Epidemiological and clinical aspects of human papillomavirus detection in the prevention of cervical cancer

Abstract

Cervical cancer is a major cause of death, and the second most frequent cancer in women worldwide. Many studies have indicated a causal relation between genital human papillomavirus (HPV) infections and cervical cancer. High-risk HPV genotypes have been detected in almost 100% of all cervical cancers, and the process of HPV mediated carcinogenesis has been partly clarified. The concept that HPV is a obligatory cause in cervical cancer development has lead to extensive research regarding the incorporation of HPV detection in (1) cervical cancer prevention programs, (2) triage of women with abnormal cervical scrapes in the screening program, and (3) follow-up of patients treated for cervical intraepithelial neoplasia (CIN). Epidemiological studies indicate that 50% of women becoming sexually active contract a genital HPV infection within 2 years. The lifetime risk of a genital HPV infection is estimated to be 80%, but very few of these women will develop cervical cancer. Several studies have shown that the persistence of genital HPV infections is especially related to the development of cervical cancer. As a result, HPV detection at a single moment was shown to be of limited clinical value in the triage of patients with abnormal cervical scrapes, or during follow-up after treatment for CIN. Furthermore, major variations in the sensitivity of different HPV detection methods, as well as differences in HPV detection related to the menstrual cycle, have shown that many facts regarding HPV transmission, replication, and detection need to be clarified, before HPV detection can be of clinical value.

Enhancement of human papilloma virus type 16 E7 specific T cell responses by local invasive procedures in patients with (pre)malignant cervical neoplasia

“…A patient was considered to have an increased or decreased response after the invasive procedures, when the number of IFN-g producing cells had changed more than 3-fold. (2), no significant response against HPV-16 E7; ND, not done; NA: not available; 1, increase; 2, decrease; 5, no change, wm; wertheim, RC, radio and chemotherapy, LD, lymphedectomy, RT, radio therapy; CT, chemotherapy; EUA, examination under anesthesia.…”

“…1,2 The majority of women infected with oncogenic HPV types do not develop cervical intraepithelial neoplasia (CIN) or cervical cancer but clear their HPV infection. The immune system plays an important role herein, as demonstrated by the observation that immunocompromised women, such as AIDS-patients, more often fail to clear an HPV infection and have an increased risk to develop cervical cancer.…”

Biofunctional organic nanocrystals for quantitative detection of pathogen deoxyribonucleic acid

“…HR-HPV genotypes are found in the majority of cervical cancer patients [1, 4,6]. Infection with high-risk genotypes HPV 16, HPV 18 and HPV 45 accounts for almost 80% of all squamous cervical carcinomas worldwide [5,9,10].…”

Patients with usual vulvar intraepithelial neoplasia-related vulvar cancer have an increased risk of cervical abnormalities

“…The majority of uVIN-related vulvar SCCs are caused by HPVs 16, 18 and 33 (Toki et al, 1991;Hording et al, 1994;Iwasawa et al, 1997;Pinto et al, 2004;Hampl et al, 2006). The development of uVIN and vulvar SCC mirrors that of cervical intraepithelial neoplasia (CIN) and cervical SCC, the latter caused by (high-risk human papillomavirus) hrHPV in nearly 100% of the cases (Walboomers et al, 1999;Bekkers et al, 2004). A subdivision on the basis of hrHPV DNA presence between the two types of vulvar SCC does not separate the two different pathways accurately.…”

“…Multicentric HPV infections affecting vulva, cervix, vagina and anus simultaneously have been described in several studies (Adamek et al, 2003;Bekkers et al, 2004;Lara-Torre and Perlman, 2004;Feng and Kiviat, 2005;Goffin et al, 2006;Hampl et al, 2007), making a thorough examination of the entire lower female anogenital tract obligatory. A decreased immune response to hrHPV has been suggested to be the cause of these multicentric hrHPV infections (Hampl et al, 2007), although it is also possible that HPV affects cervix and vulva consecutively.…”