Endometrial cancer is one of the most common gynecological malignancies, its incidence is second only to cervical cancer, but in the past 20 years, with the screening and prevention of cervical cancer and the increase of concomitant metabolic disease in developed countries, the incidence of endometrial cancer has increased significantly. 2012 latest report of endometrial cancer incidence increased by 21% compared with 2008, while the mortality rate increased by more than 100%. In our data on the 2004-2005 Chinese malignant tumor death sample review survey, the mortality rate of uterine malignant tumor was 4.32/100,000 years, ranking seventh; cervical cancer was 2.84/100,000, located in the ninth place. In recent years, in economically developed coastal areas, the incidence of endometrial cancer has also shown an increasing trend. Information published by the Beijing Municipal Health Bureau shows that endometrial cancer has become the first female reproductive tract tumor above cervical cancer in Beijing from 2008 to 2010. It is possible that endometrial cancer will become the reproductive tract tumor with the highest incidence of gynecologic malignancies in China in the future. Metabolic disease, especially obesity, has become a factor in the high incidence of endometrial cancer, and obesity also increases the risk of death in endometrial cancer patients; women with BMI greater than or equal to 30 have the highest incidence and mortality rate of endometrial cancer compared to women with BMI < 25; and obese endometrial patients have a higher mortality rate than obese ones (Chia et al. 007). The staging of endometrial cancer is divided into hormone-dependent (about 90%) and non-hormone-dependent (< 10%). Among them, endometrial cancer combined with complex hyperplasia with atypical hyperplasia accounts for more than 40%. Among the non-hormone-dependent types, plasmacytoma (ESC) is a type II endometrial cancer, accounting for 8.75%-10.16% of the uterus. Clinical data show that 50% of patients with ESC are accompanied by ectopic lesions and 1/3-1/2 of patients without myometrial infiltration have ectopic lesions. In recent years, endometrial intraepithelial carcinoma (EIC) has been found to be closely related to ESC, with EIC accounting for 89% of ESC, only 6% of endometrioid adenocarcinoma, and 56% of carcinosarcomas. ESC, along with clear cell carcinoma, has become the most malignant tissue type of endometrial cancer. Surgical pathological staging of endometrial cancer: FIGO (2009). Diagnosis of endometrial cancer mainly relies on ancillary examinations: endometrial cancer is mainly diagnosed and confirmed by ancillary examinations: vaginal color ultrasound: observation of the disease Darut course arc (15) shape dropping purpose. The diagnosis of endometrial cancer can be confirmed by the diagnostic segmental scraping and hysteroscopic biopsy pathology. After preoperative hysteroscopy or segmental diagnostic scraping and histopathological confirmation, imaging (CT, MRI, CT-PET) is routinely applied for preoperative staging, but relying on imaging cannot accurately diagnose the presence or absence of pelvic and para-aortic lymph node metastases, nor can it accurately determine whether deep muscle layers have been invaded. Therefore, preoperative diagnosis of advanced or high-risk endometrial cancer is difficult, and it cannot be decided preoperatively whether pelvic and para-aortic lymph nodes must be removed. According to the surgical pathological staging, endometrial cancer is classified into low-risk and high-risk endometrial cancer while deciding the postoperative adjuvant treatment. Low-risk endometrial cancer: tissue type is adenocarcinoma, histopathological grading is highly differentiated, no invasion of muscle or only superficial muscle layer (<1/2), no pulsed lymphatic space invasion, no pelvic and para-aortic lymph node metastasis. High-risk endometrial cancer: age >60 years, tissue type of plasmacytoma or clear cell carcinoma, histopathological grade of hypofractionation, lymphatic space invasion (LVSI), tumor occupying >1/2 of the uterine cavity, invasion of deep myometrium, invasion of cervical mesenchyme, positive pelvic and para-aortic lymph nodes. Treatment for endometrial cancer includes surgery, chemotherapy and radiotherapy. Early endometrial cancer (IA G1/G2, IB G1/G2) is treated with staged surgery: retention of abdominal irrigation fluid, TH BSO pelvic lymph node dissection para-aortic lymphadenectomy (at the level of the inferior mesenteric artery/renal artery). Patients with comorbidities may have elective lymphadenectomy, but the NCCN specifically emphasizes that random sampling should not be performed; postoperative staging should be clarified before selecting appropriate adjuvant therapy. The NCCN also suggests that radiotherapy can be administered first, with 75-80 GY of point A radiation followed by TH BSO and para-aortic lymphadenectomy. Advanced endometrial cancer (with extra-uterine metastasis confirmed by imaging or clinical evidence): tumor cytoreduction, pelvic biopsy at multiple points, and large omentectomy. Postoperative adjuvant radiotherapy. Plasma breast cancer/clear cell carcinoma, if early-onset, should be staged as ovarian cancer: abdominal irrigation, TH BSO, large omentectomy, pelvic and para-aortic lymph node dissection. Postoperative radiotherapy. Same as above for advanced stage. Preservation of fertility in early stage endometrial cancer As the incidence of endometrial cancer increases, the treatment of preservation of fertility in young early stage endometrial cancer patients is receiving more and more attention. The treatment of preserved reproductive function requires a comprehensive assessment of the patient’s condition and full communication with the patient before treatment. Indications: 1, young <40 years old; 2, early stage (stage Ia G1); 3, negative abdominal cytology; 4, no suspicious abdominal positive retroperitoneal lymph nodes found: 5, tissue type is adenocarcinoma, both positive for estrogen and progesterone receptors; 6, patient has an urgent request; 7, condition of follow-up and suspicious regular follow-up. Most of the current literature reports that the application of high-dose progestin can ensure good results. Treatment with high-dose progestin: 250-500 mg/r day of medroxyprogesterone (MPA) or 160-320 mg/day of megestrol, with a course of treatment every 3 months. Transvaginal ultrasound should be performed monthly to observe the endometrial condition, and after 3 months, diagnostic scraping or hysteroscopy should be performed to assess the efficacy and decide to continue treatment or transfer to guided fertility treatment. Good results have also been reported in the literature for localized endometrial cancer treated with hysteroscopic resection followed by high-dose progestin therapy. A recent Mtea analysis of a large sample (Am J Obstet Gynecol. 2012 Oct;207:266) showed treatment of 408 patients with endometrial cancer and 151 patients with atypical hyperplasia to preserve fertility. The results showed that the endometrial cancer group achieved a satisfactory treatment rate of 76.2%, a recurrence rate of 40.6%, and a fertility rate of 28%; the atypical hyperplasia group had a satisfactory treatment rate of 85.6%, a recurrence rate of 26%, and a fertility rate of 26.3%. At follow-up, 20 patients (3.6%) were diagnosed with ovarian cancer (concurrent or metastatic) and 10 patients (1.9%) had progressive disease, including 2 deaths, indicating that treatment with preservation of fertility is feasible for early-stage endometrial cancer. Treatment of recurrent cancer The recurrence rate of early endometrial cancer is about 10%, and it can be as high as 50% in advanced stage. Treatment of recurrent cancer includes radiotherapy and endocrine therapy. Follow up after treatment, therefore, all patients should be followed up, and patients should be informed of the clinical signs of recurrence. Every 3-6 months and every 6-12 months after two years; vaginal dissection cytology every 6 months and every year after two years; serological CA125 test; chest X-ray every year and CT/MR if necessary; genetic testing for those with family history of tumor.