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The highest-risk types are HPV 16 and 18; these are responsible for the vast majority of HPV-related cancers, including cancers of the cervix, vagina, vulva, penis, anus, and head and neck.
All HPV vaccines protect against at least HPV types 16 and 18, which cause the greatest risk of cervical cancer. The quadrivalent vaccines also protect against HPV types 6 and 11. The nonavalent vaccine Gardasil 9 provides protection against those four types (6, 11, 16, and 18), along with five other high-risk HPV types responsible for 20% of ...
Virtually all cervical cancer cases (99%) are linked to genital human papillomavirus infection (HPV); [14] [5] [6] most who have had HPV infections, however, do not develop cervical cancer. [3] [15] HPV 16 and 18 strains are responsible for approximately 70% of cervical cancer cases globally and nearly 50% of high grade cervical pre-cancers.
According to an article published 16 September 2015 in The Lancet, which reviewed the safety, efficacy, and immunogenicity of VGX-3100 in a double-blind, randomized controlled trial (phase 2b) targeting HPV-16 and HPV-18 E6 and E7 proteins for cervical intraepithelial neoplasia 2/3, it is the first therapeutic vaccine to show efficacy against ...
HPV, the human papillomavirus, causes six types of cancer, including cervical cancer. Among women aged 20 to 24, cervical cancer incidence dropped by 65% from 2012 to 2019, according to a report ...
It has been observed that HPV18 is the most prevalent type in Small cell cervical cancer. Like other types of cervical cancer it seems to be associated with high-risk (e.g. 16, 18, 31) HPV Infection. [1]
The HPV strains that Gardasil protects against are sexually transmitted, [14] specifically HPV types 6, 11, 16 and 18. [15] [16] HPV types 16 and 18 cause an estimated 70% of cervical cancers, [17] [18] and are responsible for most HPV-induced anal, [19] vulvar, vaginal, [20] and penile cancer cases. [19]
The cause of CIN is chronic infection of the cervix with HPV, especially infection with high-risk HPV types 16 or 18. It is thought that the high-risk HPV infections have the ability to inactivate tumor suppressor genes such as the p53 gene and the RB gene, thus allowing the infected cells to grow unchecked and accumulate successive mutations, eventually leading to cancer.