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View the Table of Contents for the February 15 issue of Cancer Research.
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Variation in genes affecting the bioavailability of vitamin E could impact prostate cancer risk. In a study of 982 incident prostate cancer cases and 851 matched controls drawn from a vitamin E supplementation trial, Wright and colleagues examined whether 13 variants in two key vitamin E transport genes, TTPA and SEC14L2, were associated with prostate cancer. Although no associations were observed, several variants in SEC14L2 modified the effect of the trial vitamin E supplementation on prostate cancer risk. These findings could have important implications regarding vitamin E use and the design, analysis, and interpretation of ongoing and future trials.
Jing et al. Page 1459 Oncolytic viruses exert potent antitumor effects; however, the inability of viruses to cross the endothelial barrier limits intratumoral delivery. To circumvent this problem, Jing and colleagues engineered a novel oncolytic measles virus, MV-uPA, retargeted against the tumor and vascular target urokinase receptor (uPAR). MV-uPA induced cell fusion and cytotoxicity in an uPAR-specific manner and exerted potent in vivo antitumor effects. MV-uPA infected activated endothelial cells expressing higher uPAR more efficiently than nonactivated endothelial cells. Using a murine version of MV-uPA, the authors demonstrated successful viral transduction of murine mammary tumor and, for the first time, in vivo targeting of tumor capillaries. The ability of MV-uPA to target tumor cells and capillaries makes it a promising agent for the treatment of breast cancer and other malignancies.
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Li et al. Page 1685 Monocyte chemoattractant protein 1 (CCL2) has been identified recently as a regulator of prostate cancer metastasis in the bone marrow microenvironment with CCL2 facilitating osteoclastogenesis and stimulating prostate carcinoma cell growth. Li and colleagues report that prostate cancer–derived PTHrP elevates CCL2 levels in osteoblast-derived bone marrow by increasing osteoclastic bone resorption and facilitating prostate cancer growth in bone. The authors also found that CCL2 binds to its receptor on cancer cells and stimulates release of the proangiogenic factor VEGF-A to enhance neo-blood vessel formation. These results suggest that CCL2 facilitates metastatic tumor growth via activation of tumor cells, bone resorption, and angiogenesis. Targeting CCL2 could be a promising therapeutic strategy for prostate cancer skeletal metastasis.
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