Human Papillomavirus in Cervical Cancer Screening: Important Role as Biomarker

Abstract

Cervical cytology screening has reduced cervical cancer morbidity and mortality but shows important shortcomings in terms of sensitivity and specificity. Infection with distinct types of human papillomavirus (HPV) is the primary etiologic factor in cervical carcinogenesis. This causal relationship has been exploited for the development of molecular technologies for viral detection to overcome limitations linked to cytologic cervical screening. HPV testing has been suggested for primary screening, triage of equivocal Pap smears or low-grade lesions and follow-up after treatment for cervical intraepithelial neoplasia. Determination of HPV genotype, viral load, integration status and RNA expression could further improve the effectiveness of HPV-based screening and triage strategies. The prospect of prophylactic HPV vaccination stresses the importance of modification of the current cytology-based screening approach.

Induction of Mitochondrial-Mediated Apoptosis by Morinda Citrifolia (Noni) in Human Cervical Cancer Cells

“…These cell lines were chosen for the study because they harbor the human papilloma virus (HPV) type 18 (HeLa) and type 16 (SiHa) genotypes. These HPVs have been shown in multi-institutional studies as etiological agents in the development of cervical cancer and these genotypes account for >70% of all HPV DNA positive invasive cervical cancers (Franco et al, 2001;Boulet et al, 2008).…”

“…In majority of the cases, it is associated with the presence of human papilloma virus (HPV) infection, with high-risk HPV types 16 and 18 being responsible for more than 70% of cases of cervical cancer (Boulet et al, 2008;Franco et al, 2001). Apoptosis is controlled by a balance of pro-apoptotic and anti-apoptotic genes and is the most convenient manner for tumor cell elimination.…”

Overview on Molecular Markers to Implement Cervical Cancer Prevention: Challenges and Perspectives

“…Initially, most laboratories used PCR assay with degenerated primers pair MY09/11. These primers are now been replaced by a new set of oligonucleotides pool: GP5/6 and modified GP5+/GP6+, PGMY09/11 (modified MY09/11), SPF1/2, the last one especially appropriated for formalin(fixed paraffin(embedded tissue samples, which often offer a small amount of amplifiable DNA (Boulet et al, 2008;Perrons et al, 2005). Amplification with each of these primers provides different size amplification products, resulting in varying sensitivity for HPV(DNA detection.…”

“…Nuclisens EasyQ HPV assay is a multiplex nucleic acid sequence amplification (NASBA) method, detecting FL transcripts of E6/E7 oncoproteins in a DNA background is commercially available from two companies; they are the and (Boulet et al, 2008). The test is based on the molecular beacon probe technology and on the real(time detection of five oncogenic HPV types (16, 18, 31, 33 and 45).…”

“…Studies using quantitative type(specific PCR for HR (HPV 16,18,31,33 and 45 and LR(HPV 6 and 11 showed that HPV(16 can reach a much higher viral load than the other above listed types and that only HPV(16 viral load might correlate with increased severity of cervical disease (Saunier et al, 2008). Then, all oncogenic HPV types but 16 are able to provoke cervical cancer, even when they are present at low levels (Boulet et al, 2008).…”