Avtor/Urednik		Uršič-Vrščaj, Marjetka
Naslov		Humani virusi papiloma in karcinogeneza
Prevedeni naslov		Human papillomavirusis and carcinogenesis
Tip		članek
Vir		In: Možina A, editor. Mednarodni znanstveni simpozij HPV in preprečevanje raka materičnega vratu: kje smo in kako naprej; 2005 okt 7; Ljubljana. Ljubljana: Združenje za ginekološko onkologijo, kolposkopijo in cervikalno patologijo,
Leto izdaje		2005
Obseg		str. 31-8
Jezik		slo
Abstrakt		The developmear of cervical cancer is associated with infection with high risk types of human papillomaviruses (HPV). There are over 30 known HPV types that infect anogenital region. high risk HPV types, like 16, 18, 31, and 45 are closely assotiated with anogenital malignancies and have been implicated in the etiology of most (99.7%) cervical cancers, High risk types HPV 16 and 18 accoun for nearly 70% of cases. The majoriry of cervical tumor show integration of high risk HPV DNA into the host genom. lntegration commonly disrupts the HPV virus in the E2 open reading frame; loss of E2 increases expression of E6 and E7. E6 and E7 are the most important huma papillomavirus oncogenic proteins. High risk HPV E6 leads to a down-regulation of p53 -dependant transcription and shortening of the chromosome telomerase. P53 is essential for DNA repair as it mediates either growth arrest or apoptosis in response to DNA damage in thecell. The E7 protein of higk risk HPV types binds to retinoblastoma tumor suppressor protein (pRb), which cause Rb to release the transcription factor E2F. The effect is deregulated cell cycle control and uncontrolled cellular proliferarion. The net effecc of integration of high risk HPV to the host genom is the transormation of infected ceels into a malignant phenotype.
Deskriptorji		PAPILLOMAVIRUS, HUMAN CERVIX NEOPLASMS VIRUS REPLICATION PROTEIN P53