Endometrial cancer is the seventh most common cancer in women worldwide. 
Therefore elucidation of the pathogenesis and development of effective treatment 
for endometrial cancer are important. However, several aspects of the mechanism 
of carcinogenesis in the endometrium remain unclear. Associations with genetic 
variation and mutations of cancer-related genes have been shown, but these do 
not provide a complete explanation. Therefore, in recent years, epigenetic 
mechanisms that do not involve changes in DNA sequences have been examined. 
Studies aimed at detection of aberrant DNA hypermethylation in cancer cells 
present in microscopic amounts in vivo and application of the results to cancer 
diagnosis have also started. Breakdown of the DNA mismatch repair mechanism is 
thought to play a large role in the development of endometrial cancer, with 
changes in the expression of the hMLH1 gene being particularly important. 
Silencing of genes such as APC and CHFR, Sprouty 2, RASSF1A, GPR54, CDH1, and 
RSK4 by DNA hypermethylation, onset of Lynch syndrome due to hereditary 
epimutation of hMLH1 and hMSH2 mismatch repair genes, and regulation of gene 
expression by microRNAs may also underlie the carcinogenic mechanisms of 
endometrial cancer. Further understanding of these issues may permit development 
of new therapies.