Semaphorins are a large family of molecules involved in axonal guidance during the development of the nervous system and have been recently shown to have both angiogenic and anti-angiogenic properties. Specifically, semaphorin 7A (SEMA7A) has been reported to have a chemotactic activity in neurogenesis and to be an immune modulator through α1β1integrins. SEMA7A has been shown to promote monocyte chemotaxis and induce them to produce proinflammatory mediators. In this study we explored the role of SEMA7A in a murine model of breast cancer. We show that SEMA7A is highly expressed by DA-3 murine mammary tumor cells in comparison to normal mammary cells (EpH4), and that peritoneal elicited macrophages from mammary tumor-bearing mice also express SEMA7A at higher levels compared to those derived from normal mice. We also show that murine macrophages treated with recombinant murine SEMA7A significantly increased their expression of proangiogenic molecule CXCL2/MIP-2. Gene silencing of SEMA7A in peritoneal elicited macrophages from DA-3 tumor-bearing mice resulted in decreased CXCL2/MIP-2 expression. Mice implanted with SEMA7A silenced tumor cells showed decreased angiogenesis in the tumors compared to the wild type tumors. Furthermore, peritoneal elicited macrophages from mice bearing SEMA7A-silenced tumors produce significantly (p < 0.01) lower levels of angiogenic proteins, such as CXCL2/MIP-2, CXCL1, and MMP-9, compared to those from control DA-3 mammary tumors. We postulate that SEMA7A in mammary carcinomas may skew monocytes into a pro-tumorigenic phenotype to support tumor growth. SEMA7A could prove to be valuable in establishing new research avenues toward unraveling important tumor-host immune interactions in breast cancer patients.
The classification of MFH has been recently debated. Nevertheless, our case is the second report of pediatric MFH involving the parotid gland. Surgical resection is the preferred treatment, but combined chemoradiation may be necessary in the head and neck region.
Herpes simplex virus (HSV) is regarded as a common viral pathogen that produces a wide variety of diseases. After a primary infection, which usually occurs during childhood and may or may not be clinically evident, the virus establishes a latent infection in the local sensory ganglia and can reactivate throughout the life of the individual. Fulminant hepatic failure (FHF) due to HSV infection is a clinical condition well known in pediatric, immunocompromised, and pregnant patients. It is rare in immunocompetent hosts. We report the case of a 51-year-old man with no significant past medical history who developed FHF with disseminated intravascular coagulopathy and septic shock secondary to HSV infection. The initial diagnosis was made through a frozen section of a needle liver biopsy and the presence of HSV was confirmed in the permanent section with immunohistochemistry. HSV was grown in cell culture from liver tissue obtained through an autopsy.
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