All of these can cause symptoms of abnormal uterine bleeding in women of any age, from girls who first experience menstruation to postmenopausal women. All forms of endometrial hyperplasia are caused by lack of ovulation and the resulting excess of estrogen, and the deficiency of progesterone to counteract it. This bleeding is called dysfunctional uterine bleeding. Through microscopic observation, adenomatous hyperplasia and cystic hyperplasia can be identified. In these cases, by stopping or suppressing estrogen or by using progesterone, health can be completely restored to normal. However, that is not the case with atypical hyperplasia. In atypical hyperplasia, the arrangement of the shape of the glandular epithelium and the splitting condition show that it can mutate into a carcinogenic condition if not deterred in time. The chance of its becoming adenocarcinoma can be as high as 12% to 14%, so some pathologists think of atypical hyperplasia as pre-cancer, or zero stage cancer. Because the first two categories of hyperplasia (cystic and adenomatous) may also mutate into cancer, any case of endometrial hyperplasia should be diagnosed and treated in a timely fashion to prevent future occurrence of endometrial cancer.

The cause of these three types of hyperplasia is long-term estrogen stimulation. Primate experiments also confirmed this fact. But there is evidence to show that with the long-term effects of estrogen and the lack of confrontation, most endometria will become hyperplasia in varying degrees, but only a small portion will mutate into cancer. The main reason for this may be related to the roles of estrogen receptors, time, and personal factors. During the reproductive years, women seem to have more resistance to endometrial cancer, while women

shortly before and after menopause are more prone to it. Some people think that endometrial cancer develops over time, up to as long as five years, so a long lasting menopause can develop into adenocarcinoma. The presence of hormone receptors are indispensable role of cell medium. Under normal circumstances, hormones get into the cytoplasm of cells and combine into a new complex, then enter into the nucleus and combine with chromosomes. Then, through the process of transcription, the RNA synthesis increases, resulting in a biologically active hormone. In endometrial cancer cells, there are higher levels of hormone synthesis because the receptors possess the greater affinity of the hormone. We do not know why there is a difference, that under the same conditions, 12% to 14% of the people with endometrial hyperplasia will develop cancer, while others do not. The reason is still unknown, so individual differences can be an important factor. Those women who are prone to develop cancer may possess abnormal chromosomes or DNA distribution in the cells of their endometria. A carcinogen, possibly estrogen, under a long period of stimulation, can agonize the cancer-causing gene of the nucleus and develop cancer.