Journal of Bone Oncology最新文献

{"title":"Metastatic bone disease in proximal femur. Outcome of surgical treatments. − Do we know what to do?","authors":"K. Kilk ,&nbsp;G. Kask ,&nbsp;J. Nieminen ,&nbsp;M.K. Laitinen","doi":"10.1016/j.jbo.2025.100711","DOIUrl":"10.1016/j.jbo.2025.100711","url":null,"abstract":"<div><h3>Background</h3><div>Skeletal metastases related pathological fracture reconstruction methods in proximal femur range from osteosynthesis to tumor prostheses with acetabular reconstruction, depending on lesion size and location. This retrospective study, of 299 patients surgically treated for proximal femur metastases, investigates implant survival, complications, and functional outcomes of various surgical strategies for treating pathological fractures of the proximal femur.</div></div><div><h3>Patients and methods</h3><div>This retrospective study of 299 patients surgically treated for proximal femur metastases, investigates implant survival (Kaplan–Meier), complications, and functional outcomes of different surgical strategies. The chi-test and Mann-Witney <em>U</em> test were used for analysis between groups. The subdistribution Hazard Ratio (SHR) of the role of factors affecting implant survival was calculated using competing risk analysis.</div></div><div><h3>Results</h3><div>Reconstruction methods comprised osteosynthesis (n = 59), hemiarthroplasty (n = 72), total hip replacement (THA) (n = 43), and endoprosthetic replacement (EPR) either with or without acetabular component (n = 125). The precise location and size of the metastases was evaluated. The mean implant survival was 17 months (SD 21.2). Complications occurred in 33 patients, 20 required revision surgery. In prosthesis patients, infections and dislocations were the main complications, while mechanical failure predominated in the osteosynthesis group. Mean implant failure time was 11 months, shortest in THA and osteosynthesis. Functional outcomes in 38 patients showed a mean Oxford Hip Score (OHS) of 33, with no significant differences across methods.</div></div><div><h3>Interpretation</h3><div>Patient survival is a critical factor in selecting the appropriate reconstruction method for trochanteric metastatic lesions. Osteosynthesis is suitable for patients with a limited life expectancy. In cases of metastases involving the head-neck anatomical region, arthroplasty with acetabular reconstruction offers no advantage over hemiarthroplasty. With our data there was no statistical difference in functional outcome between different surgical methods.</div></div>","PeriodicalId":48806,"journal":{"name":"Journal of Bone Oncology","volume":"54 ","pages":"Article 100711"},"PeriodicalIF":3.5,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145026898","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"RGS1 stabilized by METTL3-mediated m6A modification promotes the tumorigenicity and macrophage M2 polarization in osteosarcoma","authors":"Zhizhong Liang ,&nbsp;Yuxia Shi ,&nbsp;Mao Wang ,&nbsp;Liqiang Zhang","doi":"10.1016/j.jbo.2025.100705","DOIUrl":"10.1016/j.jbo.2025.100705","url":null,"abstract":"<div><h3>Background</h3><div>Regulators of G-protein signaling 1 (RGS1) has been reported to be involved in immune cell regulation in many cancer types. However, the specific role and mechanism in osteosarcoma (OS) progression and macrophage activation remain unclear.</div></div><div><h3>Methods</h3><div>Levels of mRNA and protein were examined using qRT-PCR and western blotting. Transwell assay, wound healing assay, EdU assay and flow cytometry were used to investigate OS cell invasion, migration, proliferation and apoptosis. Xenografts in mice were established for in vivo assay. Macrophage M2 polarization was evaluated by detecting CD206 + macrophages by flow cytometry. ELISA analysis detected IL-6 and TGF-β1 levels. Methylated RNA immunoprecipitation assay was applied to explore the specific binding of RGS1 and METTL3 (methyltransferase-like 3).</div></div><div><h3>Results</h3><div>RGS1 was highly expressed in OS tissues and cells. The silencing of RGS1 suppressed OS cell invasion, migration, growth and impaired immune response by inhibiting macrophage M2 polarization and M2 macrophage-mediated release of IL-10 and TGF-β1. Mechanistically, METTL3 promoted RGS1 m6A modification and stabilized its expression. METTL3 deficiency also inhibited OS cell invasion, migration, growth and macrophage M2 polarization, while these effects could be abolished by RGS1 overexpression. Besides that, IL–10 elevation induced by M2 macrophages promoted OS cell oncogenic phenotypes.