Cervical cancer: Epidemiology & Pathogenesis
Epidemiology
Cervical cancer is the third most common cancer among gynecologic cancers and the third highest among women with cancer. It has lower incidence and lower mortality rate than uterine cancer or ovarian cancer. Human papillomavirus (HPV) has been identified as the cause of cervical cancer and HPV is found in 99.7 percent of cervical cancer patients. The histologic classification of cervical cancer is 69% of patients with squamous cell type and 25% of patients with adenocarcinoma. The number of newly diagnosed cervical cancer worldwide is estimated at 528,000, and in 2012, 266,000 died of cervical cancer.
The two major histologic categories of cervical cancer are squamous cell type and adenocarcinoma, as discussed above, and share a risk factor that causes both types of cancer. The incidence of cervical cancer increases at the early age of sexual life, but it increases more than 1.5 times in cases between 18 and 20 years of age. Also, the risk of developing cervical cancer increases when multiple partners are involved in sex life. The risk of developing cervical cancer increases when a partner has a history of HPV infection or partners with multiple partners, even if they are partners. In addition, the risk of a sexually transmitted infection such as Chlamydia trachomatis or genital herpes is increased, and the risk is increased if a vulvar or vagina has a history of squamous intraepithelial neoplasia or cancer. Finally, patients with immune deficiency or inhibition, such as HIV infection, are known to have an increased risk of developing cervical cancer.
Pathogenesis
Let's look at the pathogenesis of cervical cancer. There are four major processes for the development of cervical cancer. The first step is that oncogenic HPV infects the metaplastic epithelium of the cervical transformation zone. The next step is to keep the HPV infection constant, and the third step is to change the epithelial cells into precancerous lesions due to persistent virus infection. The precancer then invades the carcinoma and basement membrane and develops into cervical cancer. More than 40 HPV types have been identified, 15 of which are known to cause cervical cancer, and HPV types 16 and 18 account for 70% or more of the causes of cervical cancer Respectively. In the case of squamous cell carcinoma of the squamous cell type and adenocarcinoma type, HPV 16 infection and HPV 18 infection account for 59% and 13%, respectively. 45 type. In the case of adenocarcinoma, HPV 16 infection accounted for 36 percent and HPV 18 infection accounted for 37 percent. Other cases were 45 type, 31 type, 33 type.
Next, let's look at the pathway of cervical cancer. Cervical cancer may have a direct extension or lymphatic, hematogenous spread. Direct extension can be propagated to the uterine corpus, vagina, parametria, peritoneal cavity, bladder, rectum and ovarian involvement by direct extension is rare. Ovarian metastasis of cervical cancer is observed in about 0.5 percent of squamous cell carcinoma and 1.7 percent of adenocarcinoma. The organs that are transitional due to hematogenous transmission are the main sites of the lungs, liver, and bones. The bowel, adrenal glands, and brain are rare metastatic organs. Looking at the lymph node metastasis, the external iliac node metastasizes about 43 percent and the obturator node accounts for about 26 percent. In this case, the parametrial node occupies about 21%, and it is thought that the metastasis mainly occurs in three lymph nodes.
Cervical cancer is the third most common cancer among gynecologic cancers and the third highest among women with cancer. It has lower incidence and lower mortality rate than uterine cancer or ovarian cancer. Human papillomavirus (HPV) has been identified as the cause of cervical cancer and HPV is found in 99.7 percent of cervical cancer patients. The histologic classification of cervical cancer is 69% of patients with squamous cell type and 25% of patients with adenocarcinoma. The number of newly diagnosed cervical cancer worldwide is estimated at 528,000, and in 2012, 266,000 died of cervical cancer.
The two major histologic categories of cervical cancer are squamous cell type and adenocarcinoma, as discussed above, and share a risk factor that causes both types of cancer. The incidence of cervical cancer increases at the early age of sexual life, but it increases more than 1.5 times in cases between 18 and 20 years of age. Also, the risk of developing cervical cancer increases when multiple partners are involved in sex life. The risk of developing cervical cancer increases when a partner has a history of HPV infection or partners with multiple partners, even if they are partners. In addition, the risk of a sexually transmitted infection such as Chlamydia trachomatis or genital herpes is increased, and the risk is increased if a vulvar or vagina has a history of squamous intraepithelial neoplasia or cancer. Finally, patients with immune deficiency or inhibition, such as HIV infection, are known to have an increased risk of developing cervical cancer.
Pathogenesis
Let's look at the pathogenesis of cervical cancer. There are four major processes for the development of cervical cancer. The first step is that oncogenic HPV infects the metaplastic epithelium of the cervical transformation zone. The next step is to keep the HPV infection constant, and the third step is to change the epithelial cells into precancerous lesions due to persistent virus infection. The precancer then invades the carcinoma and basement membrane and develops into cervical cancer. More than 40 HPV types have been identified, 15 of which are known to cause cervical cancer, and HPV types 16 and 18 account for 70% or more of the causes of cervical cancer Respectively. In the case of squamous cell carcinoma of the squamous cell type and adenocarcinoma type, HPV 16 infection and HPV 18 infection account for 59% and 13%, respectively. 45 type. In the case of adenocarcinoma, HPV 16 infection accounted for 36 percent and HPV 18 infection accounted for 37 percent. Other cases were 45 type, 31 type, 33 type.
Next, let's look at the pathway of cervical cancer. Cervical cancer may have a direct extension or lymphatic, hematogenous spread. Direct extension can be propagated to the uterine corpus, vagina, parametria, peritoneal cavity, bladder, rectum and ovarian involvement by direct extension is rare. Ovarian metastasis of cervical cancer is observed in about 0.5 percent of squamous cell carcinoma and 1.7 percent of adenocarcinoma. The organs that are transitional due to hematogenous transmission are the main sites of the lungs, liver, and bones. The bowel, adrenal glands, and brain are rare metastatic organs. Looking at the lymph node metastasis, the external iliac node metastasizes about 43 percent and the obturator node accounts for about 26 percent. In this case, the parametrial node occupies about 21%, and it is thought that the metastasis mainly occurs in three lymph nodes.
