추적: • co-testing

Co-testing

The cobas HPV Test provides both pooled high-risk HPV DNA results and individual detection of HPV 16 and HPV 18, the two types responsible for about 70 percent of cervical cancer. The FDA’s decision to approve the expanded use for the cobas HPV Test was based on results from the landmark ATHENA trial, which enrolled more than 47,000 women.

The study demonstrated that one in four women who are HPV 16 positive will have cervical disease within three years and that nearly 1 in 7 women with normal Pap cytology who were HPV 16 positive actually had high-grade cervical disease that was missed by cytology.

In addition, results from the ATHENA trial included a comparison of a cobas HPV Test screening strategy to alternative strategies using Pap cytology and HPV testing. The comparison showed that a strategy leveraging the ability of the cobas HPV Test to identify women testing positive for HPV 16 or 18, and using cervical cytology (Pap) as a triage, follow-up test, would allow clinicians to detect more disease without referring a significant number of women to unnecessary follow-up.

One potential advantage of the cobas 4800 HPV Test is that it provides information on HPV-16 and HPV-18 separately. HPV-16 and HPV-18 are generally considered particularly high-risk genotypes because they account for approximately 70% of invasive cervical cancers globally.13 In the ATHENA study, specific HPV genotyping was found to have a dramatic impact on the AR and RR of CIN 2 or worse and CIN 3 or worse in women with ASC-US. The AR of CIN 2 or worse among women who were HPV-16+ was 31.5%, and for CIN 3 or worse, it was 20.0%. The RR of CIN 2 or worse for women who were HPV-16+ vs women positive for a non–HPV-16/HPV-18 HR-HPV (12 other genotypes) was 3.7, and the RR of CIN 3 or worse for women positive for HPV-16 vs women positive for 12 other HR-HPV genotype(s) was 4.5. It is interesting that despite its being associated with approximately 10% of squamous cell carcinomas of the cervix, 34% of adenocarcinomas, and a very high fraction of rare but aggressive neuroendocrine carcinomas,13,23,24 HPV-18 positivity at baseline alone did not confer a significantly increased relative risk for CIN 2 or worse or CIN 3 or worse compared with the combination of all 12 other HR-HPV genotypes. This may be reflective of the finding that, in prospective trials, high-grade CIN associated with HPV-18 takes longer to develop or remains clinically occult, perhaps in the endocervical canal, compared with precancer associated with HPV-16.25–27 The effect of HPV-18 on the risk of high-grade disease will be further investigated and better defined by the 3-year follow-up phase of the ATHENA study.