</div></div><div><h3>Conclusion</h3><div>METTL3 stabilized RGS1 mRNA in an m6A-dependent manner to promote the tumorigenicity and macrophage M2 polarization in osteosarcoma, suggesting a novel insight into the therapy of osteosarcoma.</div></div>","PeriodicalId":48806,"journal":{"name":"Journal of Bone Oncology","volume":"54 ","pages":"Article 100705"},"PeriodicalIF":3.5,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144781766","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Osteofibrous dysplasia, osteofibrous Dysplasia-Like adamantinoma, and adamantinoma: A Single-center retrospective analysis","authors":"Wei Chen ,&nbsp;Qinglin Jin ,&nbsp;Shaohua Du ,&nbsp;Shuangwu Dai ,&nbsp;Changhe Hou ,&nbsp;Zixiong Lei ,&nbsp;Lin Zhong ,&nbsp;Qingzhu Wei ,&nbsp;Haomiao Li","doi":"10.1016/j.jbo.2025.100700","DOIUrl":"10.1016/j.jbo.2025.100700","url":null,"abstract":"<div><h3>Objective</h3><div>This study aimed to comprehensively investigate and contrast the imaging manifestations, pathological features, surgical interventions, and prognostic outcomes of <strong>Osteofibrous Dysplasia(OFD)</strong>, <strong>Osteofibrous Dysplasia-Like Adamantinoma(OFD-AD)</strong>, and <strong>Adamantinoma(AD)</strong>. By synthesizing disease profiles and exploring their evolutionary relationships, we sought to identify more effective diagnostic and therapeutic strategies for these conditions.</div></div><div><h3>Methods</h3><div>A retrospective analysis was conducted on patients diagnosed with OFD, OFD-AD, or AD at our institution between 2015 and 2022. The analysis included a detailed comparison of clinical presentations, imaging findings, and pathological characteristics. We also evaluated the impact of different diagnostic and treatment modalities on patient prognosis and explored potential disease evolution and transformation patterns.</div></div><div><h3>Results</h3><div>Fifty patients were included in this study: 16 with OFD, 27 with OFD-AD, and 7 with AD. The median age of onset was 14 years for OFD, 6 years for OFD-AD, and 33 years for AD. All diagnoses were confirmed through a combination of clinical evaluation, imaging (X-rays and MRI), and pathological examination. Among the patients, 2 (both with OFD-AD) were managed with observation only. Thirty-seven patients underwent intralesional resection (16 OFD, 20 OFD-AD, and 1 AD), and 11 patients had complete resection (5 OFD-AD and 6 AD). After a minimum follow-up of 24 months (range: 24–––90 months, median: 56 months), 12 patients experienced tumor recurrence (OFD: 2/16, 12.5 %; OFD-AD: 9/25, 36 %; AD: 1/6, 17 %). One patient had concurrent OFD-AD in the fibula and AD in the tibia. In another case, an OFD-AD recurrence 4 years after surgery was later diagnosed as OFD, and an OFD recurrence 2 years after surgery was reclassified as OFD-AD. No distant metastases were observed in any patient.</div></div><div><h3>Conclusion</h3><div>OFD, OFD-AD, and AD exhibit similarities in clinical and imaging presentations, and their pathological features may represent different stages of a common lesion’s evolution. These diseases have distinct age − related onset patterns and variable recurrence risks. Thus, accurate diagnosis and personalized treatment strategies based on patient characteristics are crucial for effective disease management.</div></div>","PeriodicalId":48806,"journal":{"name":"Journal of Bone Oncology","volume":"53 ","pages":"Article 100700"},"PeriodicalIF":3.4,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144519166","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Impact of treatment delay of multiple myeloma bone disease on later myeloma-related skeletal events and outcome","authors":"Eskelinen Veera ,&nbsp;Niemi Pauli ,&nbsp;Partanen Anu ,&nbsp;Kangas Jaakko ,&nbsp;E.L.Kuusisto Milla","doi":"10.1016/j.jbo.2025.100693","DOIUrl":"10.1016/j.jbo.2025.100693","url":null,"abstract":"<div><div>Limited data exists on the effect of treatment delay of multiple myeloma (MM) bone disease on the disease course. In this real-world analysis of 625 patients with newly diagnosed MM (NDMM) we aimed to investigate the impact of delay in starting bone disease treatment on later skeletal events and outcome.