Cervical intraepithelial neoplasia, or CIN, is the abnormal growth of precancerous cells in the cervix. Most cases of CIN stay the same or are eliminated by the host's immune system without intervention, but a small percentage of cases progress to become cervical cancer, usually cervical squamous cell carcinoma, or SCC (Agorastos et al., 2005). The major cause of CIN is infection with the sexually transmitted human papillomavirus (HPV), usually the high-risk HPV type 16.

CIN has four distinct grades: Grade I, or CIN1, the least risky type, represents only mild dysplasia, or abnormal cell growth (Agorastos et al., 2005) and is considered a low grade squamous intraepithelial lesion (LSIL; Park et al., 1998). Grades II and above, or CIN2+, considered high grade squamous intraepithelial lesions (HSIL; Park et al., 1998), show moderate dysplasia in CIN2, severe dysplasia in CIN3, and invasive carcinoma in CIN4 (Agorastos et al., 2005). Cases of CIN are thought by some to progress through these stages toward cancer in a linear fashion (Rapp and Chen, 1998; Agorastos et al., 2005; Hillemanns, 2005). 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 (Agorastos et al., 2005; Monnier-Benoit et al., 2005).

See also

• Cervical cancer
• Human papillomavirus

References

1. Agorastos T., Miliaras D., Lambropoulos A.F., Chrisafi S., Kotsis A., Manthos A., and 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? European Journal of Obstetrics & Gynecology and Reproductive Biology, 121(1): 99-103.
2. Hillemanns P. ,Wang X., Staehle S., Michels W., and Dannecker C. 2005. Evaluation of different treatment modalities for vulvar intraepithelial neoplasia (VIN): CO2 laser vaporization, photodynamic therapy, excision and vulvectomy. Gynecologic Oncology, In Press, Corrected Proof.
3. Monnier-Benoit S., Dalstein V., Riethmuller D., Lalaoui N., Mougin C., and Prétet J.L. 2005. Dynamics of HPV16 DNA load reflect the natural history of cervical HPV-associated lesions. Journal of Clinical Virology, In Press, Corrected Proof.
4. Park J., Sun D., Genest D.R., Trivijitsilp P., Suh I., and Crum C.P. 1998. Coexistence of Low and High Grade Squamous Intraepithelial Lesions of the Cervix: Morphologic Progression or Multiple Papillomaviruses? Gynecologic Oncology, 70(3): 386-391.
5. Rapp L. and Chen J.J. 1998. The papillomavirus E6 proteins. Biochimica et Biophysica Acta, 1378(1): F1-F19.

Oncology | Gynecology

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