Cervical Cancer
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Direct answer
Cervical cancer is a human papillomavirus-driven malignancy in which viral oncoproteins disable the two great tumour suppressors: E6 degrades p53 and E7 inactivates Rb. HPV 16 and 18 together cause about 70 per cent of cases — type 16 predominating in squamous cell carcinoma, with 18 strongly linked to adenocarcinoma. Because it evolves slowly through cervical intraepithelial neoplasia, cervical cancer is the most screenable and vaccine-preventable cancer, which is the theme of most modern exam questions.
What you must remember
- E6 and E7: E6 directs proteasomal degradation of p53, and E7 inactivates retinoblastoma protein, freeing E2F-driven cell-cycle entry — the most tested pair in this topic.
- HPV types: 16 and 18 cause about 70 per cent of cancers worldwide; 31, 33 and 45 come next; types 6 and 11 cause condylomas and low-grade lesions, not cancer.
- Precursor spectrum: koilocytic atypia and CIN 1 (low-grade, often regressing) progress through CIN 2 and 3 (high-grade, treatment warranted) over years; adenocarcinoma in situ is the glandular precursor.
- Morphology and spread: squamous cell carcinoma predominates, exophytic at the transformation zone; spread is direct into parametrium, then lymphatic to obturator and iliac nodes, with haematogenous spread late.
- Screening: Pap smear showing koilocytes, visual inspection with acetic acid in programme settings, and HPV DNA testing — recommended by WHO as the primary screen from age 30.
- Vaccination: prophylactic L1 virus-like particle vaccines, including India's indigenous quadrivalent CERVAVAC, given as two doses to girls aged 9 to 14 before sexual debut; WHO's 90-70-90 strategy targets vaccination, screening and treatment coverage by 2030.
Common confusion
E6 versus E7 is the classic memory trap: E6 pairs with p53 and E7 with Rb. The second confusion is lesion grade — CIN 1 with koilocytosis reflects productive viral infection that mostly regresses, whereas CIN 2 and 3 are true neoplasia requiring treatment. Finally, vaccination and screening are complementary, not alternatives: vaccines prevent new infection but neither treat established lesions nor replace screening in vaccinated populations.
Exam-focused takeaway
NEET-PG questions test the E6-p53 and E7-Rb pairing, the HPV type associations (16 with squamous carcinoma, 18 with adenocarcinoma, 6 and 11 with warts), the CIN-to-invasion natural history, and koilocyte recognition on cytology. Programme-level stems ask for the primary screening modality (HPV DNA testing per WHO), the vaccine schedule for girls aged 9 to 14, and the 90-70-90 elimination targets; clinical vignettes feature postcoital bleeding in a young woman. The same facts earn marks in pathology, gynaecology and community medicine.
Frequently asked questions
How does HPV cause cervical cancer?
E6 degrades p53 and E7 inactivates retinoblastoma protein, jointly disabling apoptosis and cell-cycle control; persistent high-risk infection then drives CIN and invasion.
Which HPV types cause cervical cancer?
Types 16 and 18 cause about 70 per cent of cases, then 31, 33 and 45; types 6 and 11 cause warts, not cancer.
What is the difference between CIN 1 and CIN 2-3?
CIN 1 is a low-grade productive viral lesion that usually regresses; CIN 2 and 3 are high-grade neoplasia with real progression risk, requiring treatment.
What is the current screening approach?
WHO recommends HPV DNA testing as the primary screen from age 30; Pap cytology and visual inspection with acetic acid are alternatives; positives go to colposcopy.
Who should receive the HPV vaccine and in what schedule?
Girls aged 9 to 14 before sexual debut, two doses; India's indigenous quadrivalent CERVAVAC uses the 0 and 6 month schedule.
What are the WHO 90-70-90 targets?
By 2030 — 90 per cent of girls vaccinated by 15, 70 per cent of women screened by 35 and 45, and 90 per cent of affected women treated.