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Life
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Bone Cancer: From Molecular Mechanism to Treatment
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Bone Cancer: From Molecular Mechanism to Treatment

A special issue of Life (ISSN 2075-1729). This special issue belongs to the section "Medical Research".

Deadline for manuscript submissions: 29 August 2025 | Viewed by 1432

Special Issue Editors

Dr. Chih-Yang Lin

E-Mail Website
Guest Editor
Translational Medicine Center, Shin Kong Wu Ho-Su Memorial Hospital, Taipei 111045, Taiwan
Interests: bone cancer; osteoarthritis; metastasis; angiogenesis
Dr. Syuan-Ling Lin

E-Mail Website
Guest Editor
Translational Medicine Research Center, China Medical University Hospital, Taichung City 404327, Taiwan
Interests: cancer therapy; exosomes; mesenchymal stem cells

Special Issue Information

Dear Colleagues,

The exact causes of bone cancer are currently unclear. Some bone cancers are related to genetic factors, while others result from exposure to radiation or drugs used to treat other cancers. However, the causes of most bone cancers remain unknown. In recent years, significant advancements have been made in the medical field for the treatment of bone cancer. High-dose chemotherapy has improved treatment outcomes, and the application of magnetic resonance imaging (MRI) and computed tomography (CT) scans has clearly shown the specific location, extent, and degree of invasion of bone cancer. These advancements have facilitated the complete surgical removal of bone cancer, thereby significantly increasing the success rate of limb salvage surgeries and reducing the need for amputation in a small fraction of patients with bone cancer. Consequently, the five-year survival rate for primary bone cancer can reach 70% or higher when detected and treated early. Nonetheless, if the cancer is at an advanced stage or has metastasized, the five-year survival rate can drop to below 30%. Conventional chemotherapeutic agents tend to be ineffective against metastatic bone cancer due to its heightened malignancy and propensity for invasion. Therefore, there is a pressing need to identify new pre-treatment prognostic markers and develop new targeted drugs as adjuvants for chemotherapy.

Dr. Chih-Yang Lin
Dr. Syuan-Ling Lin
Guest Editors

Manuscript Submission Information

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Keywords

  • bone cancer
  • metastasis
  • angiogenesis
  • targeted drugs
  • biomarkers

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Published Papers (2 papers)

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Research

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13 pages, 3630 KiB  
Article
NGF-TrkA Axis Enhances PDGF-C-Mediated Angiogenesis in Osteosarcoma via miR-29b-3p Suppression: A Potential Therapeutic Strategy Using Larotrectinib
by Sheng-Mou Hou, Ching-Yuan Cheng, Wei-Li Chen, En-Ming Chang and Chih-Yang Lin
Life 2025, 15(1), 99; https://doi.org/10.3390/life15010099 - 15 Jan 2025
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Abstract
Angiogenesis plays a critical role in osteosarcoma (OS) growth and metastasis. While nerve growth factor (NGF) is implicated in cancer progression, its role in OS angiogenesis remains unclear. This study explored NGF’s effects on angiogenesis and the underlying molecular mechanisms. Analysis of GEO [...] Read more.
Angiogenesis plays a critical role in osteosarcoma (OS) growth and metastasis. While nerve growth factor (NGF) is implicated in cancer progression, its role in OS angiogenesis remains unclear. This study explored NGF’s effects on angiogenesis and the underlying molecular mechanisms. Analysis of GEO (GSE16088) data identified five angiogenesis markers significantly upregulated in OS tissues. In vitro experiments demonstrated that NGF enhanced HUVEC tube formation by upregulating platelet-derived growth factor C (PDGF-C) expression and suppressing microRNA-29b-3p (miR-29b-3p). The results of tube formation assays confirmed that NGF stimulation significantly increased the angiogenic capacity of MG63/NGF cells compared to MG63 cells. Furthermore, larotrectinib, a TrkA inhibitor, effectively reduced the migration and invasion abilities of MG63/NGF cells in a dose-dependent manner. These findings suggest that the NGF-TrkA axis promotes PDGF-C-mediated angiogenesis by inhibiting miR-29b-3p signaling. Larotrectinib could serve as a potential therapeutic agent targeting NGF-mediated angiogenesis in OS, offering a promising avenue for treatment. Full article
(This article belongs to the Special Issue Bone Cancer: From Molecular Mechanism to Treatment)
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10 pages, 2232 KiB  
Case Report
Reactivating Sleeping Intramedullary Nail in a 16-Year-Old Female with Polyostotic Fibrous Dysplasia: A Case Report on Complications and Potential Solutions
by Marco Todisco, Marianna Viotto, Laura Campanacci, Giovanni Luigi Di Gennaro, Alessandro Depaoli, Gino Rocca and Giovanni Trisolino
Life 2024, 14(12), 1543; https://doi.org/10.3390/life14121543 - 25 Nov 2024
Viewed by 637
Abstract
Background: Fibrous dysplasia (FD) is a rare condition in which normal spongy and cortical bone is replaced by non-neoplastic fibrous tissue, leading to weakened bone matrix and increased risk of pathological fractures and deformities. Treating these deformities poses a significant challenge for surgeons. [...] Read more.
Background: Fibrous dysplasia (FD) is a rare condition in which normal spongy and cortical bone is replaced by non-neoplastic fibrous tissue, leading to weakened bone matrix and increased risk of pathological fractures and deformities. Treating these deformities poses a significant challenge for surgeons. While various cases of surgical stabilization and limb lengthening using intramedullary nails have been reported, there is limited evidence on the use of Motorized Intramedullary Limb-Lengthening Nails (MILLNs) in FD patients. This case report presents the clinical history of a patient with FD who underwent multiple surgical interventions to address severe lower limb length discrepancy (LLD) and angular deformity caused by multiple fractures. Case presentation: A sixteen-year-old Caucasian girl with polyostotic FD developed a severe post-traumatic LLD of 10 cm on the right side, associated with coxa vara, valgus knee, and patellar instability. The deformity of the proximal femur was addressed with a valgus and derotational femoral osteotomy. However, this procedure exacerbated the knee’s valgus deformity and only partially corrected the LLD, leading to the decision to proceed with femoral lengthening. A retrograde magnetic intramedullary nail (PRECICE, NuVasive) was utilized for this purpose. Approximately three months postoperatively, radiographs revealed the loosening of the proximal anchoring screw, while the nail had reached maximum distraction. We then proposed reactivating the previously implanted nail. Nine months after the final surgery, standing long-leg radiographs showed a residual shortening of 1 cm, with excellent healing at the fracture sites and the nail and screws remaining securely in place. The patient was monitored regularly, with the latest follow-up occurring four years and five months after the conclusion of the last lengthening procedure. Conclusions: This case report describes the reactivation of a MILLN in a patient with polyostotic fibrous dysplasia. While nail reactivation has been previously described in the literature, to our knowledge, it has not been reported for treating complications arising from FD. In cases of mechanical complications, this approach can equalize leg length discrepancies and correct deformities, avoiding additional invasive surgeries and reducing healthcare costs. As this is an off-label treatment, preoperative consent from both the patient and the parents is required. Full article
(This article belongs to the Special Issue Bone Cancer: From Molecular Mechanism to Treatment)
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