</div><div>Altogether 480 (76.8 %) patients had bone disease at the diagnosis, 282 (45.1 %) patients had a fracture at diagnosis, and 181 (29.1 %) patients had a later fracture during the follow-up. A delay in the initiation of treatment of bone disease was experienced by 221 (35.4 %) patients and tooth extraction was a main reason for the delay. Patients with a delay seemed to experience earlier and more frequent later fractures. Also, a fracture (p = 0.003) or bone disease (p &lt; 0.001) at diagnosis predicted earlier incidence of later fractures. As a bone targeted treatment, altogether 363 (58.1 %) patients received zoledronic acid, 81 (13.0 %) denosumab and 134 (21.4 %) other bone-targeted treatment. Patients treated with denosumab had poorer overall survival (OS) (p &lt; 0.001) and experienced earlier later fractures (p = 0.003). Multivariate analysis showed that bone disease at diagnosis (p = 0.043) and given bone disease treatment (p = 0.023) significantly impacted on the time to next fracture. Regarding OS, delay in osteoprotective treatment (p = 0.004) and time of the diagnosis (p &lt; 0.001) were significant factors in multivariate analysis.</div><div>To conclude, this study suggests that early initiation of bone disease treatment seemed to prevent later fractures. These findings highlight the importance of patients’ rapid access to a dentist and the start of bone targeted treatment without delay after a myeloma diagnosis.</div></div>","PeriodicalId":48806,"journal":{"name":"Journal of Bone Oncology","volume":"53 ","pages":"Article 100693"},"PeriodicalIF":3.4,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144241901","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Glutathione peroxidase 7 knockdown inhibits growth, invasion, and migration while enhancing oxidative stress and ferroptosis in osteosarcoma cells","authors":"Runze He ,&nbsp;Xiao Xiao ,&nbsp;Xinwen Tang ,&nbsp;Chen Lv","doi":"10.1016/j.jbo.2025.100692","DOIUrl":"10.1016/j.jbo.2025.100692","url":null,"abstract":"<div><h3>Background</h3><div>Glutathione peroxidase 7 (GPX7) possesses antioxidant functions and plays a crucial role in regulating cancer progression. However, relevant evidence in osteosarcoma is scarce. The current study aimed to explore the effect of GPX7 on osteosarcoma progression, oxidative stress, and ferroptosis.</div></div><div><h3>Methods</h3><div>Human osteosarcoma cells (U2OS, MG-63, and SaOS-2) were transfected with GPX7 small interfering RNA (siGPX7). Proliferation, apoptosis, invasion, migration, oxidative stress markers, Fe²⁺ levels, and ferroptosis markers were detected in human osteosarcoma cells.</div></div><div><h3>Results</h3><div>GPX7 knockdown inhibited human osteosarcoma cell proliferation, as evidenced by reduced relative cell viability and 5-Ethynyl-2′-deoxyuridine positive cells. GPX7 knockdown also showed a certain ability to promote human osteosarcoma cell apoptosis, as evidenced by increased terminal-deoxynucleotidyl transferase-mediated nick end labeling (TUNEL) positive rate and cleaved-caspase3. GPX7 knockdown decreased invasive and migration rates of human osteosarcoma cells. GPX7 knockdown increased reactive oxygen species and malondialdehyde but decreased mitochondrial membrane potential, suggesting that GPX7 knockdown enhanced oxidative stress in human osteosarcoma cells. Regarding ferroptosis markers, GPX7 knockdown increased acyl-CoA synthetase long-chain family member 4 and reduced solute carrier family 7 member 11; moreover, GPX7 knockdown increased Fe²⁺ levels; the above findings indicated that GPX7 knockdown promoted ferroptosis in human osteosarcoma cells.</div></div><div><h3>Conclusion</h3><div>GPX7 knockdown inhibits osteosarcoma cell growth, invasion, and migration while facilitating oxidative stress and ferroptosis.