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Cervical intraepithelial neoplasia

Cervical intraepithelial neoplasia, or CIN, is the abnormal growth of precancerous cells in the cervix. Most cases of CIN remain stable, or are eliminated by the host's immune system without intervention. However a small percentage of cases progress to become cervical cancer, usually cervical squamous cell carcinoma, or SCC.[1] The major cause of CIN is infection with the sexually transmitted human papillomavirus (HPV), usually the high-risk HPV types 16 or 18.

The earliest microscopic change corresponding to CIN is dysplasia of the epithelial or surface lining of the cervix, which is essentially undetectable by the woman. Cellular changes associated with HPV infection, such as koilocytes, are also commonly seen in CIN. It is usually discovered by a screening test, the Papanicolaou or "pap" smear. The purpose of this test is to diagnose the disease early, while it has not yet progressed to invasive carcinoma, and thus is easy to cure. Though epithelial dysplasia may regress spontaneously, persistent lesions must be removed, either with surgery, chemical burning, heat burning, burning with laser, or freezing (cryotherapy).


CIN has three distinct grades:

  • CIN1 (Grade I), the least risky type, represents only mild dysplasia, or abnormal cell growth[1] and is considered a low grade squamous intraepithelial lesion (LGSIL). [2]. It is confined to the basal 1/3 of the epithelium.
  • CIN2 (Grade II), as well as CIN III, are considered high grade squamous intraepithelial lesions (HSIL). [2] CIN2 represents moderate dysplasia, and is confined to the basal 2/3 of the epithelium
  • CIN3 (Grade III): In this lesion, severe dysplasia spans greater than 2/3 of the the entire epithelium, and may involve the full thickness. This lesion may also be referred to as cervical carcinoma in situ.


Cases of CIN are thought by some to progress through these stages toward cancer in a linear fashion.[1][3][4]

However, evidence suggests that cancer can occur without first detectably progressing through these stages and that a high grade intraepithelial neoplasia can occur without first existing as a lower grade.[1][5]

See also


  1. ^ a b c d Agorastos T, Miliaras D, Lambropoulos A, Chrisafi S, Kotsis A, Manthos A, Bontis J (2005). "Detection and typing of human papillomavirus DNA in uterine cervices with coexistent grade I and grade III intraepithelial neoplasia: biologic progression or independent lesions?". Eur J Obstet Gynecol Reprod Biol 121 (1): 99-103. PMID 15949888.
  2. ^ a b Park J, Sun D, Genest D, Trivijitsilp P, Suh I, Crum C (1998). "Coexistence of low and high grade squamous intraepithelial lesions of the cervix: morphologic progression or multiple papillomaviruses?". Gynecol Oncol 70 (3): 386-91. PMID 9790792.
  3. ^ Hillemanns P, Wang X, Staehle S, Michels W, Dannecker C (2006). "Evaluation of different treatment modalities for vulvar intraepithelial neoplasia (VIN): CO(2) laser vaporization, photodynamic therapy, excision and vulvectomy". Gynecol Oncol 100 (2): 271-5. PMID 16169064.
  4. ^ Rapp L, Chen J (1998). "The papillomavirus E6 proteins". Biochim Biophys Acta 1378 (1): F1-19. PMID 9739758.
  5. ^ Monnier-Benoit S, Dalstein V, Riethmuller D, Lalaoui N, Mougin C, Prétet J (2006). "Dynamics of HPV16 DNA load reflect the natural history of cervical HPV-associated lesions". J Clin Virol 35 (3): 270-7. PMID 16214397.
This article is licensed under the GNU Free Documentation License. It uses material from the Wikipedia article "Cervical_intraepithelial_neoplasia". A list of authors is available in Wikipedia.
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