B.S. Biological Sciences (Cellular Toxicology), University of Plymouth, UK (1982)
M.S. Toxicology, University of Surrey, UK (1983)
Ph.D. Genetic Toxicology/Carcinogenesis, University of Portsmouth and ICI Central Toxicology Laboratory, UK (1986)
The current focus is on genetic and epigenetic mechanisms in cancer development. The genetic basis of cancer is studied through cultured human cancer cells and whole animal approaches, including transgenic and knockout models. These models are employed to examine changes in oncogenes and tumor suppressors (e.g., K-ras, β-catenin, APC) and the influence of chemoprotective agents and anticancer drug candidates. The epigenetic basis of cancer is studied through work on histone deacetylase (HDAC) inhibitors and changes in protein acetylation in both cancer cells and normal cells treated with dietary agents/anticancer drug candidates. Sulforaphane from broccoli, garlic organosulfur and organoselenium compounds and a short-chain fatty acid derived from gut fermentation of dietary fiber (butyrate) inhibit HDAC activity in human cancer cells and trigger growth arrest/apoptosis. The molecular mechanisms are pursued. To translate this work to humans, HDACs and protein acetylation changes are being examined in volunteers undergoing screening colonoscopy exams.
Rajendran P, Dashwood WM, Li L, Kang Y, Kim E, Johnson G, Fischer K, Löhr CV, Williams DE, Ho E, Yamamoto M, Lieberman D, Dashwood RH, Nrf2 status affects tumor growth, HDAC3 gene promoter associations, and the response to sulforaphane in the colon. Clinical Epigenetics. 2015, 7:102.
Kang Y, Nian H, Rajendran P, Kim E, Dashwood WM, Pinto JT, Boardman LA, Thibodeau SN, Limburg PJ, Löhr CV, Bisson WH, Williams DE, Ho E, Dashwood RH. (2014) HDAC8 and STAT3 repress gene activity in colon cancer cells. Cell Death Disease 5:e1476. PMCID: PMC4237248
Rajendran P, Kidane AI, Yu TW, Dashwood WM, Bisson WH, Löhr CV, Ho E, Williams DE, Dashwood RH. (2013) HDAC turnover, CtIP acetylation and dysregulated DNA damage signaling in colon cancer cells treated with sulforaphane and related dietary isothiocyanates. Epigenetics 8(6):612-23. PMCID: PMC3857341
Wang R, Löhr CV, Fischer K, Dashwood WM, Greenwood JA, Ho E, Williams DE, Ashktorab H, Dashwood MR, Dashwood RH (2013) Epigenetic inactivation of endothelin-2 and endothelin-3 in colon cancer. Int J Cancer 132:1004-1012. PMC3500448.
Parasramka MA, Dashwood WM, Wang R, Saeed HH, Williams DE, Ho E,Dashwood RH (2012) A role for low-abundance miRNAs in colon cancer: the miR-206/Kruppel-like factor 4 (KLF4) axis. Clin Epigenetics 4:16.PMC3506528
Parasramka MA, Dashwood WM, Wang R, Abdelli A, Bailey GS, Williams DE, Ho E,Dashwood RH (2012) MicroRNA profiling of carcinogen-induced rat colon tumors and the influence of dietary spinach. Mol Nutr Food Res 56:1259-1269. PMC3762592
Rajendran P, Ho E, Williams DE, Dashwood RH (2011) Dietary phytochemicals, HDAC inhibition, and DNA damage/repair defects in cancer cells. Clin Epigenetic 3:4. PMC3255482
Rajendran P, Delage B, Dashwood WM, Yu TW, Wuth B, Williams DE, Ho E,Dashwood RH (2011) Histone deacetylase turnover and recovery in sulforaphane-treated colon cancer cells: competing actions of 14-3-3 and Pin1 in HDAC3/SMRT corepressor complex dissociation/reassembly. Mol Cancer 10:68. PMC3127849
Higdon JV, Delage B, Williams DE, Dashwood RH (2007) Cruciferous vegetables and human cancer risk. Pharmacol Res 55: 224-36. PMC2737735
Myzak M, Karplus PA, Chung FL, Dashwood RH (2004) A novel mechanism of chemoprotection by sulforaphane: Inhibition of histone deacetylase. Cancer Res 64:5767-74.
For a complete list of publications, please visit: http://www.ncbi.nlm.nih.gov/pubmed/?term=Dashwood%20RH%5BAuthor%5D&cauthor=true&cauthor_uid=17317210