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Intended use
Screening for risk of development of cervical cancer. 

The EIA kit HPV GP HR is an in vitro assay for the qualitative detection of DNA from Human Papillomavirus (HPV) genotypes 16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59, 66, and 68. The kit is intended to be used:
a) as primary cervical cancer risk screening test,
b) for management of women with equivocal cytology results
c) as a test-of cure for women treated for high-grade CIN in view of risk for development of cervical cancer.
Amplimers of positive samples can be used for typing with the Genotyping kit HPV GP.

In the Netherlands this HPV assay has been specifically assigned by the official Dutch Health Authority as one of the assays to be used in screening for women at risk for developing cervical cancer.

Summary and explanation
Human papillomaviruses (HPV) are small viruses containing a double-stranded, circular DNA genome of approximately 7,900 base pairs. The viral genome contains early (E), late (L) genes and an untranslated control region. At present, more than 100 different HPV types have been identified based on differences in DNA sequence. HPV types can be subdivided into mucosal types, which can infect anogenital and oraloropharyngeal mucosa, and cutaneous (skin) HPV types. Among the HPV types infecting the anogenital epithelia, a subset of HPV types has been classified as high-risk for causing alterations of the cervical mucosa and ultimately cervical cancer in women.The EIA kit HPV GP HR allows an easy and clinically valid detection of 14 high-risk HPV genotypes using GP5+/6+ PCR products encompassing a highly conserved L1 sequence according to an established method.

Principle of the procedure
The EIA kit HPV GP HR is based on the hybridization principle. During PCR-mediated amplification targeted by two universal primers, the amplified DNA fragments are labeled with biotin. The biotinylated PCR products are captured in a streptavidin-coated microplate well. After washing, the non-biotinylated complementary strands are separated by incubation with denaturation solution. After removal of non-captured strands by washing, hybridization takes place with a labeled HPV-specific probe cocktail. The label is detected with a conjugate, which is visualized by a substrate. The presence or absence of Human papillomavirus DNA in the tested sample is determined by comparing the optical density of the PCR product to that of the cut-off value.

Ordering information
REF: K-36 EIA kit HPV GP HR 96 tests
(CE marked)

Related product
REF: K-72 Genotyping kit HPV GP, version 2 20 tests
(CE marked)
REF: K-90 LMNX kit HPV GP HR 96 tests

1) Walboomers et al. (1999), Human papillomavirus, a necessary cause of invasive cervical cancer worldwide. Journal of Pathology 189, 12-19.

2) Van den Brule et al. (2002), GP5+/6+ PCR followed by reverse line blot analysis enables rapid and highthroughput identification of human papillomavirus genotypes. J Clin Microbiol 40,

3) Zielinski et al. (2003), The presense of high-risk HPV combined with specific p53 and p16INK4a expression patterns points to high-risk HPV as the main causative agent for adenocarcinoma in situ and adenocarcinoma of the cervix. Journal of Pathology 201, 535-543.

4) Snijders et al. (2005), HPV DNA detection and typing in cervical scrapes. Methods Mol Med 119, 101-14.

5) Brink et al. (2006), High concordance of results of testing for human papillomavirus in cervicovaginal samples collected by two methods, with comparison of a novel self-sampling device to a conventional endocervical brush. J Clin Microbiol 44, 2518-2523.

6) Bais et al. (2007), Human papillomavirus testing on self-sampled vaginal specimens: an effective alternative to protect nonresponders in cervical screening programs. Int J Cancer 120, 1505-1510.

7) Smeets et al. (2007), A novel algorithm for reliable detection of human papillomavirus in paraffin embedded head and neck cancer specimen. Int J Cancer 121, 2465-2472.

8) Heideman et al. (2007), Human papillomavirus-16 is the predominant type etiologically involved in penile squamous cell carcinoma. J Clin Oncol 25, 4550-4556.

9) Bardin et al. (2008), Human papillomavirus infection in women with and without cervical cancer in Warsaw, Poland. Eur J Cancer 44, 557-64.

10) Raza et al. (2010), Human papillomavirus infection in women with and without cervical cancer in Karachi, Pakistan. Br J Cancer 102, 1657-60.

11) Sherpa et al. (2010), Human papillomavirus infection in women with and without cervical cancer in Nepal. Cancer Causes Control 21, 323-30.

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