Early diagnosis and treatment of ovarian cancer remains one of the most difficult problems of oncology. Over the past 10 years, there has been a clear upward trend in the incidence of ovarian cancer in the United States and around the world. He consistently takes 2nd place in the structure of tumors of gynecologic localization (after cervical cancer), and remains the 1st place in mortality.
Currently, the etiological factors of malignant ovarian tumors are not reliably identified. There are three main hypotheses. According to the first, ovarian tumors occur in the hyperactivity of the hypothalamic-pituitary system, resulting in chronic hyperestrogenism. Estrogens do not directly lead to tumor cell transformation, but create conditions under which the likelihood of cancer in estrogen-sensitive tissues increases. Another hypothesis is based on the notions of “unceasing ovulation” (early menarche, late menopause, a small number of pregnancies, shortening of lactation). Permanent ovulation leads to damage to the epithelium of the cortical layer of the ovary, which, in turn, increases the likelihood of aberrant DNA damage with simultaneous inactivation of tumor-suppressing genes. According to the third genetic hypothesis, members of families with autosomal dominant breast and ovarian cancers are classified as high-risk individuals.
According to the world literature, hereditary forms of ovarian cancer are found in only 5-10% of patients. Advances in genetic engineering have revealed a number of oncogenes whose expression is associated with familial forms of ovarian cancer.
There is a relationship between the frequency of tumors of various morphological types and the age of patients. The peak in the incidence of ovarian cancer is noted between 60 and 70 years of life, but recently it has been recorded 10 years earlier.
Ovarian cancer is primary, secondary and metastatic.
The specific frequency of primary cancer is not more than 5%. In primary cancer, the tumor is formed from the surface epithelium of the ovary, therefore, there is no mixture of benign and malignant elements. Primary cancer is called a malignant tumor, primarily affecting the ovary. According to the histological structure, primary ovarian cancer is a malignant epithelial tumor of a glandular or papillary structure.
Secondary ovarian cancer (cystadenocarcinoma) is most common and accounts for 80–85% of all forms of ovarian cancer; develops on the background of benign or borderline tumors. Most often, secondary ovarian cancer occurs in serous papillary, less often in mucinous cystadenomas. Endometrioid cystadenocarcinoma also belongs to secondary lesions of the ovaries.
Metastatic ovarian cancer (Krukenberg tumor)
is a metastasis of the primary lesion, which is most often located in the gastrointestinal tract, stomach, mammary gland, thyroid gland, uterus.
Metastases from malignant tumors of the gastrointestinal tract spread through the hematogenous, retrograde-lymphogenous and implant pathways. Metastases are usually bilateral. In 60–70% of cases, ascites occurs. The tumor is growing very fast. Macroscopically metastatic tumor is whitish, nodular, often fibrous in section. It may be dense or testovato consistency, which depends on the ratio of stroma and parenchyma of the tumor, as well as secondary changes in the form of edema or necrosis. Microscopically, in metastatic cancer, cricoid circular cells filled with mucus are detected.
Currently, the Unified International Classification has been adopted, which reflects both the stage of the process and the histological type of the tumor.
The stage of the tumor process is established on the basis of clinical examination and during surgery.