“…However, the general acceptance is that HSIL do not regress spontaneously [16]. Additionally, early studies suggested that less than 30% of HSIL progress further into invasive carcinoma within 10 years [17]. During malignant transformation, the DNA of HPV is able to integrate into the host genome at random positions [18,19].…”
Section: Cervical Cancer and Human Papilloma Virusesmentioning
Cervical cancer is caused by Human papillomavirus (HPV) in virtually all cases. These HPV-induced cancers express the viral oncogenes E6 and E7 and are therefore potentially recognized by the immune system. Despite the abundant presence of these foreign antigens, the immune system is unable to cope with the tumor. Due to the constant immunological pressure, cervical cancers can evolve different immune evasion strategies, which will be described in the current review. Several approaches for immunotherapy of cervical cancer are currently under development, which aim at inducing strong HPV-specific immunity. Besides the reinforcement of potent anti-tumor immune responses, immunotherapy could also enhance HPV-specific T regulatory cells. Supplementary strategies that neutralize an immunosuppressive milieu may have great potential. These strategies are discussed as well.
“…However, the general acceptance is that HSIL do not regress spontaneously [16]. Additionally, early studies suggested that less than 30% of HSIL progress further into invasive carcinoma within 10 years [17]. During malignant transformation, the DNA of HPV is able to integrate into the host genome at random positions [18,19].…”
Section: Cervical Cancer and Human Papilloma Virusesmentioning
Cervical cancer is caused by Human papillomavirus (HPV) in virtually all cases. These HPV-induced cancers express the viral oncogenes E6 and E7 and are therefore potentially recognized by the immune system. Despite the abundant presence of these foreign antigens, the immune system is unable to cope with the tumor. Due to the constant immunological pressure, cervical cancers can evolve different immune evasion strategies, which will be described in the current review. Several approaches for immunotherapy of cervical cancer are currently under development, which aim at inducing strong HPV-specific immunity. Besides the reinforcement of potent anti-tumor immune responses, immunotherapy could also enhance HPV-specific T regulatory cells. Supplementary strategies that neutralize an immunosuppressive milieu may have great potential. These strategies are discussed as well.
“…Indeed some studies have reported a second peak in later life and this is most pronounced in developing countries. In Australia, 12% of men and 6% of women aged 30-39 years report more than one partner in the previous year [15] .…”
Section: Risk Of Hpv Infection According To Agementioning
Preventive human papillomavirus (HPV) L1 vaccines are safe and efficient to prevent infection and lesions of vaccine- specific HPV types in women from 15 to 26 years, but also in older age groups. Clearly, public health funds are to be spent to organize programs for vaccination of young adolescents. Immunobridging studies and clinical trials have shown that HPV vaccines generate significantly higher plasma antibodies than following natural infections in women up to 55 years and prevent up to 90.5% (95% CI 73.7–97.5) vaccine-specific HPV infections and lesions in women aged 24–45 years who are HPV DNA-negative at the time of vaccination. However, data from clinical trials with HPV L1 vaccines in older women (older than 25 years) are still scarce compared to the amount of evidence from trials in women younger than 26 years. Information from large population-based studies indicates that older women remain at risk of infection by high-risk HPV and the risk of persistent high-risk HPV infection is significantly higher than in young women, leading to a higher risk of progressing disease and carcinoma. The natural history of HPV infection remains enigmatic as we do not know if the immune mechanisms that clear the HPV infection offer prolonged protection. On the contrary, some data indicate that seroconversion after a natural infection only partially protects against re-infection. Given the large proportions of adult men and women that change sexual partners, the protective effects of HPV L1 vaccines may offer an extra benefit against HPV-related genital diseases within a much shorter time period than after vaccination of prepubertal adolescents.
“…However, the medical histories of children in the Oxford Survey have taught us that it is not only in patients with advanced cancers that the immune system is defective. We also know from screening tests for cervical carcinoma that a cancer in situ may regress spontaneously but is unlikely to do so if the patient is over 40 years of age [10]; and by including African children in cancer studies, we have learnt that common accompaniments of a sharply localised cancer of the immune system are chronic malaria and acquired immunity to the Epstein-Barr virus [7]. It is also becoming increasingly obvious that for everyone, but particularly children and old persons, there must be a direct connection between mortality from other causes and the proportion of recognised cancers.…”
Section: Possible Nature Of the Association Between Cancers And The Imentioning
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