|1.||Kurakata, Shinichi: 2 articles (02/2009 - 09/2008)|
|2.||Fujiwara, Kosaku: 2 articles (02/2009 - 09/2008)|
|3.||Reynolds, Lisa A: 1 article (02/2009)|
|4.||Marlow, Laura A: 1 article (02/2009)|
|5.||Sebo, Thomas: 1 article (02/2009)|
|6.||Zhang, Ying: 1 article (02/2009)|
|7.||Wadsworth, J Trad: 1 article (02/2009)|
|8.||Cleland, Alan S: 1 article (02/2009)|
|9.||Copland, John A: 1 article (02/2009)|
|10.||Grant, Clive: 1 article (02/2009)|
09/01/2008 - "We conclude that RS5444 inhibits both initiation and progression of colon tumors in the AOM model of sporadic colon carcinogenesis."
09/01/2008 - "Furthermore, exposure to RS5444 during the course of AOM treatment effectively blocked colon tumor formation after withdrawal of the agonist. "
04/13/2006 - "RS5444 plus paclitaxel demonstrated additive antiproliferative activity in cell culture and minimal ATC tumor growth in vivo. "
09/01/2008 - "The high affinity peroxisome proliferator-activated receptor-gamma agonist RS5444 inhibits both initiation and progression of colon tumors in azoxymethane-treated mice."
09/01/2008 - "RS5444 did not inhibit DNA synthesis in tumor cells, suggesting that PPARgamma activity was impaired in adenomas. "
|2.||Lung Neoplasms (Lung Cancer)
02/15/2009 - "We further implicate RhoB as a key signaling effector for the growth inhibition of ATC, as treatment with a histone deacetylase inhibitor shown to increase RhoB expression in lung cancer cells caused the up-regulation of RhoB in ATC cells accompanied by increased expression of p21 and inhibition of cell proliferation; this effect occurred even in ATC cells that were unresponsive to RS5444 due to a lack of expression of PPARgamma. "
|2.||Histone Deacetylase Inhibitors
|4.||DNA (Deoxyribonucleic Acid)