</div></div>","PeriodicalId":48806,"journal":{"name":"Journal of Bone Oncology","volume":"53 ","pages":"Article 100692"},"PeriodicalIF":3.4,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144480639","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Management of aromatase inhibitor-associated bone loss (AIBL) in women with hormone-sensitive breast cancer: An updated joint position statement of the IOF, CABS, ECTS, IEG, ESCEO, IMS, and SIOG","authors":"Peyman Hadji ,&nbsp;Matty Aapro ,&nbsp;Nasser Al-Dagri ,&nbsp;Majed Alokail ,&nbsp;Emmanuel Biver ,&nbsp;Jean-Jacques Body ,&nbsp;Maria Luisa Brandi ,&nbsp;Janet Brown ,&nbsp;Cyrille Confavreux ,&nbsp;Bernard Cortet ,&nbsp;Matthew Drake ,&nbsp;Peter Ebeling ,&nbsp;Erik Fink Eriksen ,&nbsp;Ghada El-Hajj Fuleihan ,&nbsp;Theresa A. Guise ,&nbsp;Nick C. Harvey ,&nbsp;Andreas Kurth ,&nbsp;Bente Langdahl ,&nbsp;Willem Lems ,&nbsp;Radmila Matijevic ,&nbsp;Robert Coleman","doi":"10.1016/j.jbo.2025.100694","DOIUrl":"10.1016/j.jbo.2025.100694","url":null,"abstract":"<div><h3>Background</h3><div>Women with hormone-responsive breast cancer who receive adjuvant endocrine treatment with aromatase inhibitors (AI) are known to be at higher fracture risk due to a marked increase in bone resorption. In 2017, several interdisciplinary cancer and bone societies involved in the management of women with AI-associated bone loss (AIBL) published a joint position statement comprising evidence-based recommendations and a practical management algorithm for the assessment of fracture risk and optimal treatment of this patient population.</div></div><div><h3>Patients and methods</h3><div>In order to provide updated recommendations that reflect recent advances in the assessment and management of AIBL since publication of the 2017 joint position statement, a systematic literature review was undertaken to identify relevant studies for analysis, including systematic reviews and meta-analyses. Individual trials identified were assessed for their level of evidence based on design, size, follow-up, and evaluation of safety, as well as the impact of bone directed treatments on breast cancer outcomes.</div></div><div><h3>Results</h3><div>New evidence was combined with the existing recommendations to provide an updated joint position statement regarding fracture risk assessment and implementation of bone-directed therapy.</div></div><div><h3>Conclusion</h3><div>Current published literature, including recent clinical trial reports, systematic reviews and meta-analyses, continue to affirm the high risk of fractures in women with breast cancer who are receiving adjuvant AI treatment, a risk which has been observed to increase with the commonly used approach of extended duration AI therapy (&gt;5 years). Risk factors for fracture and risk assessment in this patient population as well as the most suitable treatment modalities have been updated. Finally, the influence of bone protective treatments on breast cancer outcomes such as incidence of bone metastasis and breast cancer related overall survival have been included.</div></div>","PeriodicalId":48806,"journal":{"name":"Journal of Bone Oncology","volume":"53 ","pages":"Article 100694"},"PeriodicalIF":3.4,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144662193","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"COPB2 as a key regulator of cell growth in human osteosarcoma cells: Potential therapeutic target and prognostic indicator","authors":"Yunpeng Cui ,&nbsp;Xuedong Shi ,&nbsp;Qiwei Wang ,&nbsp;Wence Wu ,&nbsp;Yuanxing Pan ,&nbsp;Bing Wang ,&nbsp;Mingxing Lei","doi":"10.1016/j.jbo.2025.100702","DOIUrl":"10.1016/j.jbo.2025.100702","url":null,"abstract":"<div><h3>Purpose</h3><div>Coatomer protein complex subunit beta 2 (COPB2) is a crucial component of the coatomer protein complex I, responsible for vesicle transport. Previous studies have indicated that COPB2 is highly expressed in malignant tumors and is involved in cell proliferation and apoptosis. However, the role of COPB2 in osteosarcoma and its underlying mechanisms remain unclear. This study aimed to investigate the impact of COPB2 on proliferation, apoptosis, and colony formation in human osteosarcoma cells, as well as to explore potential mechanisms.</div></div><div><h3>Methods</h3><div>Kaplan-Meier survival analysis was conducted to assess the association between COPB2 expression and the prognosis of osteosarcoma patients using data extracted from the Cancer Genome Atlas (TCGA) database. Additionally, COPB2 expression was examined in osteosarcoma tissue samples and four osteosarcoma cell lines using immunohistochemistry and quantitative real-time PCR (qRT-PCR). COPB2 expression was downregulated using siRNA in U2OS and SAOS-2 human osteosarcoma cells. Cell proliferation and colony formation were assessed using Cellomics/Celigo and Giemsa staining, respectively. Flow cytometry was used to evaluate cell cycle distribution and apoptosis. Tumor growth was evaluated in vivo model. Furthermore, the regulation mechanism of COPB2 on osteosarcoma cells was investigated using the Human Phospho-Kinase Array Kit.