Osteosarcoma

CD36⁺ CAFs drive immunosuppressive metabolic reprogramming via the OxLDL-PPARG-ANGPTL4 axis, promoting CD8⁺ T cell exhaustion and resistance to immunotherapy in osteosarcoma. Targeting this pathway with VitE alleviated CAF-mediated immune suppression and enhanced PD-1 blockade responses in preclinical models, providing a rationale for metabolism-based combinatorial strategies in osteosarcoma.

P2, N=70, Active, not recruiting, M.D. Anderson Cancer Center | Not yet recruiting --> Active, not recruiting | Initiation date: May 2026 --> Dec 2025

Doxorubicin (DOX) forms stable π-π stacking complexes with PDA, creating a versatile chemotherapeutic delivery platform...We hypothesize that this integrated approach will demonstrate enhanced antitumor efficacy while promoting functional bone reconstruction. Comprehensive in vitro evaluations will elucidate the underlying mechanisms and provide preclinical validation for this precision oncology strategy.

Importantly, multiomics analyses reveal a unique mechanism of action: APT NPs induce the upregulation of the stress-responsive gene DNA damage-inducible transcript 4 (DDIT4), which inhibits the mammalian target of the rapamycin complex 1 (mTORC1) signaling pathway...In vivo, the MCF-7 tumor-bearing mouse model confirms potent antitumor efficacy without significant side effects. This work not only introduces a hypoxia-insensitive PDT agent but also provides novel insights into the mechanistic interaction between transcriptional and metabolic regulation in PDT, highlighting the potential of AIE-active materials for cancer therapy.

None malignant transformations occurred following denosumab or radiotherapy...SM-GCTB and osteosarcoma arise from benign GCTB but differ in morphology and prognosis. Because malignant transformation is exceptionally rare and symptomatic, a patient-centered, symptom-driven follow-up strategy is preferred over routine lifelong radiologic surveillance.

This review systematically synthesizes: BME composition and tumor-induced reprogramming, Mechanistic roles in metastasis and treatment resistance, Emerging targeted therapies and translational trade-offs. By positioning the BME as both a pathogenic driver and therapeutic vulnerability, we aim to inform future strategies for tissue-specific microenvironmental targeting in bone malignancies.

Taken together, these findings suggest that FGF-23 promotes osteosarcoma cell migration and may contribute to metastasis through coordinated regulation of the miR-4463/LOXL2 axis via ERK, p38, and JNK signaling. Targeting FGF-23 or its downstream signaling cascades may offer a promising therapeutic approach for metastatic osteosarcoma.

CONCLUSIONS PPOS can present as a lesion smaller than 2 cm. An integrated imaging-pathology workup and early resection can yield favorable short-term outcomes.

Adjuvant drugs can reduce inflammation and neuropathic pain, including corticosteroids, gabapentinoid agents such as gabapentin or pregabalin, lidocaine patches, tricyclic antidepressants such as amitriptyline, nortriptyline, and desipramine, or selective serotonin-norepinephrine reuptake inhibitors such as duloxetine and venlafaxine. The present investigation aims to synthesize currently available data on periosteal osteosarcomas, including common clinical, histologic, and radiographic presentations. In addition, this review aims to further examine the potential for biomarkers and provide recommendations for treatment and future research direction.

Our preclinical study investigates the possible therapeutic mechanism of plumbagin against osteosarcoma, indicating that plumbagin exhibited anti-osteosarcoma features via regulation of core target genes associated with autophagy. Current research findings may provide the scientific ideas and evidences for screening bioactive compound against osteosarcoma.

This review explores chondrosarcoma subtypes, diagnostic approaches, prognostic factors, and molecular alterations, followed by a discussion of current and emerging treatment strategies. Emphasis is placed on clinical trials investigating targeted therapies or immunotherapies for advanced chondrosarcoma, including inhibitors of IDH1/2 and multiple kinases, death receptor 5 agonism, and other potential new therapeutic approaches.

This study emphasizes the value of molecular techniques in improving the diagnosis and management of maxillofacial OS. However, further research is needed to fully understand the molecular complexity and optimize therapeutic strategies.