Prospective studies with follow-up information are needed to define relative risk factors involved in the progression from EmGD to a full-blown ESC and further develop optimal clinical management.
Validations from multiple institutions should be carried out to confirm the previous findings and make this diagnose feasible worldwide.
The early recognizable entity EmGD provides an opportunity to identity molecular alterations in the initiation of ESC. Stem cells with epigenetic alterations might be the source of the malignant transformation, which is currently being pursued in our laboratory.
A p53 protein based early detection assay needs to be developed for ESC. This assay can be used initially for those high risk patients, then apply to general use when appropriate.
Animal models with genetic manipulations such as p53, IMP3, Nrf2, and BRCA etc to further understand initial genetic alterations in the process of endometrial serous carcinogenesis.