Cervical cancer arises from hyperplasia of epithelial cells from cervix. It is the second most common cancer in women worldwide and has increasingly become a major cause of cancer death in developing countries due to weak consciousness of cancer preventions, poor sanitary conditions and limited medical technology (Parkin, Bary, Ferlay
& Pisani, 2005). Eighty-three percent of cases were found in developing countries that have access to only 5% of global cancer resources (Denny,
2005). In the essay, the histology of the cervical transformation zone and histopathology during the different stages of the cervical intraepithelial neoplasia and carcinoma in situ will be described, incorporated with the risk factors of infection of the transformation zone with the Human
The cervical transformation zone is the mucosa where the simple columnar epithelium
non-keratinizing squamous epithelium of the ectocervix meet and undergo metaplasia from columnar to squamous differentiation (Carr &
Sellors, 2004). The position of the transformation zone is changeable.
The estrogen level decreases with an increase in age, which causes the cervix to shrink. Therefore, the transformation zone shifts from
ectocervix towards and into the endocervix (Castle et al., 2006). Most cervical cancer occurs at the transformation zone. This region is vulnerable and relative easily to have lesions compared with vaginal and other cervical epithelia although HPVs infections are equally commonly
(Castle et al., 2004). The transformation zone is of significance in cervical cancer study and the precise reason for its vulnerability is still unclear.
Cervical intraepithelial neoplasia (CIN) is the premalignant lesion that squamous cells abnormally develop (dysplasia) on cervical epithelium.
CIN is diagnosed according to histological characteristics including differentiation, maturation and stratification of cells. Additionally, analyzing mitotic figures and nuclear abnormalities, such as high nuclear-cytoplasmic ratio, enlarged nuclei and increased intensity of nuclear staining (hyperchromasia) help to classify the CIN into an accurate stage (Martin & O’Leary, 2011). CIN is graded as CNI1 CNI2 and
CIN3 depending on the percentage of the epithelia thickness replaced by undifferentiated dysplastic cells (Wentzensen et al., 2009). CIN1 is mild dysplasia and confined to the lower one third of the epithelium. The basal cells lack differentiation or orderly stratification. They have irregular, enlarged
nuclear-cytoplasmic ratio. The upper cells can still mature normally with minimal nuclear abnormalities. However, mitotic figures are not obvious in this stage. In moderate dysplastic CNI2, the dysplastic cells have
similar characteristics with those of CNI1 and extend upwards but are restricted to lower two-thirds of the epithelium. On the other hand, nuclear abnormalities are more obvious. Mitotic figures with abnormal forms become more prevalent (Sellors & Sankaranaravanan, 2003). CIN3 is considered as severe dysplasia with abnormal cells present in upper third of the epithelium. Mitotic figures with abnormal forms are numerous throughout the epithelium (Reich, Lahousen, Pickel,
Tamussino & Winter, 2002). Carcinoma in situ (CIS) is the most serious stage of CIN3. At early stage of CIN3 cells in the superficial epithelium may still undergo differentiation and maturity. However, when it develops to CIS the dysplasia cells will be present throughout whole thickness of the epithelium and are about to invade the basal membrane.
CIS sometimes is named stage zero of cervical cancer since the epithelium have totally lost differentiation and stratification but dysplasia does not involve the deep tissues. In terms of risks of developing into an