Cervical squamous intraepithelial neoplasia

Cervical intraepithelial neoplasia (CIN)
Updated: 02/29/2020
© Jun Wang, MD, PhD


General features
  • AKA Squamous Intraepithelial Lesion (SIL)
  • Precancerous changes
  • Human papilloma virus associated
  • Usually start from cervical transformation zone
  • Bethesda system (High and low grade)
  • Low grade: CIN I
  • High grade: CIN II and III
  • Low grade dysplasia tend to regress
  • Much higher risk for development of invasive cancer if high grade
Clinical presentations
  • Most time identified due to screening with Pap test
Key risk factors
  • Human papilloma virus infection, especially high risk group, such as HPV 16 and 18
  • Most HPV infections will regress, even without treatment 
Key pathogenesis
  • HPV products
    • E6: Promotes degradation of p53, abnormal activation of telomerase  
    • E7: Inactivates retinoblastoma 1, a tumor suppressor
  • P16 overexpression in high grade dysplasia and cancers
Key Laboratory findings
  • Pap smears
  • HPV test
Key morphological features
Markers of dysplasia
  • Diffuse p16 reactivity
  • Proliferation (Ki67 reactivity) beyond basal layer
Management
  • LSIL: Controversial since most lesions regress
  • HSIL:
Cone biopsy
LEEP
Electrodiathermy
Cryosurgery
Laser
Long term followup
Intraepithelial lesions in anogential areas
  • Similar etiology and terminology
  • Same morphology in cytological examination
  • Vulva: Vulvar intraepithelial neoplasm; incidence increasing; more common in women 20 to 35 years; multifocal, VIN I-III
  • Vagina: Vaginal intraepithelial neoplasia; uncommon; Mean age ~50-60 years; VAIN I-III
  • Anus:  Anal intraepithelial neoplasia; perianal skin or anal canal in flat mucosa or with condyloma acuminatum; HIV+ patients are at increased risk, often have high risk HPV types within low grade lesions; AIN I-III



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