</div></div><div><h3>Results</h3><div>Patients with high COPB2 expression exhibited shorter overall survival and disease-free survival compared to those with low COPB2 expression. COPB2 was found to be highly expressed in osteosarcoma tissue samples and cell lines. Silencing of COPB2 significantly inhibited cell proliferation and colony formation. Additionally, COPB2 silencing altered the cell cycle distribution, leading to cell cycle arrest in the G2 phase, and promoted cell apoptosis in osteosarcoma cells. Further investigations revealed that COPB2 silencing inhibited tumor growth and lung metastases of osteosarcoma cells in vivo, and its effects on cell proliferation and apoptosis may be mediated through the regulation of kinase phosphorylation levels.</div></div><div><h3>Conclusions</h3><div>COPB2 expression is increased in osteosarcoma cells and plays a crucial role in cell growth regulation. Silencing of COPB2 inhibits cell proliferation, colony formation, and promotes cell apoptosis. Furthermore, COPB2 silencing inhibits tumor growth in vivo, suggesting its potential as an important therapeutic target in treating osteosarcoma.</div></div>","PeriodicalId":48806,"journal":{"name":"Journal of Bone Oncology","volume":"53 ","pages":"Article 100702"},"PeriodicalIF":3.4,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144653531","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Yin Yang 1 protein-activated N-acetyltransferase 10 drives cell malignant progression of osteosarcoma through ac4C acetylation of integrin β3","authors":"Fan Yang,&nbsp;Mao Wang","doi":"10.1016/j.jbo.2025.100701","DOIUrl":"10.1016/j.jbo.2025.100701","url":null,"abstract":"<div><h3>Background</h3><div>N-acetyltransferase 10 (NAT10) acts as the “writer” of N4-acetylcytidine (ac4C) modification in tumor progression, including osteosarcoma (OS). Its molecular mechanism in OS remains not fully clear. This study endeavored to disclose the upstream and downstream mechanism of NAT10 related to Yin Yang 1 protein (YY1) and integrin β3 (ITGB3) in OS.</div></div><div><h3>Methods</h3><div>Gene mRNA and protein levels were assayed via real-time quantitative PCR and Western blotting. Cell counting kit-8, EdU assay, flow cytometry/TUNEL staining assay, transwell assay, and scratch assay were conducted to assess cell viability, proliferation, apoptosis, invasion, and migration. Interaction analysis was completed through ac4C RNA immunoprecipitation (ac4c RIP), RIP, chromatin IP and dual-luciferase reporter assay. <em>In vivo</em> assay was carried out using xenograft models in mice.</div></div><div><h3>Results</h3><div>OS tissues and cells showed the high expression of NAT10. Cell proliferation, invasion, and migration were suppressed but apoptosis was enhanced in NAT10-silenced OS cells. GSE237541 dataset has predicted the inhibition of ITGB3 after NAT10 knockdown, and PACES website predicted ac4C site in ITGB3. Furthermore, it was found that NAT10 could up-regulate ITGB3 expression by mediating ac4C acetylation. ITGB3 overexpression recused OS cell progression inhibition caused by NAT10 knockdown. Jaspar predicted the binding between YY1 and NAT10 promoter. YY1 could activate the transcriptional regulation of NAT10 to increase NAT10 expression, and YY1 depletion blocked cell malignant behaviors via reducing NAT10 expression. More importantly, YY1 interacted with NAT10 to up-regulate ITGB3 expression. <em>In vivo</em>, NAT10/ITGB3 axis also promoted OS tumor growth in mice.</div></div><div><h3>Conclusion</h3><div>YY1 was firstly affirmed to regulate transcription of NAT10, and NAT10 was firstly indicated to mediate ac4C modification of ITGB3. YY1-activated NAT10 could affect ITGB3 and then modulated the malignant development of OS.