Malignant Epithelial Tumors: Cervical Cancer
Cervical cancer is a major cause of cancer-related mortality among women worldwide. The peak incidence occurs between 40 and 49 years of age. Key risk factors include early onset of sexual activity and multiple sexual partners, which significantly increase the risk of infection with high-risk human papillomavirus (HPV) types—the primary etiologic agent.
Carcinoma extremely rarely arises on normal mucosa. Tumors are invariably preceded by cervical intraepithelial neoplasia (CIN). There are two main pathological forms:
- Microinvasive carcinoma. Characterized by the penetration of anaplastic epithelium beyond the basement membrane to a depth of up to 3 mm. The surface epithelium retains features of severe dysplasia (CIN3). The underlying stroma shows edema, inflammatory infiltration, and fibroblast proliferation. Invasion of lymphatic and blood vessels can already occur at this stage.
- Invasive squamous cell carcinoma. Most commonly seen in women aged 45–55 years. It can be well-, moderately, or poorly differentiated.
Histologically, invasive carcinoma is divided into two variants:
- Keratinizing: cells accumulate keratohyalin forming characteristic "cancer pearls"; mitotic activity is low.
- Non-keratinizing: composed of polygonal or oval cells with eosinophilic cytoplasm. Intercellular bridges are absent, and nuclei range from monomorphic to markedly polymorphic. A high mitotic rate, including atypical mitoses, is typical.
Growth Pattern and Metastasis of Carcinoma
The clinical course and symptoms (primarily abnormal vaginal bleeding) depend on the growth pattern of the tumor. It may grow exophytically (as papillomas or polyps) or endophytically (infiltrating tissues with ulcer formation).
The tumor aggressively invades the surrounding parametrial tissue, bladder wall, and rectum. This leads to severe complications—the formation of vesicovaginal and rectovaginal fistulas, which inevitably result in septic conditions.
Spread of tumor cells occurs via three pathways:
- Lymphogenic: pelvic, retroperitoneal, and (retrogradely) inguinal lymph nodes are affected.
- Hematogenous: metastases most commonly settle in the lungs, liver, and bones.
- Implantation: dissemination along serosal surfaces leads to peritoneal carcinomatosis.
Endometriosis: Etiopathogenesis of a Tumor-Like Process
Endometriosis is the proliferation of tissue morphologically similar to the endometrium outside its normal anatomical location. This pathology rivals uterine fibroids and inflammatory diseases in frequency, and frequently coexists with endometrial hyperplasia.
The pathogenesis is based on genetic mutations, hormonal dysregulation, and failure of cellular immunity (macrophages and natural killer cells), which normally should eliminate ectopic endometrial cells.
Modern pathomorphology distinguishes three main theories regarding the origin of endometriosis:
- Implantation theory: endometrial cells are regurgitated into the peritoneal cavity during retrograde menstruation, spread via lymph and blood vessels, or are surgically transplanted.
- Metaplastic theory: under the influence of trauma, inflammation, or hormones, the epithelium of other organs, peritoneal mesothelium, or vascular endothelium transforms into endometrium-like tissue.
- Dysontogenetic theory: lesions develop from embryonic remnants—derivatives of the Mullerian ducts.
Morphology of Adenomyosis
Adenomyosis, or internal endometriosis, is the penetration and growth of the endometrium directly into the thickness of the uterine muscular layer (myometrium). Mechanical trauma (abortions, manual exploration, diagnostic curettage) serves as the trigger, disrupting the boundary between the basal layer of the endometrium and the myometrium.
Depending on the depth of uterine wall involvement, three degrees of adenomyosis are distinguished:
- Glands and stroma are confined to the submucosal layer of the myometrium.
- Heterotopic foci reach the middle of the muscular layer's thickness.
- The entire thickness of the uterine wall is affected.
Macroscopically, the uterine wall appears honeycombed, and cut sections reveal characteristic bluish "eyes" (glandular spaces) oozing blood. Microscopic examination with hematoxylin and eosin staining demonstrates endometrial glands surrounded by cellular stroma (lymphocytes, macrophages, fibroblasts). The foci undergo menstrual cyclic changes, leading to the formation of hemorrhagic cysts in the myometrium over time. The process manifests with pain, heavy bleeding, and infertility, although malignant transformation is uncommon.