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    • The ability of tumors to progress

    2019-05-22

    The ability of tumors to progress to more malignant phenotypes depends on tumor microenvironment. Blood capillaries, made up of endothelial cells, are usually static under physiological conditions but are induced to proliferate by direct exposure to angiogenic factors, for instance, vascular endothelial growth factor (VEGF) [30]. The proliferation and migration of endothelial glucose transporter play an important role in tumor angiogenesis [31]. As we all know, angiogenesis, development of new blood vessels from preexisting vascular bed, plays important roles during tumor growth and metastasis [32]. Significantly, the concept that malignant neoplasm onset, growth, and invasion rely on angiogenesis is broadly recognized and accepted [33,34]. Theoretically, cancer cells, like normal cells, also need the delivery of oxygen as well as nutrients through blood vessels to survive and grow. In situ carcinoma, there seems to be a prolonged dormant period during which the cancer is not angiogenic, and is restrained in growth [35]. When sufficient cancer cells have transformed to the angiogenic phenotype from the quiescent phenotype, neovascularization may initiate, and thus rapid tumor growth can proceed. Through the literatures, we found that gene function of ‘angiogenesis’ has already been established to be important for OS. For example, previous studies have implicated that high recurrence rate and metastatic potential of OS are connected with high levels of angiogenesis [36,37]. Moreover, Wang et al. [38] have used differential co-expression network to find that angiogenesis is closely related to OS progression and metastasis. Most importantly, suppression of cancer angiogenesis has been regarded as an attractive strategy for tumor therapy [39]. Thus, anti-angiogenic therapy might be a consideration for OS patients, with the majority of OS showing high vascularization [40]. During the tumor occurrence and metastasis, cancer cells 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 glucose transporter to the lung.