Background 18F-fluorodeoxyglucose positron emission tomography/computed tomography (18F-FDG-PET/CT) is useful for assessing location, metastasis, staging, and recurrence of malignant tumors. Tenosynovial giant cell tumor (TSGCT) is a benign tumor; however, some studies have reported that TSGCTs have a high uptake of FDG. Few studies have reported on the detailed evaluation of TSGCT using 18F-FDG-PET/CT. The purpose of the current study is to evaluate the image characteristics and locations, particularly where possible, with or without, extra-articular invasion from TSGCT of the knee in 18F-FDG-PET/CT could occur. Methods We retrospectively reviewed the patients with TSGCT who were diagnosed pathologically either by biopsy or surgical specimen. Furthermore, we evaluated the difference of the maximum standardized uptake value (SUVmax) between diffused TSGCT with extra-articular invasion and TSGCT with intra-articular localization in the knee. Results The study consisted of 20 patients with TSGCT. The mean SUVmax of TSGCT was 12.0 ± 6.50. There were five patients with TSGCT arising in the knee with extra-articular invasion and six with TSGCT with intra-articular localization. The mean SUVmax of TSGCT with extra-articular invasion and those with intra-articular localization were 14.3 ± 6.00 and 5.94 ± 3.89, respectively. TSGCT with extra-articular invasion had significantly higher SUVmax than TSGCT with intra-articular localization (p < 0.05). Conclusions TSGCT revealed high FDG uptake. Furthermore, SUVmax was higher in diffused TSGCT with extra-articular invasion than in intra-articular localized TSGCT; this may reflect its local aggressiveness.

An 83-year-old woman presented with a 1-year history of a growing mass on the lateral surface of the right knee. Magnetic resonance imaging revealed a large soft tissue tumor in the subcutis of the right knee. The mass in the right knee rapidly increased, due to hemorrhage from the tumor. A needle biopsy revealed that the diagnosis was synovial sarcoma. The patient underwent wide excision and lateral collateral ligament reconstruction using the plantaris tendon. The patient had a Musculoskeletal Tumor Society Score of 86% at the lateset follow-up. In conclusion, reconstruction of the lateral collateral ligament using the plantaris tendon may be useful for preserving the function of the knee joint after resection of the soft tissue due to sarcoma of the knee.

Giant cell tumor of bone (GCTB) is an intermediate and locally aggressive bone tumor. Alpha-tricalcium phosphate (alpha-TCP) is an adjustable bone substitute used to fill various sizes of bone cavities after curettage for GCTB. This study aimed to evaluate the surgical outcome of packing with alpha-TCP followed by curettage and phenol-ethanol ablation. We retrospectively reviewed data of 16 patients with GCTB who underwent primary surgery in our institute between January 2009 and April 2021. Data of Campanacci grading system; number of local recurrences and distant metastases; local recurrence-free survival rate using the Kaplan-Meier method; oncological outcomes; and complications after surgery (secondary osteoarthritis and postoperative fracture) were evaluated in this study. Regarding the Campanacci grading system, 2 patients were classified as grade I, 14 as grade II, and none as grade III. The 5-year local recurrence-free survival rate was 77.8% in all cases. Lung metastasis was not detected in this study. Oncological outcomes were: continuous disease free, 13 patients; alive with disease, 3 patients; and no evidence of disease or death of disease, none of the patients. Secondary osteoarthritis after surgery was not detected in the present study. Packing with alpha-TCP followed by curettage and phenol-ethanol ablation for appendicular GCTB may be safe and effective in suppressing the risk of secondary osteoarthritis.Abbreviations: CPC = calcium phosphate cement, GCTB = giant cell tumor of bone, K-L = Kellgren-Lawrence, LRFS = local recurrence-free survival, MPa = megapascal, PMMA = poly methyl methacrylate, TCP = tricalcium phosphate.

Hip rotationplasty is a surgical method used to treat malignant tumors of the proximal femur. A 52-year-old woman, who underwent hip rotationplasty for Ewing sarcoma of the proximal left femur at the age of 24, fell and hit the left buttock. The patient was then admitted to the Department of Orthopedic Surgery, Graduate School of Medicine, University of the Ryukyus. Radiography and computed tomography (CT) revealed a comminuted fracture of the reconstructed bone distally. The patient underwent open reduction and internal fixation (ORIF) and external fixator. External fixation was removed 1 month after the surgery. At two years after surgery, at the latest follow-up, bone union was confirmed by 3-dimensional CT. The combination of ORIF and temporal external fixation was effective for the reconstructed bone fractures after hip rotationplasty.

Since methotrexate (MTX) resistance of osteosarcoma is a frequent cause of poor prognosis, new treatment strategies are needed to overcome this recalcitrant problem. The present study investigated if MTX resistance increased malignancy of osteosarcoma cells and its possible mechanism, via histone-H3 lysine-methylation status. We also propose a new therapeutic strategy for MTX resistant osteosarcoma. MTX resistant 143B osteosarcoma cells (143B-MTXR) were established from 143B parental osteosarcoma cells (143B-P) by culturing the cells with increasing concentrations of MTX stepwise (0.04 μM to 100 μM) for 12 months. The degree of malignancy of the isogenic pair of 143B-MTXR and 143B-P cells was compared by testing clonogenic capacity in cell culture, on both plastic and soft agar. Malignancy was also compared by tumor growth in orthotopic xenograft mouse models by implantation of 2.5 × 105 cells in the tibia of nude mice. Histone-H3 lysine-methylation status was determined by Western immunoblotting. 143B-MTXR and 143B-P cells were also tested for methionine addiction by sensitivity to recombinant methioninase (rMETase). Welch’s t-test was performed to statistically evaluate results and a probability value ≤ 0.05 was defined as statistically-significant difference. The mouse studies were approved by Institutional Animal Care and Use Committee of AntiCancer Inc. After 12 months selection in increasing concentrations of MTX, we isolated 143B-MTXR cells, which had an MTX IC50 of 384 μM compared to 143B-P cells, which had an IC50 of 0.27 μM, demonstrating that the 143B-MTXR cells acquired a 1422-fold resistance to MTX. In cell culture, 143B-MTXR cells had reduced clonogenic capacity on plastic and in soft agar (P &lt; 0.01), indicating reduction in malignancy. In orthotopic xenograft nude-mouse studies, 143B-MTXR cells formed much smaller tumors than 143B-P cells (P &lt; 0.01), further indicating that 143B-MTXR cells lost malignancy. 143B-MTXR cells showed an increase of histone H3K9me3 (P = 0.01), H3K27me3 (P &lt; 0.01), and H3K79me3 (P &lt; 0.01) methylation, which may account in part for their decreased malignancy. However, there was no difference in methylation of H3K4me3 (P = 0.12) or H3K36me3 (P = 0.29). The 143B-MTXR cells had an IC50 of 0.358 U/ml for rMETase, similar to an IC50 of 0.38 U/ml for 143B-P cells, indicating the 143B-MTXR cells did not lose their methionine addiction. The increase in histone H3K9me3, H3K27me3, and H3K79me3 shown in the present study in 143B-MTXR cells suggested potential biomarkers of methotrexate-resistance. MTX resistant osteosarcoma may be treated by methionine restriction with rMETase, as the MTX-resistant osteosarcoma cells are highly methionine addicted. Citation Format: Yusuke Aoki, Yasunori Tome, Hiromichi Oshiro, Ryo Katsuki, Kohei Mizuta, Kotaro Nishida, Robert M. Hoffman. Alteration of malignancy and histone-H3 lysine-methylation status in osteosarcoma cells which acquire methotrexate resistance in vitro. [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 3896.