FDA approved HPV, Chlamydia, Gonorrhea and Trichomonas testing

women ages 21 years and older  =  Pap, reflex to Aptima HPV if ASC-US 

women ages 30 years and older (ACOG limits age to 65)  =  Pap + Aptima HPV 

ThinPrep® Pap test

Introduced in the 1940s, Pap testing has been the single greatest contributor to the overall decline in cervical cancer. Then, the 1996 launch of the Hologic ThinPrep® Pap test propelled screening success to new heights, contributing to a further 28% reduction in invasive cancers in the U.S. To date, ThinPrep® has become the most widely used Pap test in the country,1 with hundreds of published, peer-reviewed studies demonstrating significant benefits over the conventional Pap smear.

Multiple Tests From One Sample*

Today, accurate Pap testing is even more critical in light of extended Pap testing intervals. A negative HPV test can keep patients from follow-up appointments for years, while a false negative HPV result can give cervical disease a chance to advance undetected. The ThinPrep® Pap Test is the only liquid-based pap test FDA-approved/cleared for HPV, Chlamydia/Gonorrhea and Trichomonas testing out of the same vial.

Why did we choose Aptima HPV Transcription Mediated Amplification (TMA) mRNA Assay?

In our findings, it is the most reliable, most convenient, most sensitive and specific test available for HPV detection.

  

Multiple Advantages over Polymerase Chain Reaction (PCR), Cervista and Hybrid Capture 2 (HC2):

1.  Multiple tests FDA approved on ThinPrep sample: HPV, Trichomonas, CT and GC.

2.  Less possibility of carry over and contamination, therefore decreasing the chances of false positive results and increasing specificity.

3.  Trusted high sensitivity.

4.  Less complexity means less chance of errors.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC427873/                                                  http://jcm.asm.org/content/49/2/557.full

The facts are clear: Screening with Pap+HPV Together provides the best possible protection against cervical cancer for women ages 30 to 65.  Evidence and guidelines support this.

*Detection of Results of these tests should only be interpreted in conjunction with information available from clinical evaluation of the patient history.  Although these tests are very effective, a negative Result, interpreted on its own, does not necessarily rule out an infection.  These tests are dependent on collection methods, patient factors, stage of infection and the presence of interfering substances such as excessive or unapproved lubricant.

Performance Characteristics and Product Inserts

Click on a test, or collection method, below to view the Data sheet

ThinPrep FDA

ThinPrep FDA

ThinPrep FDA

ThinPrep FDA

Cervical cancer is one of the most common female cancers in the world. HPV is the etiological agent responsible for more than 99% of all cervical cancers.1, 2, 3 HPV is a common sexually transmitted DNA virus comprised of more than 100 genotypes.1 The HPV viral genome is a double-stranded circular DNA approximately 7900 base pairs in length. The genome has eight overlapping open reading frames. There are six early (E) genes, two late (L) genes, and one untranslated long control region. The L1 and L2 genes encode the major and minor capsid proteins. Early genes regulate HPV viral replication. The E6 and E7 genes of high-risk HPV genotypes are known oncogenes. Proteins expressed from E6/E7 polycistronic mRNA alter cellular p53 and retinoblastoma protein functions, leading to disruption of cell-cycle check points and cell genome instability.1, 4 Fourteen HPV genotypes are considered pathogenic or high-risk for cervical disease.5 Multiple studies have linked genotypes 16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59, 66, and 68 to disease progression.2, 6, 7 Women with a persistent infection with one of these types have an increased risk for developing severe dysplasia or cervical carcinoma.5, 8 HPV infections are very common and most women will clear HPV infections within 6 to 12 months.2, 9 The presence of HPV nucleic acid does not mean that cervical dysplasia or cervical cancer is present. However, an effective approach for detection of cervical disease is to target those oncogenic elements of HPV that foster persistent viral infection and cellular transformation.10

Transcription-mediated amplification (TMA) is an isothermal, single-tube nucleic acid amplification system utilizing two enzymes, RNA polymerase and reverse transcriptase, to rapidly amplify the target RNA/DNA, enabling the simultaneous detection of multiple pathogenic organisms in a single tube. TMA technology allows a clinical laboratory to perform nucleic acid test (NAT) assays for blood screening with fewer steps, less processing time, and faster results. It is used in molecular biologyforensics, and medicine for the rapid identification and diagnosis of pathogenic organisms, In contrast to similar techniques such as polymerase chain reaction and ligase chain reaction, this method involves RNA transcription (via RNA polymerase) and DNA synthesis (via reverse transcriptase) to produce an RNA amplicon (the source or product of amplification) from a target nucleic acid. This technique can be used to target both RNA and DNA.

Transcription-mediated amplification has several advantages compared to other amplification methods including:

  • TMA is isothermal; a water bath or heat block is used instead of a thermal cycler.

  • TMA produces RNA amplicon rather than DNA amplicon. Since RNA is more labile in a laboratory environment, this reduces the possibility of carry-over contamination.

  • TMA produces 100–1000 copies per cycle (PCR and LCR exponentially doubles each cycle). This results in a 10 billion fold increase of DNA (or RNA) copies within about 15–30 minutes.

