Cervical cancer pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Nima Nasiri, M.D.[2], Aida Javanbakht, M.D.


It is established that human papillomavirus (HPV) is the main cause of development of cervical neoplasia, only high risk strain of HPV can cause cervical cancer among women who are affected. This is because of HPV produced proteins E7 which alters epithelium of cervix mainly at junctional zone between the columnar epithelium of the endocervix and the squamous epithelium of the ectocervix.



High risk strains of HPV, mainly HPV types 16 and 18 had been identified as a potent cause of cancer of cervix. HPV plays main role in pathogenesis of cervical cancer and it is widely related to disrupting cell cycle growth and regulations, summary of these include:[1]

There are other cofactors that cause progression of cervical neoplasia, some of these include:[2][3][4]


Associated Conditions:

Conditions associated with cervical cancer include:[7]

Gross Pathology:

Gross pathological changes can be visualized by colposcopy and biopsy and application of a 3% acetic acid solution on biopsy speciemen and inspection under bright filtered light microscopy with 10 to 15 fold magnification. Findings in gross pathology of patients with cervical cancer include:[8]

Microscopic pathology

Microscopic morphology of low‐grade squamous intraepithelial lesions (CIN 1) include:[9]

High‐grade dysplasia (CIN 2 and 3) is characterized by the following features:

  • Loss of maturation
  • Nuclear crowding
  • Loss of nuclear polarity
  • Prominent cytonuclear atypia, increase in nuclear‐to‐cytoplasmic ratios
  • Irregular nuclear contours and coarse chromatin.
  • Increased proliferation and mitotic changes in the upper part of the epithelium.
  • In CIN2, most cytonuclear abnormalities are seen in the lower and middle third of the epithelium.
  • CIN3 characteristic features include:
    • Full‐thickness cytonuclear atypia
    • Minimal to absent maturation
    • Numerous mitotic activities




  1. Burd EM (January 2003). "Human papillomavirus and cervical cancer". Clin. Microbiol. Rev. 16 (1): 1–17. PMC 145302. PMID 12525422.
  2. Arends MJ, Buckley CH, Wells M (February 1998). "Aetiology, pathogenesis, and pathology of cervical neoplasia". J. Clin. Pathol. 51 (2): 96–103. PMID 9602680.
  3. zur Hausen H (December 1982). "Human genital cancer: synergism between two virus infections or synergism between a virus infection and initiating events?". Lancet. 2 (8312): 1370–2. PMID 6129466.
  4. Vanakankovit N, Taneepanichskul S (January 2008). "Effect of oral contraceptives on risk of cervical cancer". J Med Assoc Thai. 91 (1): 7–12. PMID 18386537.
  5. . doi:10.1016/S1674-8301(11)60020-1. Check |doi= value (help). Missing or empty |title= (help)
  6. Shi, Ting-Yan; Chen, Xiao-Jun; Zhu, Mei-Ling; Wang, Meng-Yun; He, Jing; Yu, Ke-Da; Shao, Zhi-Ming; Sun, Meng-Hong; Zhou, Xiao-Yan; Cheng, Xi; Wu, Xiaohua; Wei, Qingyi (2013). "A pri-miR-218variant and risk of cervical carcinoma in Chinese women". BMC Cancer. 13 (1). doi:10.1186/1471-2407-13-19. ISSN 1471-2407.
  7. Ogino, Ichiro; Okamoto, Naoyuki; Ono, Yoshimi; Kitamura, Tatsuo; Nakayama, Hiroki (2003). "Pelvic insufficiency fractures in postmenopausal woman with advanced cervical cancer treated by radiotherapy". Radiotherapy and Oncology. 68 (1): 61–67. doi:10.1016/S0167-8140(03)00128-2. ISSN 0167-8140.
  8. Burd, E. M. (2003). "Human Papillomavirus and Cervical Cancer". Clinical Microbiology Reviews. 16 (1): 1–17. doi:10.1128/CMR.16.1.1-17.2003. ISSN 0893-8512.
  9. Kalof, A. N; Cooper, K. (2006). "Our approach to squamous intraepithelial lesions of the uterine cervix". Journal of Clinical Pathology. 60 (5): 449–455. doi:10.1136/jcp.2005.036426. ISSN 0021-9746.

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