</div></div>","PeriodicalId":48806,"journal":{"name":"Journal of Bone Oncology","volume":"53 ","pages":"Article 100701"},"PeriodicalIF":3.4,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144653532","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effectiveness of rehabilitation treatment for bone metastasis patients without surgical intervention: A propensity score matching analysis","authors":"Ryo Yoshikawa ,&nbsp;Yasumitsu Fujii ,&nbsp;Ryoga Kashima ,&nbsp;Wataru Saho ,&nbsp;Risa Harada ,&nbsp;Daisuke Makiura ,&nbsp;Katsuya Fujiwara ,&nbsp;Junichiro Inoue ,&nbsp;Yoshiki Takeoka ,&nbsp;Ryoko Sawada ,&nbsp;Naomasa Fukase ,&nbsp;Keisuke Oe ,&nbsp;Hitomi Hara ,&nbsp;Kenichiro Kakutani ,&nbsp;Toshihiro Akisue ,&nbsp;Yoshitada Sakai","doi":"10.1016/j.jbo.2025.100703","DOIUrl":"10.1016/j.jbo.2025.100703","url":null,"abstract":"<div><div>Evidence regarding the effectiveness of rehabilitation treatments in patients with bone metastases remains limited. This study evaluated the implementation and effectiveness of rehabilitation in patients with bone metastases who did not undergo surgery. This retrospective study included 200 patients with nonsurgically treated bone metastases at our institution. The patients were categorized into a rehabilitation group (R group, n = 61) and a non-rehabilitation group (N group, n = 139). Over the course of one month, we compared activities of daily living (ADL), assessed using the Barthel Index (BI), quality of life (QOL), measured using the EuroQoL-5 Dimension (EQ-5D), and demographic and clinical characteristics. Propensity score matching was conducted to minimize selection bias. After matching, 31 patients in each group were included in the analysis. No statistically significant differences were observed in baseline BI and EQ-5D scores between the two groups. In the R group, BI improved significantly from 80 (interquartile range [IQR]: 60–100) to 90 (IQR: 70–100), and EQ-5D improved from 0.444 (IQR: 0.282–0.608) to 0.608 (IQR: 0.533–0.768). In contrast, no improvements were observed in either score in the N group. Chemotherapy was identified as a significant factor associated with improvements in BI (odds ratio 4.03) and EQ-5D (odds ratio 5.29). Rehabilitation may be a valuable treatment option for nonsurgically treated patients with bone metastases, warranting further validation in prospective studies.</div></div>","PeriodicalId":48806,"journal":{"name":"Journal of Bone Oncology","volume":"53 ","pages":"Article 100703"},"PeriodicalIF":3.4,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144678759","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exploring bone-tumor interactions through 3D in vitro models: Implications for primary and metastatic cancers","authors":"Nicolas Cristini ,&nbsp;Mohamadreza Tavakoli ,&nbsp;Mehdi Sanati ,&nbsp;Saber Amin Yavari","doi":"10.1016/j.jbo.2025.100698","DOIUrl":"10.1016/j.jbo.2025.100698","url":null,"abstract":"<div><div>Bone tissue serves as a perfect hosting site where metastatic cancer cells of the most prevalent cancer types, such as prostate and breast cancers, as well as the native bone sarcomas, can further proliferate, advancing the disease stage with the consequential decline of the patient’s prognosis. Understanding how the bone niche interacts with tumor cells and the mechanisms leading to drug resistance is a crucial step for enabling the identification of effective cancer therapies. Nevertheless, bone tumor research and the development of new effective anticancer drugs have been hampered for a long time due to the limitations of preclinical models. Traditional 2D cultures and animal models have failed to accurately replicate the human bone cancer microenvironment, driving researchers to develop 3D <em>in vitro</em> bone models using tissue-engineered bone constructs and advanced technologies like microfluidics and additive manufacturing. While a complete reproduction of the bone tumor microenvironment (TME), including all relevant cell types, stromal elements, and biophysical cues, remains elusive, targeted inclusion of key components has advanced the physiological relevance of these models. The following review evaluates the biomimetic approaches that have been used to recapitulate the bone TME through 3D <em>in vitro</em> models, with particular attention to recent studies aimed at more accurately mimicking the complexity of bone TME, highlighting future directions and the advancements required to overcome present limitations.</div></div>","PeriodicalId":48806,"journal":{"name":"Journal of Bone Oncology","volume":"53 ","pages":"Article 100698"},"PeriodicalIF":3.4,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144314338","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}