From: http://www.gen-probe.com

Bibliography 1. Doorbar, J. 2006. Molecular biology of human papillomavirus infection and cervical cancer. Clin Sci (Lond). 110(5):525-41. 2. Monsonego J., F.X. Bosch, P. Coursaget, J.T. Cox, E. Franco, I. Frazer, R. Sankaranarayanan, J. Schiller, A. Singer, T.C. Wright Jr, W. Kinney, C.J. Meijer, J. Linder, E. McGoogan, and C. Meijer. 2004. Cervical cancer control, priorities and new directions. Int J Cancer. 108(3):329-33. Erratum in: Int J Cancer. 108(6):945. 3. Walboomers, J. M., M.V. Jacobs, M.M. Manos, F.X. Bosch, J.A. Kummer, K.V. Shah, P.J. Snijders, J. Peto, C. J. Meijer, N. Muñoz. 1999. Human papillomavirus is a necessary cause of invasive cervical cancer worldwide. J Pathol. 189:12-19. 4. Lambert P.F., H. Pan, H.C. Pitot, A. Liem, M. Jackson, and A.E. Griep. 1993. Epidermal cancer associated with expression of human papillomavirus type 16 E6 and E7 oncogenes in the skin of transgenic mice. Proc Natl Acad Sci U S A. 90(12):5583-7. 5. Kjaer S.K., A.J.C. van den Brule, G., Paull, E.I. Svare, M.E. Sherman, B.L. Thomsen, M. Suntum, J.E. Bock, P.A. Poll, and C.J.L.M. Meijer. 2002. Type specific persistence of high risk human papillomavirus (HPV) as indicator of high grade cervical squamous intraepithelial lesions in young women: population based prospective follow up study. BMJ. 325(7364): 572-579. 6. Burd, E.M. 2003. Human papillomavirus and cervical cancer. Clin Microbiol Rev. 16(1):1-17. 7. Li N., S. Franceschi, R. Howell-Jones, P. J. Snijders, G. M. Clifford. 2010. Human papillomavirus type distribution in 30,848 invasive cervical cancers worldwide: Variation by geographical region, histological type and year of publication. Int J Cancer, n/a. doi: 10.1002/ ijc.25396. 8. Cuschieri, K.S., M.J. Whitley, H.A. Cubie. 2004. Human papillomavirus type specific DNA and RNA persistence--implications for cervical disease progression and monitoring. J. Med. Virol. 73(1): 65-70. 9. Baseman, J.G., and L.A. Koutsky. 2005. The epidemiology of human papillomavirus infections. J Clin Virol. 32 Suppl 1:S16-24. 10. Czegledy J., C. Losif, B.G. Hansson, M. Evander, L. Gergely, and G. Wadell. 1995. Can a test for E6/E7 transcripts of human papillomavirus type 16 serve as a diagnostic tool for the detection of micrometastasis in cervical cancer? Int J Cancer. 64(3):211-5. 11. Kacian, D.L. and T.J. Fultz. 1995. Nucleic acid sequence amplification methods. U. S. Patent 5,399,491. 12. Arnold, L.J., P. W. Hammond, W. A. Wiese, and N. C. Nelson. 1989. Assay formats involving acridinium-ester-labeled DNA probes. Clin Chem. 35: 1588-1594. 13. Nelson, N.C., A. BenCheikh, E. Matsuda, and M. Becker. 1996. Simultaneous detection of multiple nucleic acid targets in a homogeneous format. Biochem. 35:8429-8438. 14. Wright TC, Jr., Massad LS, Dunton CJ, Spitzer M, Wilkinson EJ, and Solomon D. 2007. 2006 Consensus Guidelines for the Management of Women with Abnormal Cervical Cancer Screening Tests. Am J Obstet Gynecol 197 (4); 346-355. 15. Datta, S. D., L. A. Koutsky, S. Ratelle, E. R. Unger, J. Shlay, T. McClain, B. Weaver, P. Kerndt, J. Zenilman, M. Hagensee, C. J. Suhr, and H. Weinstock. 2008. Human Papillomavirus Infection and Cervical Cytology in Women Screened for Cervical Cancer in the United States, 2003–2005. Annals Int Med. 148:493. 16. Clifford, G.M., S. Gallus, R. Herrero, N. Muñoz, P. J. F. Snijders, S. Vaccarella, P. T. H. Anh, C. Ferreccio, N. T. Hieu, E. Matos, M. Molano, R. Rajkumar, G. Ronco , S. de Sanjosé, H. R. Shin, S. Sukvirach, J. O. Thomas, S. Tunsakul, C. J. L. M. Meijer, S. Franceschi, and the IARC HPV Prevalence Surveys Study Group. 2005. Worldwide distribution of human papillomavirus types in cytologically normal women in the International Agency for Research on Cancer HPV prevalence surveys: a pooled Analysis. The Lancet. 366, 991. 17. Stoler, M.H., T.C. Wright, Jr., J. Cuzick, J. Dockter, J. Reid, D. Getman, C. Giachetti. 2013. Aptima HPV assay performance in women with atypical squamous cells of undetermined significance cytology results. American Journal of Obstetrics & Gynecology. 208(2):144-145. 18. Pretorius R.G., W. H. Zhang, J. L. Belinson, et al. 2004. Colposcopically directed biopsy, random cervical biopsy, and endocervical curettage in the diagnosis of cervical intraepithelial neoplasia II or worse. Am J Obstet Gynecol. 191:430-434. 19. Pretorius R.G., R. J. Kim, J. L. Belinson, P. Elson, Y-L Qiao. 2006. Inflation of sensitivity of cervical cancer screening tests secondary to correlated error in colposcopy. J Low Genit Tract Dis. 10(1):5-9. 20. Kondratovich, M.V. and W. A. Yousef. 2005. Evaluation of Accuracy and ‘Optimal’ Cutoff of Diagnostic Devices in the Same Study. ASA Section on Statistics in Epidemiology. 901:2547-2551.

CLINICAL PATHOLOGY ASSOCIATES ABILENE, TX

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