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• W2049817132 abstract "The attribution of specific human papillomavirus (HPV) types to invasive cervical cancer (ICC) is important to predict the efficacy of current and future HPV vaccine programs and to decide which HPV types should be included in HPV-based screening tests.Although ICC is assumed to originate from a single transformed cell, its attribution to an individual HPV type is complicated by the increasingly frequent detection of multiple HPV types in cervical samples.1 A previous article by Wentzensen et al.2 in this journal used different algorithms to assess the potential range of attribution of specific HPV types to various grades of cervical disease in the United States. This cross-sectional study included 1,670 women who were referred to colposcopy because of abnormal cytology or histology, among whom only 107 had ICC. The HPV detection method was based on the linear array assay, a very sensitive test capable of detecting 37 HPV types. In this report, we have replicated the algorithms used by Wentzensen et al. in a much larger number of ICC cases (1,728 histologically confirmed ICC cases) derived from the IARC Multicentric Case–Control Study (IMCCS). The IMCCS was carried out between 1990 and 1999 and included nine study areas (Brazil, Mali, Morocco, Paraguay, Philippines, Thailand, Peru, India and Algeria). In the IMCCS, the overall presence of HPV DNA was determined using a general GP5+/6+ primer-mediated PCR. HPV positivity was assessed by hybridization of PCR products in an enzyme immunoassay using two HPV oligoprobe cocktails that, together, detect 33 HPV types: HPV6, 11, 16, 18, 26, 31, 33, 34, 35, 39, 40, 42, 43, 44, 45, 51, 52, 53, 54, 56, 57, 58, 59, 61, 66, 68, 70, 72 (equivalent to CP4137), 73 (MM9), 82 (equivalent to IS39 and MM4 subtypes), 83 (equivalent to MM7), CP6108 and CP8304. Subsequent HPV typing was performed by reverse-line blot hybridization of PCR products, as described earlier.3, 4 For India and Algeria, the oligoprobe cocktail was extended to include HPV types 55, 71 (equivalent to CP8061) and 84 (equivalent to MM8). The IMCCS also included two studies from Spain and Colombia which, however, employed different primers (MY09/11 consensus primer) and, therefore, were not included in the present analysis. By analogy with Wentzensen et al.2 and Insinga et al.,5 attribution of multiple HPV types in our present report was based on the “proportional” and “hierarchical” algorithms. In the “proportional” approach, attribution of cervical disease to an HPV type was based on the frequency of that type as a single infection within the study. For example, in a multiple infection consisting of HPV16, 31 and 53 where frequencies in single infections are 50%, 15% and 20% for the respective types, the case would be split between the three types (50/85 for HPV16, 15/85 for HPV31 and 20/85 for HPV53). Conversely, in the “hierarchical” approach, instead of a partial attribution, a case with multiple HPV types was completely attributed to the type, among those present in the coinfection, most frequently found in single infections. In the above example, the case would be, therefore, fully attributed to HPV16. Due to the small number of single infections (only 69 out of 107 ICC, of which 44 with HPV16), Wentzensen et al. had to base attribution algorithms for ICC on the overall frequency of HPV types, rather than on the frequency of types in single infections. To note, while the proportional algorithm can attribute cases to HPV types with low oncogenic potential, the hierarchical attribution favors the most frequent types in cancer, particularly HPV16. Ninety-four percent of cervical cancer cases in the IMCCS were infected with at least one HPV type. Among HPV-positive women, two types were detected in 9.8%, and three or more types in 1.1% of women. Overall, the most common HPV types were, in decreasing order, HPV16, 18, 45, 33, 31 and 52. The attribution to HPV16 ranged from a minimum of 50.1% among single infections to 54.4% using the proportional attribution, to 55.2% using the hierarchical attribution (Table 1). The corresponding attribution estimates for HPV18 were 14.8%, 17.2% and 17.0%, respectively. The combined percentage for the two oncogenic types HPV16 and 18, which are included in the current vaccines, ranged from 64.9% (single infections) to 72.1% (hierarchical attribution) while the combined percentage for the seven most important oncogenic types (16, 18, 45, 33, 31, 52 and 58) varied from 77.7% (single infections) to 86.9% (hierarchical attribution; Table 1). The fraction of multiple infections among HPV-positive cases in our study was substantially lower (11% vs. 34%) than that of Wentzensen et al. In fact, the HPV detection method we used, GP5+/6+ PCR, is known to be less sensitive for multiple HPV infections than linear array,6 the method used by Wentzensen et al. Most likely, the GP5+/6+ PCR assay (that uses two universal primers) suffers more from competition between different HPV types than the linear array (that uses multiple type-specific primers). Therefore, we observed smaller differences in the attributions. Nonetheless, the two studies showed fairly similar attribution estimates according to the proportional or hierarchical algorithms, although results were based on smaller numbers in Wentzensen et al. The range of attribution to HPV18, however, shifted toward higher values in the IMCCS compared to Wentzensen et al. The ICC cases of the two studies differed by age (mean age = 46.8 years in Wentzensen et al.; 49.5 years in the IMCCS) and by study location, which was the United States in Wentzensen et al., but a wide range of medium/low-resource countries in the IMCCS. Attributable fractions for specific and combined HPV types are, however, known to vary little across geographical areas,1, 7 with the possible exception of a slight over-representation of HPV58 in Eastern Asia.1 Whether the lower sensitivity of the GP5+/6+ PCR assay may favor the HPV type most likely to be the one associated with ICC is unclear. Without using complex functional assays to explore the mechanistic basis for assigning an etiological role to a given HPV type, the attribution of an ICC to an individual type when multiple types are detected is impossible, and different algorithms can thus be helpful. The present analysis showed that, despite the use of a PCR technique with a relatively lower sensitivity for the detection of multiple types and the consequently smaller fraction of multiple HPV infections, attribution estimates within the IMCCS were similar, although more robust, especially for less frequent HPV types, to those presented by Wentzensen et al. Salvatore Vaccarella Tel.: +33-4-72-73-8402, Fax: +33-4-72-73-8345 [email protected]*, Gary M. Clifford*, Rebecca Howell-Jones*, Peter J.F. Snijders , Silvia Franceschi*, * International Agency for Research on Cancer, Lyon, France, VU University Medical Center, Amsterdam, The Netherlands" @default.
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• W2049817132 title "Author's reply to: Multiple human papillomavirus genotype infections in cervical cancer progression in the study to understand cervical cancer early endpoints and determinants" @default.
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• W2049817132 doi "https://doi.org/10.1002/ijc.25774" @default.
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