Malignant epithelial tumors: cervical cancer
Cervical cancer consistently ranks seventh in the structure of cancer mortality among women in the Russian Federation. The peak incidence occurs at the age of 40–49 years. Key risk factors include early sexual debut and frequent partner changes, which repeatedly increase the risk of infection with the human papillomavirus (HPV), the main etiological agent.
Carcinoma extremely rarely arises against the background of a healthy mucosa. The tumor is always preceded by cervical intraepithelial neoplasia (CIN). There are two main forms of the pathology:
- Microinvasive cancer. Characterized by the growth of anaplastic epithelium beyond the basement membrane to a depth of up to 3 mm. The surface epithelium retains the picture of severe dysplasia (CIN3). In the underlying stroma, edema, inflammatory infiltration, and fibroblast proliferation are observed. Already at this stage, invasion into lymphatic and blood vessels is possible.
- Invasive squamous cell carcinoma. Occurs predominantly at 45–55 years of age. It can be high-, moderate-, and low-differentiated.
According to its histological structure, invasive cancer is divided into two variants:
- Keratinizing: cells accumulate keratohyalin with the formation of specific "cancer pearls"; mitotic activity is low.
- Non-keratinizing: consists of polygonal or oval cells with eosinophilic cytoplasm. Intercellular bridges are absent, and nuclei vary from monomorphic to markedly polymorphic. A large number of mitoses, including atypical ones, is characteristic.
Growth pattern and metastasis of carcinoma
The clinical course and symptoms (primarily spotting) depend on the growth pattern of the tumor. It can grow exophytically (in the form of papillomas or polyps) or endophytically (infiltrating tissues with the formation of ulcers).
The tumor aggressively invades the adjacent parametrium, the walls of the urinary bladder and rectum. This leads to severe complications—the formation of vesicovaginal and rectovaginal fistulas, which inevitably entails septic conditions.
The spread of tumor cells occurs via three pathways:
- Lymphogenous: pelvic and retroperitoneal nodes are affected, as well as (retrogradely) inguinal lymph nodes.
- Hematogenous: metastases most commonly settle in the lung tissue, liver, and bones.
- Implantation: dissemination along the serous membranes leads to peritoneal carcinomatosis.
Endometriosis: etiopathogenesis of the tumor-like process
Endometriosis is the proliferation of tissue morphologically similar to the endometrium outside its normal localization. This pathology competes in frequency with myomas and inflammatory diseases, while frequently being combined with endometrial hyperplasia.
The pathogenesis is based on genetic mutations, failures in hormonal regulation, and cellular immunity failure (macrophages and natural killers), which normally must eliminate misplaced endometrial cells.
Three theories of the origin of endometriosis dominate modern pathomorphology:
- Implantation: endometrial cells are cast into the abdominal cavity during retrograde menstruation, spread through the lymphatic and blood vessels, or are surgically transplanted.
- Metaplastic: under the influence of trauma, inflammation, or hormones, the epithelium of other organs, the peritoneal mesothelium, or the vascular endothelium transforms into endometrioid-like tissue.
- Dysontogenetic: foci develop from embryonic remnants—remnants of the mullerian duct.
Morphology of adenomyosis
Adenomyosis, or internal endometriosis, is the penetration and proliferation of the endometrium directly into the thickness of the muscular layer of the uterus (myometrium). Mechanical traumas (abortions, manual examination, diagnostic curettage) serve as triggers, destroying the border between the basal layer of the endometrium and the myometrium.
Depending on the depth of wall involvement, three degrees of adenomyosis are distinguished:
- Glands and stroma are limited to the submucosal layer of the myometrium.
- Heterotopias reach the middle of the thickness of the muscular coat.
- The entire thickness of the uterine wall is affected.
Macroscopically, the uterine wall appears honeycombed, and on cross-section, characteristic bluish "eyes" (passages) exuding blood are visible. Microscopic examination with hematoxylin and eosin staining demonstrates endometrial glands surrounded by cellular stroma (lymphocytes, macrophages, fibroblasts). The foci are subject to menstrual changes, which is why hemorrhagic cysts eventually form in the myometrium. The process manifests with pain, heavy bleeding, and infertility, although malignant transformation is not typical for it.
Briefly: answers to topical questions
What three degrees of dysplasia and precancerous changes precede cervical cancer?
Cervical cancer is preceded by cervical intraepithelial neoplasia (CIN), which has three degrees of severity. The morphological picture depends on the depth of involvement of the stratified squamous epithelium:
- Mild dysplasia (CIN1) — pathological cell changes are limited to the lower 1/3 of the epithelial layer.
- Moderate dysplasia (CIN2) — atypical cells affect the lower 2/3 of the epithelial layer.
- Severe dysplasia (CIN3 / Carcinoma in situ) — the entire epithelial layer is affected throughout its entire thickness.
A specific sign of precancerous changes is the presence of koilocytes—cells with a halo around the nucleus, reflecting the cytopathic effect of papillomavirus infection.
What clinical symptoms and complications does endophytic cervical cancer cause?
Endophytic growth of cervical cancer has an infiltrative or ulcerative character. Spotting vaginal discharge is characteristic of cervical cancer.
The tumor rapidly invades the surrounding cervical stroma, urinary bladder, and rectum. Possible complications:
- Fistula formation — rectovaginal and vesicovaginal.
- Septic complications — develop as a result of the formation of such fistulas.
Class and exam questions
How is adenomyosis classified according to the depth of involvement?
Three degrees are distinguished: in the first, only the submucosal part of the myometrium is affected; in the second, the process reaches the middle of the muscular layer; and in the third, the entire thickness of the uterine wall is involved in the pathological process.
How does peritoneal carcinomatosis develop in cervical cancer?
Peritoneal carcinomatosis occurs as a result of implantation metastasis, when tumor cells detach from the primary node and disseminate over the surface of the serous membranes of the abdominal cavity.
What else to study on this topic
- Histological picture of uterine leiomyosarcoma
- Features of external endometriosis and its localization
- Severity grades of cervical intraepithelial neoplasia (CIN 1-3)
- Morphological differences of atypical mitoses in squamous cell carcinoma
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