Tumor hypoxia has been associated with increased malignancy, likelihood of metastasis, and increased resistance to radiotherapy and chemotherapy in human medicine. Hypoxia-inducible factor-1 (HIF-1) is a key transcription factor that is induced by tumor hypoxia and regulates the pathways involved in cellular response and adaptation to the hostile tumor microenvironment. HIF-1 induces transcription of different proteins, including Ca-IX and Glut-1, which are considered endogenous markers of chronic hypoxia in solid tumors in humans. In this study, sections from 40 canine sarcomas (20 histiocytic sarcomas and 20 low-grade soft-tissue sarcomas) were immunostained for these markers. Expression of Glut-1 was scored based on percentage of positive staining cells (0 ¼ <1%; 1 ¼ 1%-50%; 2 ¼ >50%) and intensity of cellular staining (1 ¼ weak; 2 ¼ strong); Ca-IX was scored based on percentage of positive cells (0 ¼ <1%; 1 ¼ 1%-30%; 2 ¼ >30%). Intratumoral microvessel density was measured using CD31 to assess intratumoral neoangiogenesis. Histiocytic sarcomas showed statistically significant higher Glut-1 immunoreactivity and angiogenesis than did low-grade soft-tissue sarcomas. Intratumoral microvessel density in histiocytic sarcomas was positively associated with Glut-1 immunoreactivity score. These findings suggest a potential role of hypoxia in the biology of these tumors and may provide a base for investigation of the potential prognostic use of these markers in naturally occurring canine tumors.

A nine-month-old entire female terrier cross was presented with intermittent anorexia, vomiting and recent onset of abdominal pain and distension. A diagnosis of unilateral hydronephrosis was made following ultrasound examination and intravenous urography, but no cause was identified. Subsequent ureteronephrectomy and histology of the affected kidney showed ureteric atresia as the cause of obstruction. Uterus unicornis was also identified and ovariohysterectomy was performed. The combination of structural abnormalities can be explained by an in-utero developmental error of their common embryological precursor, the mesonephric duct.

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