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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 4152

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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Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Life is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

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

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Published Papers (3 papers)

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Research

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13 pages, 3630 KB  
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
Cited by 1 | Viewed by 1281
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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Review

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34 pages, 2583 KB  
Review
Galectin-3 Release in the Bone Marrow Microenvironment Promotes Drug Resistance and Relapse in Acute Myeloid Leukemia
by Cansu Yıldırım
Life 2025, 15(6), 937; https://doi.org/10.3390/life15060937 - 10 Jun 2025
Viewed by 921
Abstract
Reciprocal signaling between acute myeloid leukemia (AML) cells and the surrounding bone-marrow microenvironment (BMME) promotes AML progression through several mechanisms. One of the most important mechanisms is the induction of Galectin-3 (Gal-3) expression by AML cells and bone marrow mesenchymal stromal cells (BM-MSCs). [...] Read more.
Reciprocal signaling between acute myeloid leukemia (AML) cells and the surrounding bone-marrow microenvironment (BMME) promotes AML progression through several mechanisms. One of the most important mechanisms is the induction of Galectin-3 (Gal-3) expression by AML cells and bone marrow mesenchymal stromal cells (BM-MSCs). Emerging evidence indicates that Gal-3 upregulation in the BMME promotes AML cell adhesion and survival, leading to the development of chemotherapy resistance, relapse, and poor prognosis. Identifying the biological function and critical signaling pathways of Gal-3 may contribute to overcoming acquired drug resistance and preventing post-treatment relapse. Gal-3 is involved in several molecular signaling pathways, including PI3K/AKT/mTOR, Ras/Raf/MEK/ERK, JAK/STAT, JNK, Wnt/β-catenin, PLC/PKC and NF-κB, which are interconnected to promote AML cell survival and resistance to chemotherapy. This review focuses on the biological effects, molecular mechanisms of action and regulation of Gal-3 in the pathogenesis and progression of AML. The therapeutic potential of potent synthetic small-molecule Gal-3 inhibitors in high-risk patients with AML is also discussed based on preclinical and clinical evidence from several human diseases. Currently, the effect of these Gal-3 inhibitors in AML has not been investigated either in vitro or in vivo. The findings provide a rationale for targeting Gal-3 that may be a very promising therapeutic approach, especially for patients with relapsed/refractory AML, and may enhance the efficacy of conventional chemotherapeutic drugs and/or immune checkpoint inhibitors. Full article
(This article belongs to the Special Issue Bone Cancer: From Molecular Mechanism to Treatment)
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Other

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10 pages, 2232 KB  
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 1357
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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