In recent decades, the incidence of cancer of the body of the uterus has steadily increased, which, apparently, is associated with an increase in the life expectancy of women and their stay in the postmenopausal period. Cancer of the body of the uterus occurs mainly in postmenopausal women, the average age of patients is 60-62 years. During the life of cancer of the endometrium 2-3% of women become ill.
There are two pathogenetic variants of uterine body cancer – hormone-dependent and autonomous.
Hormone-dependent cancer of the uterus occurs in approximately 70% of cases, and long-term hyperextension plays a role in the pathogenesis of this cancer variant. The latter can be both absolute and relative and can result from anovulation, feminizing ovarian tumors, excessive peripheral conversion of androgens to estrogens (in obesity, diabetes mellitus), estrogenic influences (in hormone replacement therapy with estrogen, treatment of breast cancer with tamoxifen with the formation of metabolites with estrogenic activity), etc. Hormone-dependent cancer of the uterus is preceded by the sequential occurrence of hyperplastic and precancerous processes of the endometrium. As a rule, it is a highly differentiated adenocarcinoma that is sensitive to hormonal therapy. The risk factors for hormone-dependent cancer of the uterus are infertility, lack of childbirth in history, late menopause, obesity, diabetes mellitus, hypertension, hereditary burden cancer with endocrine-metabolic pathogenesis (breast cancer, endometrium, ovary, colon), hormone-producing ovarian tumors, postmenopausal estrogen replacement therapy, the use of tamoxifen in the treatment of breast cancer.
In retrospective studies, information was obtained about the dependence of the risk of uterine cancer and the severity of the endometrial hyperplastic process. Uterine cancer occurs in 1% of patients with glandular hyperplasia, in 3% with glandular-cystic, in 8% with simple atypical hyperplasia and in 29% with complex atypical hyperplasia. However, postmenopausal risk is higher than at another age.
Autonomous pathogenetic variant of endometrial cancer occurs in less than 30% of cases, occurs against the background of endometrial atrophy in the absence of hyperestrogenism in patients without metabolic and endocrine disorders. It is believed that pronounced depression of the T-system of immunity plays a role in the development of an autonomous variant of endometrial cancer, in the context of impaired adaptation homeostasis and hypercorticism. Changes in immunity consist in a significant decrease in the absolute and relative number of T-lymphocytes, inhibition of all subpopulations of T-lymphocytes and their theophylline-sensitive forms, a large number of lymphocytes with blocked receptors.
Autonomic uterine cancer develops at an older age. No risk factors have been identified for this option. As a rule, it appears in thin older women without previous hyperplastic processes. A history of postmenopausal bleeding may occur on the background of endometrial atrophy. The tumor has low differentiation, low sensitivity to hormonal therapy, early invasion of the myometrium and metastasis occur.
Classification of uterine cancer depending on its prevalence is based on clinical or on clinical and histological data.
Clinical classification (FIGO, 1971) is used before surgery or in inoperable patients:
Stage 0 – in situ cancer.
Stage I – the tumor is limited to the body of the uterus.
Stage II – the tumor spreads to the cervix, without going beyond
Stage III – the tumor spreads within the pelvis.
Stage IV – a tumor invades adjacent organs or spreads over
IVA – the tumor grows into the bladder or rectum.
IVB – distant metastases.
Intraoperative data and histological examination allows you to select
morphological stages of uterine cancer (FIGO, 1988):
Stage ΙΙΒ – spreading to the stroma of the cervix.
Stage ΙΙΙΑ – the germination of a tumor in the serous membrane of the uterus, metastases in the fallopian tubes or ovaries, tumor cells in the washes from the abdominal cavity.
Stage II – spread to the vagina.
Stage C – metastases to the pelvic or lumbar lymph nodes.
Stage IVA – germination of the mucous membrane of the bladder or rectum. Stage IVB – distant metastases to the inguinal lymph nodes.
Based on this classification and the results of histological examination,
patients after surgery plan the subsequent stages of treatment.
Histologically, endometrial cancer is most often represented by:
• adenocarcinoma (papillary, secretory, with squamous metaplasia);
• mucinous cancer;
• papillary serous cancer;
• clear cell carcinoma;
• squamous cell carcinoma;
• undifferentiated cancer.
In 80% of cases, endometrial cancer is adenocarcinoma Depending on the severity of tissue and cell atypism, there are three degrees of differentiation of uterine cancer (FIGO, 1989):
• highly differentiated cancer (G1);
• moderately differentiated cancer (G2);
• low grade cancer (G3).
The clinical picture of uterine cancer is to some extent dependent on the menstrual function. In menstruating women, endometrial cancer can be manifested by abundant long periods, often irregular, acyclic bleeding. However, in 75% of cases, endometrial cancer develops in postmenopausal women and causes the appearance of blood discharge from the genital tract, which is called postmenopausal bleeding. Blood discharge may be scanty, smearing or copious. They occur in postmenopause in 90% of patients with endometrial cancer; in 8% of cases with diagnosed cancer, its clinical manifestations are absent. In addition to blood discharge, patients may experience purulent discharge, and pyometra can form during stenosis of the cervical canal. Pains, if they are not caused by pyometra, appear late, with a common cancer process with infiltrates in the pelvis. In case of compression of the ureter infiltrate with the emergence of a block of kidney pain localized in the lumbar region. In some cases, ascites or mass lesions can form in the pelvis (with metastases in the ovaries, omentum).