† These authors contributed equally to this work ABSTRACT: An eight-year-old, intact male Rottweiler dog was presented due to anorexia, lethargy, ataxia and imbalance. Cerebellar and thyroid masses were identified using 0.3T magnetic resonance imaging. The 18 F-fluorodeoxyglucose uptakes of the masses were elevated on positron emission tomography and 7 T-magnetic resonance imaging fusion imaging. At 113 days after the initial presentation, new nodular lesions were observed in the skin, liver and spleen. Histopathology revealed multiple lesions of disseminated histiocytic sarcoma in the cerebellum, liver, spleen and skin, whereas the thyroid lesions were diagnosed as mixed medullary-follicular thyroid carcinoma. The primary site of the disseminated histiocytic sarcoma was found to be in the cerebellum. To our knowledge, this is the first case report to describe the imaging and histopathological findings of extracranial metastasis of a primary intracranial histiocytic sarcoma in a dog.
Giant cell tumors (GCT) of the skull are rare and only a few case series with limited number of cases have been reported till date. In the cranium, GCT usually occurs in the sphenoid and temporal bone, and occipital condyle GCTs are very rare. We report a rare presentation of GCT of the occipital condyle manifested as occipital condyle syndrome. Despite gross total resection, they can recur aggressively; presence of cortical breach might be an indicator of aggressiveness prompting early postoperative imaging and adjuvant therapy.
MutT Homolog1 (MTH1) is an enzyme responsible for removing oxidized nucleotides from cells. Activation of MTH1 is reported in many cancer cells and is thought to be responsible for imparting resistance towards anticancer drugs. While there are several mechanisms for the activation of MTH1 in cancer cells, this study aimed to evaluate the role of mutant Isocitrate Dehydrogenase1 (mIDH1) - mediated reactive oxygen species (ROS) in the activation of MutT Homolog1 in glioma cells. MTH1 was found to be upregulated in both mIDH1 expressed and 2- HG treated cells. mIDH1 and its product, 2-HG, increased the ROS levels in the cultured glioblastoma cells. Further, increased expression and activity of MTH1 was observed in glioma tissues harboring mIDH1 compared to tissues with wild-type IDH1. Our study unveils a novel mechanism of activation of MTH1 in cells harboring mutant IDH1.
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