Histologic comparison of hereditary nonpolyposis colorectal cancer associated with MSH2 and MLH1 and colorectal cancer from the general population

1999 ◽  
Vol 42 (6) ◽  
pp. 722-726 ◽  
Author(s):  
Maniamparmpil Shashidharan ◽  
Thomas Smyrk ◽  
Kevin M. Lin ◽  
Charles A. Ternent ◽  
Alan G. Thorson ◽  
...  
1998 ◽  
Vol 41 (4) ◽  
pp. 428-433 ◽  
Author(s):  
Kevin M. Lin ◽  
M. Shashidharan ◽  
Charles A. Ternent ◽  
Alan G. Thorson ◽  
Garnet J. Blatchford ◽  
...  

2007 ◽  
Vol 17 (2) ◽  
pp. 447-454 ◽  
Author(s):  
N. J. Wood ◽  
N. A. Quinton ◽  
S. Burdall ◽  
E. Sheridan ◽  
S. R. Duffy

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


2014 ◽  
Vol 133 (3) ◽  
pp. 526-530 ◽  
Author(s):  
Zohreh Ketabi ◽  
Anne-Marie Gerdes ◽  
Berit Mosgaard ◽  
Steen Ladelund ◽  
Inge Bernstein

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