**2. Risk factors**

In 2017, the American Cancer Society (Cancer Statistic Center) estimated that there will be 12,820 new cervical cancer patients and 4210 deaths. The incidence rate for cervical cancer from 2009 through 2017 is 7.6 per 100,000 women; the rate of death from 2010 through 2014 is 2.3 per 100,000 women. The incidence and death rates for cervical cancer in Latin America are still high; for example, in Venezuela, the annual average of new cervical cancer cases from

**Figure 1.** Age-standardized cervical cancer: Incidence and mortality. Rates by world area. GLOBOCAN 2008.

In developed countries, most patients are diagnosed in the early stage of the disease or with pre-malignant lesions susceptible to effective treatment. Nevertheless, with the current migratory movement of women, there is an upturn of advanced stage cervical cancer, especially among women who miss their routine gynecologic evaluation or belong to immigrant's

In Latin America, cervical cancer occupies the second position after breast cancer and is the most common cause of cancer deaths among women, primarily in young women. For public

2010 through 2014 was 4019, with a standardized rate on 2014 of 24.88.

32 Cervical Cancer - Screening, Treatment and Prevention - Universal Protocols for Ultimate Control

groups without suitable medical assistance.

Most of the risk factors for developing cervical cancer are associated with a compromised immune response that allows HPV infection, the etiologic agent of nearly all cases of cervical cancer. These factors include the following.

• Early first sexual intercourse; the risk increases if the first sexual activity is before 21 years of age [11, 12], being approximately 1.5% when first sexual activity is at 18–20 years of age and younger.

exposure and shared risk factors; however, subsequent data comparing sisters and half-sisters

Uterine Cervical Cancer Screening

35

http://dx.doi.org/10.5772/intechopen.72606

Research has been done to identify genetic alterations that can make women more susceptible

To date, results show a large polymorphism diversity in a wide variety of genes, including those regulating immunity and susceptibility [19–21] and generating a large amount of immune mechanism (cytokines production, angiogenesis, tumor suppression pathways, tran-

The causal role of HPV in all common and non-common histologic types has been firmly established biologically and epidemiologically and has led to a new carcinogenic model for cervical cancer: HPV acquisition, HPV persistence, progression of pre-malignant lesion to invasive cancer [25, 26]. Human papillomavirus is acquired through sexual contact; most population prevalence reaches its peak few years after the median age of initiation of sexual

Most HVP infections are transient, lasting no more than 1 or 2 years [27]. Persistent HPV infection for 1–2 years, especially by HPV 16 predicts development of CIN 3 (cervical intraepithelial neoplasia) or malignant changes. The probability of untreated CIN 3 transforming into an invasive cancer is 30%, although 1% of treated CIN 3 transforms into an invasive

There are more than 100 HPV types; high-risk types 16, 18, 31, 35, and 39 are linked to malignant transformation [29]. Type 18 infection progresses with bad prognosis based on recorded

High-risk HPV infection may generate some of the following cell biologic alterations leading to malignant transformation. Two of the eight proteins encoded by the HPV genome, E6 and E7, accounts for most carcinogenic effects of high-risk HPV types. They promote carcinogen-

• They interfere with important tumor suppressor pathways; E6 inhibits the p53 tumor suppressor by promoting its proteasomal degradation, while E7 disrupts the retinoblastoma (Rb) pathway [30, 31], or activates oncogenes via EGFR (epidermal growth factor receptor)

• They induce telomerase enzyme activation related with the unlimited potential of neoplas-

• E6 and E7 abrogate cell cycle checkpoints and induce genomic instability. Both can induce abnormal centrosome numbers and centrosome abnormalities. They also have synergistic

effects on centrosome abnormalities and chromosomal instability [35, 36].

to cervical cancer because of less resistance to HPV infection and persistent infection.

far exceed shared environments.

scription activation) [22–24].

intercourse.

cancer [28].

survival rates.

[32, 33].

esis in several ways:

tic cells replication [34].

**4. Human papillomavirus**

