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• W7699552 startingPage "285" @default.
• W7699552 abstract "Epidemiologic evidence supporting a major chemopreventive role for vitamin D in various malignancies is strong. Likewise the use of the active metabolite of vitamin D, 1,25(OH)(2)D(3), and its analogs to prevent and/or treat a wide variety of malignancies in animals is well established. The evidence has been less compelling for epidermal carcinogenesis perhaps because the same agent that produces vitamin D in the skin, UVB radiation (UVR), is also the same agent that results in most epidermal malignancies. However, recent studies indicate that the role of vitamin D and its receptor (VDR) in protecting against the development of epidermal tumors deserves a closer look. One such study found mice lacking the VDR were quite sensitive to epidermal tumor formation following the administration of the carcinogen DMBA. A more recent study showed that these mice were similarly more sensitive to tumor formation following UVR, results we have confirmed. The epidermis of the VDR null mouse is hyperproliferative with gross distortion of hair follicles, structures that may provide the origin for the tumors found in the skin following such treatment. Two interacting pathways critical for epidermal and hair follicle function, beta-catenin and hedgehog (Hh), result in epidermal tumors when they are activated abnormally. Thus, we considered the possibility that loss of VDR predisposes to epidermal tumor formation by activation of either or both beta-catenin and Hh signaling. We determined that all elements of the Hh signaling pathway are upregulated in the epidermis and utricles of the VDR null mouse, and that 1,25(OH)(2)D(3) suppresses the expression of these elements in normal mouse skin. In addition we observed that the transcriptional activity of beta-catenin was increased in keratinocytes lacking the VDR. These results lead us to the hypothesis that the VDR with its ligand 1,25(OH)(2)D(3) functions as a tumor suppressor with respect to epidermal tumor formation in response to UVR by regulating Hh and beta-catenin signaling." @default.
• W7699552 created "2016-06-24" @default.
• W7699552 creator A5032781101 @default.
• W7699552 date "2020-01-01" @default.
• W7699552 modified "2023-10-09" @default.
• W7699552 title "The Vitamin D Receptor as Tumor Suppressor in Skin" @default.
• W7699552 cites W1484268538 @default.
• W7699552 cites W1488908620 @default.
• W7699552 cites W1492801490 @default.
• W7699552 cites W1496700429 @default.
• W7699552 cites W1510470032 @default.
• W7699552 cites W1513900203 @default.
• W7699552 cites W1520833254 @default.
• W7699552 cites W1523788432 @default.
• W7699552 cites W1590561990 @default.
• W7699552 cites W1605072294 @default.
• W7699552 cites W1711175242 @default.
• W7699552 cites W1767001524 @default.
• W7699552 cites W1873156815 @default.
• W7699552 cites W1880207624 @default.
• W7699552 cites W1885898936 @default.
• W7699552 cites W1937240320 @default.
• W7699552 cites W1947526212 @default.
• W7699552 cites W1968306291 @default.
• W7699552 cites W1970741980 @default.
• W7699552 cites W1971055997 @default.
• W7699552 cites W1971616572 @default.
• W7699552 cites W1972181361 @default.
• W7699552 cites W1974648584 @default.
• W7699552 cites W1975593226 @default.
• W7699552 cites W1978243004 @default.
• W7699552 cites W1978828082 @default.
• W7699552 cites W1979303488 @default.
• W7699552 cites W1979512659 @default.
• W7699552 cites W1980877070 @default.
• W7699552 cites W1981000910 @default.
• W7699552 cites W1981900473 @default.
• W7699552 cites W1983437978 @default.
• W7699552 cites W1983442041 @default.
• W7699552 cites W1986388219 @default.
• W7699552 cites W1989224577 @default.
• W7699552 cites W1989813145 @default.
• W7699552 cites W1990768206 @default.
• W7699552 cites W1990956955 @default.
• W7699552 cites W1993569127 @default.
• W7699552 cites W1995459339 @default.
• W7699552 cites W1997673869 @default.
• W7699552 cites W1998176709 @default.
• W7699552 cites W1998314871 @default.
• W7699552 cites W1998995917 @default.
• W7699552 cites W2001884779 @default.
• W7699552 cites W2002189255 @default.
• W7699552 cites W2002404925 @default.
• W7699552 cites W2003006686 @default.
• W7699552 cites W2003875170 @default.
• W7699552 cites W2004360930 @default.
• W7699552 cites W2004630197 @default.
• W7699552 cites W2005032514 @default.
• W7699552 cites W2005186319 @default.
• W7699552 cites W2005675731 @default.
• W7699552 cites W2005891610 @default.
• W7699552 cites W2005943555 @default.
• W7699552 cites W2006381191 @default.
• W7699552 cites W2006565377 @default.
• W7699552 cites W2007205568 @default.
• W7699552 cites W2007223760 @default.
• W7699552 cites W2007374663 @default.
• W7699552 cites W2009108161 @default.
• W7699552 cites W2009230970 @default.
• W7699552 cites W2009410210 @default.
• W7699552 cites W2010076661 @default.
• W7699552 cites W2011842366 @default.
• W7699552 cites W2012071848 @default.
• W7699552 cites W2012382826 @default.
• W7699552 cites W2013735942 @default.
• W7699552 cites W2014444464 @default.
• W7699552 cites W2014751142 @default.
• W7699552 cites W2018730905 @default.
• W7699552 cites W2019966492 @default.
• W7699552 cites W2021182462 @default.
• W7699552 cites W2021264322 @default.
• W7699552 cites W2021354108 @default.
• W7699552 cites W2022548910 @default.
• W7699552 cites W2023743167 @default.
• W7699552 cites W2024357543 @default.
• W7699552 cites W2024513156 @default.
• W7699552 cites W2026194974 @default.
• W7699552 cites W2027823566 @default.
• W7699552 cites W2029728577 @default.
• W7699552 cites W2030627408 @default.
• W7699552 cites W2031074006 @default.
• W7699552 cites W2031197720 @default.
• W7699552 cites W2034347152 @default.
• W7699552 cites W2035235887 @default.
• W7699552 cites W2035740499 @default.
• W7699552 cites W2039390906 @default.
• W7699552 cites W2040512937 @default.
• W7699552 cites W2040619287 @default.

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