Abstract
Persistent HPV infection plays a major role in cervical cancer. This study was undertaken to identify HPV types in a cohort of Indian women with locally advanced cervical cancer as well as to determine the physical state and/or site of viral integration in the host genome. Pretreatment biopsies (n = 270) from patients were screened for HPV infection by a high throughput HPV genotyping assay based on luminex xMAP technology as well as MY09/11 PCR and SPF1/2 PCR. Overall HPV positivity was observed to be 95%, with HPV16 being most common (63%) followed by infection with HPV18. Integration status of the virus was identified using Amplification of Papillomavirus Oncogene Transcripts (APOT) assay in a subset of samples positive for HPV16 and/or HPV18 (n = 86) and with an adequate follow-up. The data was correlated with clinical outcome of the patients. Integration of the viral genome was observed in 79% of the cases and a preference for integration into the chromosomal loci 1p, 3q, 6q, 11q, 13q and 20q was seen. Clinical data revealed that the physical state of the virus (integrated or episomal) could be an important prognostic marker for cervical cancer.
Highlights
Cervical cancer is the third most common cancer among women worldwide and the most common cancer found in Indian women
HPV genotyping by high throughput luminex array there are a few reports on different high risk HPVs in Indian women, here we report 15 high risk HPVs, 3 intermediate risk and 6 low risk HPV types using the high throughput luminex array
Out of 169 HPV positive samples, 168 samples were positive for one or more high risk HPV (HR-HPV) types indicating a high association of cervical cancer with HR-HPV infection
Summary
Cervical cancer is the third most common cancer among women worldwide and the most common cancer found in Indian women. Most of the high risk HPV (HR-HPV) infections (90%) regress spontaneously and only in about 10% cases the infection persists and progresses to high-grade cervical intraepithelial neoplasia. This generally occurs through integration of the HPV genome into the host chromosome with associated loss or disruption of E2 [3]. Viral E2 gene has the ability to repress viral E6 and E7 oncogenes in cells harbouring integrated HPV DNA [4]. In most of the cases integration of HRHPV genome gives rise to fusion transcripts comprising of viral oncogenes E6, E7 and adjacent cellular sequences [6,7,8,9]. In vitro studies have demonstrated that the viral-cellular fusion transcripts are more stable and impart the cells with a selective growth advantage as compared to the episomal counterparts [10,11]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
