Cervical cancer pathogenesis is driven by HPV-mediated malignant transformation within the cervical transformation zone, progressing from low-grade dysplasia (CN1/L-SIL) to high-grade lesions (CN2/3/H-SIL) via inhibition of tumor suppressor genes p53 and RB. Endometriosis represents a multifactorial pathology defined as the presence of functional endometrial glands and stroma outside the uterine cavity, resulting in local inflammation, adhesions, and potential ovarian malignancy through retrograde menstruation or metaplasia. These concepts illustrate how specific viral oncogenesis mechanisms and ectopic tissue implantation theories underpin diagnostic classification systems (WHO/Bethesda) and risk stratification protocols in gynecological pathology.
Cervical cancer pathogenesis is driven by HPV-mediated malignant transformation within the cervical transformation zone, progressing from low-grade dysplasia (CN1/L-SIL) to high-grade lesions (CN2/3/…