**4. Classification of precancers and invasive cancers**

1. Low-grade squamous intraepithelial lesion (LSIL): occurs due to persistent HPV infection; cervical intraepithelial neoplasia grade 1 (CIN1);

mild squamous dysplasia; flat condyloma; koilocytotic atypia; koilocytosis.


an invasive epithelial tumour composed of squamous cells of varying degrees of differentiation.

#### **4.1. Associated risk factors**

**3. Natural history of cervical cancer**

**3.2. The development of cervical cancer**

**3.3. The HPV epidemiology: HPV: The causal factor**

High-risk 16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59;

cofactors are early sexual exposures and multiple partners.

**4. Classification of precancers and invasive cancers**

due to the protection from cell-mediated immunity.

1. Low-grade squamous intraepithelial lesion (LSIL):

cervical intraepithelial neoplasia grade 1 (CIN1);

occurs due to persistent HPV infection;

Low-risk 6, 11, 40, 42, 43, 44, 54, 61, 70, 72, 81.

os and finally to the distal cervical canal when age increases.

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

referred to as the transformation zone (IARC, 2005; WHO, 2006).

Squamous epithelium and columnar epithelium are both types of epithelium lining in the

The squamocolumnar junction is the junction between squamous epithelium and columnar epithelium and it migrates from the periphery of the ectocervix inward towards the external

The process by which the columnar epithelium is replaced by stratified squamous epithelium is termed as squamous metaplasia and the area where this transformation takes place is

The cervix is protected by stratified squamous cell epithelium from injuries by toxins and from infections. The human papilloma virus (HPV) primarily targets the squamous cells, and persistent infection by the high-risk strains leads to change of cells to metaplasia and dyspla-

HPV16 and 18 are responsible for the development of all the precancers and invasive cancers

HPV transmission occurs through skin and mucous contact during sexual contact, and the

Persistent HPV infections cause cervical cancers but most of the HPV infections are transient

sia, which is the precancer stage and this occurs in the transformation zone—TZ.

**3.1. Histology**

surface of the cervix.

of the uterine cervix.

**3.4. HPV transmission**

HPV types:

Cervical cancer begins with abnormal changes in the cervical tissue. The risk of developing these abnormal changes has been associated with the following factors: relationship to sexual intercourse; many partners during lifetime; frequent intercourse; early onset of sexual activity; first pregnancy in teenage years; multiparity (several children) by mid 20s; venereal diseases; genital herpes (herpes simplex virus type 2—HSV-2); human papilloma virus (HPV); race: incidence higher in blacks and Hispanics; low socioeconomic status; poor genital hygiene; cigarette smoking; peak incidence over 40 years.

#### **4.2. Signs and symptoms**

post-coital or unexplained vaginal spotting or bleeding; persistent vaginal discharge; pelvic pain.

#### **4.3. Five-year survival rates**

Adenocarcinomas of the cervix have a worse prognosis than squamous cell cancers.

Squamous cell carcinoma, adenocarcinoma:

Stage 0 = 100%; Stage I = 60–85%; Stage II = 40–60%; Stage III = up to 40%; Stage IV = <15%.
