PT  - JOURNAL ARTICLE
AU  - N. J. Wood
AU  - N. A. Quinton
AU  - S. Burdall
AU  - E. Sheridan
AU  - S. R. Duffy
TI  - Exploring the potential chemopreventative effect of aspirin and rofecoxib on hereditary nonpolyposis colorectal cancer–like endometrial cancer cells <em>in vitro</em> through mechanisms involving apoptosis, the cell cycle, and mismatch repair gene expression
AID  - 10.1111/j.1525-1438.2007.00867.x
DP  - 2007 Feb 01
TA  - International Journal of Gynecologic Cancer
PG  - 447--454
VI  - 17
IP  - 2
4099  - http://ijgc.bmj.com/content/17/2/447.short
4100  - http://ijgc.bmj.com/content/17/2/447.full
SO  - Int J Gynecol Cancer2007 Feb 01; 17
AB  - Women in hereditary nonpolyposis colorectal cancer (HNPCC) families have up to a 71% lifetime risk for developing endometrial cancer (EC). This compares to the female lifetime risk for colorectal cancer (CRC) in HNPCC of 60%. The basis of HNPCC is an inherited mutation in a mismatch repair gene (MMR). Aspirin and COX2 inhibitors seem to have a chemoprotective effect on CRC in the general population and are the subject of prospective clinical studies in patients at high risk for CRC including HNPCC. There is no evidence that these agents have any protective effect against EC in the general population. This study investigated the effect of aspirin and a COX2 inhibitor (rofecoxib) on an HNPCC EC cell line model (Ishikawa) by assessing the effect on proliferation, apoptosis, the cell cycle, and MMR gene expression. Aspirin inhibits EC cell proliferation by inducing apoptosis and changes in the cell cycle. This effect is not mediated by changes in MMR gene (hMSH2) expression as assessed by quantitative reverse transcription–polymerase chain reaction. Rofecoxib inhibits EC cell proliferation; this did not appear to be mediated by induction of apoptosis, by alterations of the cell cycle, or by changes in MMR gene expression