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  • Introduction Schwannoma is a benign tumor of neuroectodermal

    2019-05-16

    Introduction Schwannoma is a benign tumor of neuroectodermal derivation that originates from Schwann protein kinase which cover the peripheral nerves [3]. Approximately 25–40% of all schwannomas occur in the head and neck. These tumors most commonly arise in the soft tissues of the head and neck and on the flexor surfaces of the upper and lower extremities [3]. Intraosseous schwannoma is a slow growing tumor and the patient is usually asymptomatic. Swelling is the most common complaint at presentation. Intraosseous schwannoma is a rare entity and in this study we are reporting a case of a schwannoma in the femur [3].
    Case Report
    Discussion Schwannoma is a slow-growing benign tumor derived from Schwann cells, the sheath cells that cover myelinated nerve fibers [1]. Patients with schwannoma are usually symptom-free and swelling is the most common complaint at presentation [3]. Intraosseous schwannomas are rare and they account for less than 0.2% among the primary bone tumors. The preoperative diagnosis of intraosseous schwannoma is challenging because of its rarity [2]. Schwannomas can affect the bone either by an extra osseous soft tissue mass that causing bony erosion or it can arise from nerves that course through a canal in a bone causing erosion of the bone and creating a dumbbell-shaped configuration. Less commonly, schwannoma can originate centrally from the medullary cavity of the bone [4]. This was reviewed at multidisciplinary sarcoma rounds. This is quite an unusual case of a bone cortically based nerve sheath tumor with a large soft tissue component. The pathology was reviewed for both interpretation and to ensure there were no sampling or administrative errors. Once it was confirmed after multidisciplinary discussion, the patient was brought to the operating theater for resection of the posterior thigh soft tissue mass with bone grafting femur as required (Figs. 1–4).
    Conclusion
    Conflict of interest statement
    Introduction Osteosarcoma is the most common bone tumour in children, adolescents and young adults [1,2]. Risk factors for osteosarcoma are outlined in Table 1. It is most common between the ages of 10–19, and the incidence rate for the condition ranges between one and five cases per one million people [1,3–6]. It has a variable prognosis, and the main factors affecting disease course have been highlighted in Table 2. Current treatment for osteosarcoma has achieved a universal cure rate of 65% [7]. When diagnosed, patients commence induction chemotherapy [8,9]. The tumour is surgically resected and analysed, and if 90% or more of the tumour is necrosed, the chemotherapy regime is continued to eliminate micrometastasis [1,10]. However, there is no standardised treatment for osteosarcoma that has failed to respond to the first chemotherapy regime [11]. Thus, researchers have attempted to identify potential drugs to fulfil this role. One such drug is sorafenib, which is sold under the trade name “Nexavar” [9]. This literature review evaluates the mechanism of action and efficacy of sorafenib in the treatment of osteosarcoma refractory to chemotherapy.
    Methodology The terms “sorafenib OR Nexavar” and “osteosarcoma” were used to search the PUBMED database. The initial search was conducted during March 2016, and was repeated in April 2016. The searches were repeated and the original paper was reviewed in January 2017 to account for new evidence. Both preclinical and clinical data sources were evaluated. The oldest article discussing osteosarcoma and sorafenib was from 2009 [24].
    Discussion
    Limitations of the review Sorafenib is a relatively new drug. More so, the combination of sorafenib with other drugs for osteosarcoma is a treatment modality that has existed in the literature for a mere 12 months. Thus, large scale data and relationships are not yet available. More clinical data is required to properly evaluate the efficacy of sorafenib and sorafenib combination therapy as a second line treatment for osteosarcoma. In particular, denosumab and sorafenib is a combination that demands further evaluation. Additionally, both phase II trials were conducted by the Italian Sarcoma Group. All other clinical evidence evaluated was on a far smaller scale. Thus, to ensure validity of the data, sorafenib must undergo further clinical trials conducted by other research institutions. Finally, all future clinical trials should focus on sorafenib in the context of combination therapy, as this review has foregrounded evidence suggesting that Nucleolytic reaction is ineffective in isolation [39,40].