| Cervical cancer is one of the most frequent malignant tumors in female, its incidence is the first place in the developing countries and the second only behind breast cancer. Based on statistical data from the World Health Organization, around 500,000 new cases of the cervical cancer are reported yearly in the world, and near 20,000 patients, with 80% from the developing countries, die from the disease. In China, the prevalence of cervical cancer is 14.6 per 10,000, and is considerably highly level compared with that in other countries. Recent years, increasing data of investigation indicate that the cervical cancer in young women tends to be increased. According to epidemiological and biological studies, human papillomavirus (HPV) infection is considered to be an important pathogenic pathway in the induction of the development of cervical cancer and precancerous lesion. HPV DNA can be detected in almost all cervical cancer samples in the world. In 1995, International Agency for Research on cancer (IARC) symposium pointed out clearly that HPV infection is the chief cause of cervical cancer.HPV is a kind of double-strands, closure and circular DNA virus, which infects human skin and mucous membrane, showing philo-epithelium, -tissue and -host specificities. No cross infection interspecies has been found. HPV-DNA is divided into three regions by its function, early gene, late gene and long control region. Over110 types of HPV have been identified currently, about 30 types can be isolated from infected genital tract, and over 20 types are found to be associated with cervix tumor. HPV can be divided into two groups according to its philo-tissue specificity, cutaneous and genital tract HPV. On the basis of the oncogenic potential, the HPV genotypes have been classified into two groups, low risk HPV types, such as HPV6, 11, 42, 43, 44, 54, 61, 70, 72, 81, cp6 108, which are associated with exogenous condyloma of gential tract crissum skin and vagina subjacent, flat condyloma and cervical intra-epithelial neoplasia I (CIN I ); high risk HPV types, such as HPV16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59, 68, 73, 82, which are associated with cervical intra-epithelial neoplasia III (CIN III) and invasion cervical cancer. The most frequent types are HPV 16 and HPV 18, then HPV 58, 52, 56. HPV phenotyping is associated with histologic typing and clinical stages of the cervical cancer. HPV 16 is observed to be associated most strongly with squamous cell carcinoma, HPV 18 is associated most strongly with adenocarcinoma, HPV16 or mixed types of HPV 16 and HPV 18 are associated with lower-grade clinical stages (0- II stages), and HPV 18 is associated with higher-grade clinical stages (III-IVstages) and poor prognosis.As a common sexually transmitted disease, HPV infection is a often transient disease. About 80% HPV infection is temporal, and generally virus is cleared in 7-12 months. In remaining 20% cases, virus is cleared in 3 years. Only in lower number of cases (< 4%) HPV infection is persistent, leading to persistent cervical intra-epithelial neoplasia or the development of cervical cancer. Although HPV infection is chief cause of cervical cancer, only few women with HPV infection develop cervical cancer. Statistical data demonstrate that sexual activity, organism immune state, copiousness, long-term oral contraceptive, smoking, nutrition, social factor, other microorganism infection in gential tract, et al, are also involved in the pathogenesis.HPV carcinogenesis is associated with integration of HPV DNA with humanDNA. In benign lesions, HPV genome is often present in free shape. In HPV-associated malignant tumors, HPV DNA often is integrated into host genome. To date, the chief gene of integration of HPV which causes carcinogenesis is E6, E7, and E2. Integration of HPV DNA into host genome cause the absence of the E2 gene fragment, resulting in overexpression of E6 and E7 and cell transformation. E6 and E7 proteins bind to tumor suppressor proteins p53 and pRb proteins, respectively, which promotes p53 and pRb degradation and inactivation, then induces cell transformation and cancer cell formation. HPV infection affects immunologic systems, leading to the abnormalities of cell immunity, humoral immunity and local immunity. HPV can escape host immunologic surveillance, especially cell-mediated immune surveillance. It is one of the mechanism of immune escape that early protein of HPV regulates local immunity reaction, and cytokine secretion by cervical tumor cells induces immune suppression, and promotes tumor multiplication. HPV-related diseases are also associated with systematical immune state. Previous work has found that the incidence of HPV infection and cervix lesion is increased in HIV positive women. Anti-HIV therapy can effectively prevents cervix lesions. E6 oncoprotein is a kind of multifunctional protein that leads to normal cell escaping growth limit of senescence process through activation of telomerase.Substantial epidemiologic and molecular biological data have proved that HPV infection is chief cause of cervical cancer and precancerosis, so HPV testing can be used for screening cervical cancer. Since HPV can not grow in vitro, it can not be cultured using routine methods. Currently, HPV DNA detection is mainly performed by molecular biologic methods, including nucleic acid hybridization and polymerase chain reaction (PCR). Nucleic acid hybridization includes Southern bolt, dot blot hybridization, in situ hybridization, hybrid capture DNA analyses, gene chip technology. PCR has a liability for cross-contamination among samples and high falsepositive rates. Recent years, various new diagnostic methods based on PCR technique have been used in basic and clinical research, including the combination of the beacon primer method and reverse line blotting, real-time PCR-based fluorescent assay, indirect in situ PCR hybridization, fluorescence quantitation PCR. Hybrid Capture 2 (HC- II) method, designed by Digene company, have demonstrated better sensitivity and specificity and has been applied to screen on a large scale. This method has been utilized around the world for screening and diagnosing cervical cancer.Since positive rates of HPV testing are affected largely by age, many scholars do not recommend that HPV DNA testing be used for primary screening. The combination of HPV testing with cervical cytology can enhance sensitivity, therefore, HPV testing is considered to be a supplemental method for screening initial cervix cytology. Women aged < 30 years, who were positive for high-risk HPV types, should be reexamined 1 year later. If there is still positive for HPV, colposcopy seems necessary. Women with HPV positive and = 30 years tend to persistent infection, being associated with cervix high-grade lesions.HPV is main biological cause of cervical cancer development, so HPV vaccine administration is the most basic means to prevent and treat cervical cancer. HPV vaccine includes prophylactic and remedial vaccine. Development of specific vaccine is limited greatly, because HPV could not be cultured in vitro successfully and no ideal animal model is available for in vivo HPV infection. Furthermore, the effectiveness of vaccine is largely affected by various HPV types, variation and difference of endemic distribution. With the development of molecular biology and genetic engineering, HPV vaccine will become specific and effective means for preventing cervical cancer in the near future.Cervical cancer is one of the main malignant tumors that threaten woman health, and its age of onset tends to be young. Persistent HPV infection is the chiefcause of cervical cancer. Its cure rate can reach 100%, if early diagnosis is generated. Early screening, early discovery and early treatment show very important significance. Recently, scholars at home and abroad are busy with developing a simple, accuracy, inexpensive screening method and HPV vaccine. It is believed that cervical cancer will be the first malignant tumor which is prevented and eradicated overall through immunization in the near future.
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