مقالات پذیرفته شده در هفتمین کنگره بین المللی زیست پزشکی
Treatment of cervical cancer caused by HPV review article
Treatment of cervical cancer caused by HPV review article
Toktam Hajipour Moghadam,1Saman Hakimian,2,*
1. Department of Microbiology, Faculty of Advanced Science & Technology, Tehran Medical Sciences, Islamic Azad University, Tehran, Iran 2. M.sc student of Microbiology Islamic Azad University Central Tehran Branch,Iran,Tehran
Introduction: HPV is a double-stranded DNA tumor virus known to cause cancers of the anus, oropharynx, penis, and cervix.
How can cervical cancer be prevented?The most effective ways to prevent cervical cancer are to vaccinate girls against HPV, before their first sexual contact, and to screen women aged 30- 49 years or according to the national guideline.
vaccines have shown promising results in recent years , the implementation of universal HPV vaccination strategies is expensive for developing countries, especially for populous countries such as China and India, and the multivalent vaccines cannot completely cover all the major types of HPV infections in these countries.
Due to the huge economic burden posed by cervical screening and vaccination programs, many women in both developed and developing countries are still unprotected from HPV infections and its related cervical cancers.
Key Factors that Contribute to HPV Persistence and Cervical Carcinogenesis: Host Susceptibilities to Latent HPV Infections and Cervical Cancer Like many other types of malignancies, cervical cancer is a chronic complex disease caused by a combination of inherited genetic factors and external environmental influences.
Methods: Key Factors that Contribute to HPV Persistence and Cervical Carcinogenesis: Host Susceptibilities to Latent HPV Infections and Cervical Cancer Like many other types of malignancies, cervical cancer is a chronic complex disease caused by a combination of inherited genetic factors and external environmental influences.
Obvious evidence of genetic factors contributing to cervical carcinogenesis can be proved by warts, hypogammaglobulinemia, immunodeficiency, and myelokathexis syndrome (WHIM) and hereditary nonpolyposis colorectal cancer (Lynch) syndrome, two autosomal dominant genetic disorder characterized by extensive HPV infection and high risk of cervical cancer.
Although HPV infection may be the triggering factor, studies showthat a linkage between genetic factors and immune functions are correlated to cervical carcinogenesis and infection by themajor subtypes of high-risk.A small fraction of people infected with the type of high-risk HPV will develop cancer, which usually arise many years after initial infection.
There are several approaches to screening for cervical cancer, including cytological testing (Pap test), HPV DNA testing for high-risk strains of the HPV virus, and visual inspection of the cervix with acetic acid (VIA), with or without magnification.
Results: There are several approaches to screening for cervical cancer, including cytological testing (Pap test), HPV DNA testing for high-risk strains of the HPV virus, and visual inspection of the cervix with acetic acid (VIA), with or without magnification.
Cytological testing is the most common screening method in developed countries, but it requires trained technicians and good laboratories that are often unavailable in developing countries.
Effectiveness of Screening Methods All HPV screening methods, when done properly, can detect most precancerous lesions; none, however, is perfect.Even in developed countries, the results of Pap tests are much less reliable than many people realize.
Conclusion: The oncogenes of high-risk HPVs are retained and expressed in HPV induced cancers and their expression may have effects on the tumor microenvironment (TME).In contrast to the immune suppressive activities seen in HPV infection, HPV induced cancers such as head and neck squamous cell carcinomas (HNSCC) often demonstrate increased infiltration and activation of multiple immune cell types within the TME, indicative of an immune-hot phenotype.