Pathogenesis of cancer of the Cervix; Etiology, Risk factor and Co carcinogen serotypes, Cells

Cervical cancer develops through a multi-step process driven by persistent infection with high-risk human papillomavirus (HPV), particularly HPV types 16 and 18. The pathogenesis involves viral oncogenes, genetic mutations, and immune evasion.

Pathogenesis of Cervical Cancer
HPV Infection & Viral Integration

HPV infects basal epithelial cells at the transformation zone of the cervix.

The virus produces E6 and E7 oncoproteins, which inactivate tumor suppressor genes (p53 and Rb), leading to uncontrolled cell growth.

Cellular Dysplasia & Precancerous Lesions

Persistent HPV infection causes cervical intraepithelial neoplasia (CIN), classified as:

CIN 1 (mild dysplasia)

CIN 2 (moderate dysplasia)

CIN 3 (severe dysplasia, carcinoma in situ)

Progression to Invasive Cancer

Accumulation of genetic mutations leads to malignant transformation.

Tumor cells invade the basement membrane, spreading to deeper tissues.

Metastasis & Immune Evasion

Cancer cells spread via lymphatic and hematogenous routes to distant organs.

HPV-infected cells evade immune detection by downregulating antigen presentation.

Risk Factors
Early sexual activity & multiple partners

Smoking & immunosuppression

Long-term oral contraceptive use

Lack of HPV vaccination & screening

#Cervix