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.

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SUMMARYAIDS is an increasingly common diagnosis seen by neurologists and neurosurgeons alike. Although the more common brain lesions associated with AIDS are due to central nervous system lymphomas, toxoplasma encephalitis or progressive multifocal leukoencephalopathy, relatively recent clinical evidence has shown that AIDS-independent cerebral tumours can arise as well, albeit less commonly. Previous incidents have been reported with HIV and AIDS patients presenting with cerebral astrocytomas. To our knowledge, there has never been a report in the literature of a brainstem anaplastic glioma occurring in an AIDS or HIV patient. We report a 55-year-old patient with HIV and brainstem anaplastic glioma. Its presentation, diagnostic difficulty, scans, histology and subsequent treatment are discussed. We also review the relevant literature on gliomas in HIV/AIDS patients. BACKGROUND

Key Clinical MessageAcute myeloid leukemia (AML) with t(8:16) is an infrequent acute leukemia subtype. It can occur de novo or more frequently therapy-related. The presence of blasts with monocytoid morphology and erythrophagocytosis suggest the presence of the t(8;16).