HPV 1618 vaccine could prevent 70 of cervical cancers

Munoz N, Bosch FX, de Saniose S et al. International Agency for Research on Cancer Multlcenter Cervical Study Group. N Engl J Med2003; 348: 518-27.

Fig. 1 HPV types in cervical cancer membrane, differentiate, and become epithelial cells. Virus replication and assembly is tightly linked to the differentiation program of epithelial cells. Infectious virions are produced only in the terminally differentiated cell and are shed as virus-laden squamous cells.

The HPV genome codes for eight proteins (open reading frames). The late L1 and L2 genes code for the viral capsid proteins, the early proteins E1 and E2 are responsible for viral replication and transcription, and E4 seems to aid virus release from infected cells (Spence et al. 2005). The early genes of the high-risk HPV types (E6 and E7) encode the main transforming proteins. These genes are capable of immortalization of epithelial cells and are thought to play a role in the initiation of the oncogenic process. The protein products of these early genes interfere with the normal function of tumor suppressor genes. HPV E6 is able to interact with p53, leading to its dysfunction, thereby impairing its ability to block the cell cycle when DNA errors occur. E6 also keeps the telomerase length above its critical point, protecting the cell from apoptosis. HPV E7 binds to retinoblastoma protein (pRb) and activates genes that start the cell cycle, leading to tissue proliferation. E5 has also been implicated in cellular transformation.

It is now widely accepted that high-risk HPV infections are a necessary, but not sufficient, cause of virtually all cases of cervical cancer worldwide (Fig. 2) and are a likely cause of a substantial proportion of other anogenital neoplasms and oral squamous cell carcinomas. An estimated 85% of anal cancers; 50% of the cancers of the vulva, vagina, and penis; 20% of oropharyngeal cancers; and 10% of laryngeal and esophageal cancers are attributable to HPV (CDC 2004).

Infection with low oncogenic risk HPV types, such as HPV 6 and 11, can cause benign lesions of the anogenital areas known as condylomata acuminata (genital warts), as well as a large proportion of low-grade squamous intraepithelial lesions of the cervix. Low-risk HPV clinical infections are responsible for substantial morbidity and invoke high costs associated with the treatment of clinically relevant lesions.

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  • cancer epithelial
    It is now widely accepted that high-risk HPV infections are a necessary, but not sufficient, cause of virtually all cases of cervical cancer worldwide (Fig. 2) and are a likely cause of a substantial proportion of other anogenital neoplasms and oral squamous cell carcinomas. An estimated 85% of anal cancers; 50% of the cancers of the vulva, vagina, and penis; 20% of oropharyngeal cancers; and 10% of laryngeal and esophageal cancers are attributable to HPV (CDC 2004).
    5 years ago

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