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    • During the tumor occurrence and metastasis cancer cells can

    2019-04-29

    During the tumor occurrence and metastasis, cancer 5-aminosalicylic acid can modulate the immune system of the host to find strategies that enable them to survive from the immune surveillance [41]. Cancer immunoediting is one of the two major strategies to get away from immune surveillance [42]. Innate and adaptive immunity appear to contribute to cancer immunoediting [43]. Previously, lymphocytes and IFNγ have indicated to prevent tumor immunoediting, thereby preventing the selection of less immunogenic tumor cells [44]. Indeed, immune cells (for example, macrophages cells) release soluble agents like chemokines and cytokines promoting the migration and infiltration of leukocytes that exert important functions in tumor development [45]. OS is frequently infiltrated by immune cells including macrophages and T cells [46]. Moreover, macrophage migration inhibitory factor is an proinflammatory cytokine which exerts an crucial function in the immune system [47]. Macrophage migration inhibitory factor contributes to cell proliferation, survival, and tumor-related angiogenesis [48,49]. Moreover, Han et al. [50] have suggested that macrophage migration inhibitory factor can serve as a prognostic marker and a potential therapeutic target for OS. Interestingly, a link between p53 and IFN system was recently discovered in regulating tumor suppression and immunity [51]. Abnormalities of p53 gene in OS occur with a high incidences approaching 50% of all cases [52]. Currently, growing evidence implicates that the immune system is a fundamental player in cancer and a key determinant of prognosis and response to therapy [53,54]. While, understanding the crosstalk between OS cells and the immune system, and how they drive tumorigenesis is still in its infancy. Hence, it is urgently needed to develop novel drugs that would potentiate the immune system in OS patients to act against this disease by means of immunomodulatory methods.
    Conflicts of Interest
    Introduction Giant cell tumor of bone (GCTB) is an invasive benign bone tumor consisting of proliferative mononuclear cells and osteoclast-like multinucleated giant cells. It has the tendency to relapse. GCTB accounts for 4–5% of primary bone tumors. The incidence of lung metastasis in patients with GCTB is about 1–9% [1–5]. Viswanathan et al. [3] reported that two mechanisms are related to lung metastasis: a self-limiting process of transformation and vascular transfer. Because both lung tissue and GCTB tissue have a rich blood supply, the tumor cells may invade the interstitium and destroy the vessel walls, facilitating hematogenous metastasis to the lung. Studies and reports of lung metastasis of GCTB are rare because of the low incidence of lung metastasis. The biological behavior and clinical features of GCTB are difficult to predict [6,7]. Some researchers have attempted to analyze related clinical factors of lung metastasis, such as age, sex, primary tumor site, tumor stage, primary tumor treatment, and recurrence. However, the numbers of patients were small, and different results were reported among the studies. High-level evidence from large-sample data is lacking. Therefore, the present study focused on a large number of patients with lung metastasis in a single center. The purpose was to elucidate the clinical characteristics and risk factors for pulmonary metastasis of GCTB.
    Materials and methods
    Results
    Discussion Finch and Gleave [10] reported pulmonary metastasis of benign GCTB for the first time in 1926. Initial pulmonary metastases are rare, and most appear after the operation of the primary tumor. Previous studies have shown that most pulmonary 5-aminosalicylic acid metastases were found several months to 3 years postoperatively [3,11,12]. However, some metastases occurred more than 10 years postoperatively [6,7]; the longest occurred at 49 years postoperatively [13]. Such case reports are very rare. The rate of lung metastasis from GCTB is very low, and only small samples of affected patients have been reported in the literature. Campanacci et al. [1] reported 280 cases of GCTB in 1987, and the lung metastasis rate among these cases was 2.1%. Dominkus et al. [4] reported 649 cases of GCTB, and 2.1% of them had lung metastasis. In 2010, Errani et al. [5] reported 349 cases of GCTB, and the lung metastasis rate was 4.0%. In our center, Sung et al. [14] reported that 6 of 111 patients with GCTB had pulmonary metastasis in 1982, and Niu et al. [9] reported that the rate of lung metastasis was 3.4% among 621 cases of GCTB in 2012. The clinical characteristics of lung metastatic lesions were analyzed in the present study. Most lesions were multiple and located in the bilateral lungs, and they were mainly distributed in the peripheral lung. These characteristics are similar to those of metastases of other malignant tumors. However, the biological behavior of pulmonary metastasis of GCTB differs from that of other tumors. In general, the vast majority of GCTB metastases progress slowly. The doubling time of GCTB lung metastasis is significantly longer than that of other tumors [15].