providing new mechanistic insight and a potential therapeutic framework for targeting inflammation-associated OS progression.

P=N/A, N=90, Completed, Istituto Ortopedico Rizzoli

The resulting pro-inflammatory microenvironment contributed to the establishment of a lung pre-metastatic niche, thereby promoting OS lung metastasis. These findings underscore the critical role of OS-derived exosomes in lung metastasis and suggest that exosomal miR-27a-3p may serve as a promising therapeutic target in OS lung metastasis.

Subsequent imaging revealed no evidence of metastatic disease, and re-excision showed no residual tumor. Primary superficial Ewing sarcoma is extremely rare, and this is only the second molecularly confirmed case of rectal origin.

PTEN loss occurred frequently (59% 12/22 mice), and contributed to osteosarcomagenesis, as demonstrated by tumor initiation with in vivo CRISPR/Cas9-mediated deletion experiments (2 mice). Together, these results demonstrate that a preclinical model of osteosarcoma can generate the genomic heterogeneity and complexity of the human disease, thereby facilitating research into mechanisms of tumor initiation and drivers of progression and relapse.

Therefore, fisetin-induced autophagy in osteosarcoma cells may be associated with the reactive oxygen species (ROS)/FOXO3 axis, thereby promoting ferroptosis. These findings highlight fisetin's potential as a unique therapy for osteosarcoma.

No significant systemic toxicity was observed. [225Ac]Ac-Macropa-PEG4-IF3 is a translational orphan alpha therapeutic for osteosarcoma with excellent radiochemical stability and potency and low off-target toxicity.

In vitro findings preliminarily suggest that exosomal circVANGL1 may promote DDP resistance in OS cells by regulating the miR-145-5p/E2F3 axis.

Emerging topics such as diagnostic biomarkers, therapeutic targets, and miRNA-related signaling pathways in glioma tumors are central to recent research. This analysis can assist researchers and scientific policymakers in identifying knowledge gaps, strengthening international collaborations, and directing future research efforts.