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The body is made up of hundreds of millions of living cells. Normal body cells grow, divide, and die in an orderly fashion. Cancer begins when cells in a part of the body start to grow out of control. Cancer cells grow in a different manner to normal cells. Instead of dying, cancer cells continue to grow and form new, abnormal cells. They growing out of control and can invade other tissue.
The cervix is the lower part of the uterus. The cervix connects the body of the uterus to the vagina. The part of the cervix closest to the body of the uterus is called endocevix. The part next to the vagina is the exocervix. There are two main types of cells covering the cervix; squamous cells on the exocervix and glandular cells on the endocervix. There is a transformation zone where these two types of cell meet and most cervical cancer start in the transformation zone. Most cervical cancers begin in the cells lining the cervix. These cells do not suddenly change into cancer. Instead, the normal cells of the cervix first gradually develop pre-cancerous change that turn into cancer. Cervical cancers and cervical pre-cancers are classified by how they look under microscope. There are two main types of cervical cancers: squamous cell carcinoma and adenocarcinoma. Squamous cell carcinoma is from the squamous cells that cover the surface of the exocervix and take part in 80% to 90% of cervical cancer. These cells are like squamous cells under the microscope and often be found at where the exocervix join the endocervix. Most of the remaining cervical cancers are adenocarcinomas. It develops from the mucus-producing gland cells of the endocervix. Although almost all cervical cancers are either squamous cells carcinoma or adenocarcinomas, other types of cancer also can develop in the cervix such as melanoma, sarcoma and lymphoma occur more commonly in other parts of the body.
HPV and Cervical Cancer
Human papillomavirus is regarded as the vector that confers susceptibility to neoplastic conversion or that directly incites transmutation to a malignant phenotype in some infected epithelial cells. Some genes have instructions for controlling when our cells grow and divide; oncogenes can promote cell division and tumor suppressor genes can slow down cell division or cause cells to die at the right time. Cells become cancer cells when there is damage or mutation of the DNA. Normal cell have the ability to repair the damage DNA or die if the DNA cannot be fixed. In cancer cells the damage DNA is not repaired or the cell do not die. Instead it goes on making new cells that the body does not need. These new cells will all have the same damaged DNA as the first cell does. Cancer can be cause by DNA mutation that turn on oncogenes or turn off tumor suppressor genes. Much research has been done to characterize the Human Papilloma Virus (HPV) causes the production of two proteins known as E6 and E7. When these proteins are produced, they turn off tumor suppressor genes and allow the cervical lining cells to grow uncontrollably. The HPV, a Papovavirus, is a small double-stranded DNA virus with a diameter of 55 nm. It is encased in a protein capsid with the viral genome existing in a circular or epitomal configuration. The viral genome can be divided into three regions: the Upstream Regulatory Region (URR), the Early Region (E) and the Late Region (L). The Early Region is responsible for maintaining high numbers of HPV and the oncogenic types also encode for the proteins that promote the transformation of the host cell to cancer. The E6 and E7 regions in the Early Region are responsible for the oncogenic properties of the HPV. There are 120 types of HPV being found with about 20%-30% unclassified. Type 16, 18, 31, 35, 45, 51, 52 and 56 are considered high risk types because of the association of lower genital tract cancer and pre-cancer.
Infection Transmission Pathway of HPV
The infection transmission pathway of HPV first started when HPV is transmitted sexually from one host to another. The HPV may persist in the genital tract for a very long time. Genital-to-genital transmission happens when viruses enter into the host cells through micro-trauma at the fourchette, labia minora or vagina. The viruses take up to three months after exposure to show any clinical lesion and 20 years to show carcinomatous change. Some of the infection may be without any visible expression. The HPV virus loses it protein capsule after invades the genital cell. The HPV DNA therefore exists in the host cell without its shell. But to be infective the capsule is required. Infective HPV maybe found only in the upper layers of the epithelium where infective genomes of HPV are released as dying koilocytes. The two late regions of the HPV produce proteins for the construction of the capsid of the infective HPV genome. Infection is usually found at the basal cell layer and it does not go through the basement membrane of the genital epithelium. There are two main courses of female genital tract infection; transient infection and persistent infection. There are 65% of infected individuals show disease expressions and other may quickly resolve due to a complex interplay of host, viral and environmental factors with resultant increased dominance over the viral intruder. The infection becomes persistent when the virus escapes the hostâ€™s immune reaction. The persistent of the viral genome in the hostâ€™s cells may ultimately result in the cervical changes leading to carcinoma.
The persistent HPV infection leads to cervical change. There are some genes responsible for repairing damages, mistakes or mutation of DNA during cell replication; the p53 and Rb of the retinoblastoma gene. Apoptosis occurs when the damage is irreparable and the abnormal cell would be destroyed. In persistent HPV infection the anti-oncogenic activity p53 and Rb is blocked by the production of proteins by E6 and E7 from the HPV. As a result, the host cells growth uninhibited and lack of repair of damaged cells. Abnormal cells than proliferate and integrate with viral DNA into the host cellular DNA. As a result, the immortalization of the host cell becomes capable of invasion. Some of the wildly growing cells may develop irreparable, permanent changes in the genetic structure and eventually produce cancerous cells. After the HPV occupy the host cells, there are many cellular changes occur in the epithelial squamous which is detectable by cytology. The koilocytic atypia occur when the host cell nucleus is displaced to the side with a hollow appearance of cytoplasm. As the disease advances, the squamous cells begin to show sign of change in size and shape with sometimes nuclear changes. This change is known as Atypical Squamous Cells of Undertermined Signifiance (ASCUS). Similarly, for the cervical glandular cell is called Atypical Glandular Cells of Undertermined Signifiance (AGUS). About 60% of the cases may regress spontaneously, 20%-35% would persist unchanged and the remaining 10% are likely to develop High Grade Intra-epithelial Lesion (HGIL) with increase cellular changes, reduce in nuclear to cytoplasmic ratio and mitotic elements. Cervical intra-epithelial neoplasia (CIN) III or carcinoma in situ develops when the whole epithelium is replaced by mutant cells. The squamous cells continuous to grow and break through the basement membrane and invasion may occur. In Caucasian women, it takes about 15 years after the peak incidence of CIN III to develop invasive cancer.
Invasive cancers perform two primary modes of extension: local spread and metastasis via lymphatic and hematogenous routes. Cervical cancer may exhibit an ulcerative or exophytic appearance. Local spread includes extension to the endocervix and vaginal fornices, followed by progressive infiltration of parametrial tissues, uterine corpus, bladder or rectum. Stepwise, lymphatic extension may occur. Pelvic nodes become involved before common iliac and para-aortic lymph mode chains. It may continuous to spread through hematogenous route to distant implant such as lungs, bone, liver, parenchyma or other tissue. The change of metastasis rise as the size and expanse of tumor increase.
HPV infection is common and most people are able to clear the infection on its own. Sometimes the infection does not cure and become chronic. Although HPV can be spread during sex, it is not necessary for the HPV to be spread. Infection of HPV can be spread from one part of the body to another through skin-to-skin contact. So to prevent HPV infection, never allow another person to have contact with anal and genital area. However, HPV does not completely explain what causes cervical cancer. Most women with HPV do not get cervical cancer whereas some risk factors, like smoking and HIV infection, influence which women exposed to HPV are more likely to develop cervical cancer. Researches are being done on many other risk factors such as usage of diethylstilbestrol, oral contraceptives, chlamydia infection, family history and multiple full-term pregnancies.