Differences in HPV 16- and HPV 18 E6/E7 oncogene expression between in situ and invasive adenocarcinomas of the cervix uteri

Abstract

To evaluate the importance of high-risk human papillomavirus (HPV) types in in situ and invasive adeno- and adenosquamous carcinomas (ACISs/ACs, and ASCISs/ASCs) of the cervix uteri, we analyzed HPV infection and HPV 16- and HPV 18 E6/E7 oncogene expression in different histologic subtypes. Using the polymerase chain reaction (PCR) technique, 29 of 33 (88%) ACISs, 2 of 2 (100%) ASCISs, 46 of 54 (85%) ACs, and 8 of 10 (80%) ASCs were found to be HPV 16- and/or HPV 18-positive. In 25 of 35 (71%), 10 of 35 (29%), and 4 of 35 (11%) ACISs/ASCISs, HPV 16, HPV 18, and HPV 16 and HPV 18 were detected, respectively. Invasive ACs/ASCs were more frequently infected with HPV 18 (36 of 64, 56%) than with HPV 16 (28 of 64, 44%). Ten (16%) of these cases were positive for HPV 16 and HPV 18. In ACISs/ASCISs, HPV 16 oncogene expression predominated (62%) relative to HPV 18 (25%) expression, whereas in invasive ACs/ASCs, only 21% of the cases expressed HPV 16, but 48% of the cases expressed HPV 18 oncogenes. Thus, detection of HPV 18 in ACISs/ASCISs might be associated with an increased risk of progression. HPV oncogene expression was not dependent on histologic subtype of in situ or invasive AC. Normal glandular epithelia and glandular dysplasias (GDs, n = 4) were always negative concerning HPV oncogene expression. In HPV 16- and HPV 18-double-infected cases, HPV 18 oncogene expression was most frequently detected, and we did not find a coexpression of HPV 16- and HPV 18-specific oncogenes in purely glandular lesions or in cases with an additional CIN (cervical intraepithelial neoplasia) II or CIN III. HPV E6/E7 expression of the same HPV type in both in situ or invasive ACs and associated CIN II/III suggest that these lesions might be histogenetically related.

Prevalence of human papillomavirus DNA in various histological subtypes of cervical adenocarcinoma: a population-based study

“…8 As to the role of HPV on the cervical adenocarcinoma, HPV 18 was reported to be a preferential type in cervical adenocarcinoma in contrast to HPV 16 in cervical squamous cell carcinoma. 5,6,19 Nonetheless, the causal linkage of HPV infection to the cervical adenocarcinoma has not been considered as strong as it is for the squamous cell carcinoma of the cervix. 5,6 However, the recent more sensitive techniques have made it possible to identify the higher rate of HPV infection in adenocarcinoma with a frequency of 85% or more.…”

“…5,6 However, the recent more sensitive techniques have made it possible to identify the higher rate of HPV infection in adenocarcinoma with a frequency of 85% or more. [19][20][21] In this study, we used a recently developed HPV DNA Chip for the detection of HPV DNA in 82 of 135 cases. This method is based on the polymerase chain reaction with an advantage to detect single and multiple infection of 22 HPV genotypes at once and has reported to be a very sensitive method comparable with Hybrid Capture II assay.…”

Coexisting high-grade glandular and squamous cervical lesions and human papillomavirus infections

“…High-risk human papillomavirus was detected in 66 -100% of patients with ACIS (Anciaux et al, 1997;Riethdorf et al, 2000). Approximately 48% of all women diagnosed with ACIS have coexisting squamous lesions (Colgan and Lickrish, 1990;Leary et al, 1991;Higgins et al, 1992;Duggan et al, 1995;Anciaux et al, 1997;McLachlin et al, 1997;Pirog et al, 2000;Riethdorf et al, 2000Riethdorf et al, , 2002Madeleine et al, 2001), but the frequency of specific hr-HPV genotypes in patients with ACIS has not been studied in relation with the presence or absence of coexisting CIN lesions. In this study, the frequency of specific hr-HPV genotypes in patients with ACIS and coexisting CIN is compared with its frequency in patients with ACIS without coexisting CIN, and patients with CIN without ACIS, in order to gain more insight into the relation between hr-HPV infections and the development of coexisting squamous and glandular lesions.…”

“…Only limited studies are available on the frequency of hr-HPV genotypes in premalignant glandular lesions and the number of patients in most studies is rather low (see Table 1) (Colgan and Lickrish, 1990;Leary et al, 1991;Higgins et al, 1992;Duggan et al, 1995;Anciaux et al, 1997;McLachlin et al, 1997;Pirog et al, 2000;Riethdorf et al, 2000Riethdorf et al, , 2002Madeleine et al, 2001). High-risk human papillomavirus was detected in 66 -100% of patients with ACIS (Anciaux et al, 1997;Riethdorf et al, 2000). Approximately 48% of all women diagnosed with ACIS have coexisting squamous lesions (Colgan and Lickrish, 1990;Leary et al, 1991;Higgins et al, 1992;Duggan et al, 1995;Anciaux et al, 1997;McLachlin et al, 1997;Pirog et al, 2000;Riethdorf et al, 2000Riethdorf et al, , 2002Madeleine et al, 2001), but the frequency of specific hr-HPV genotypes in patients with ACIS has not been studied in relation with the presence or absence of coexisting CIN lesions.…”

Screening of microsatellite markers in penile cancer reveals differences between metastatic and nonmetastatic carcinomas

“…The amplification of HPV 6/11 DNA with specific primer sequences F-TACACTGCTGGACAACATGC and R-GTGCGCAGATGGGACACAC and of HPV 16 DNA with specific primer sequences F-CCCAGCTG TAATCATGCATGGAGA and R-GTGTGCCCATTAA CAGGTCTTCCA was detected in a duplex PCR as described by Husnjak et al 16 For the amplification of HPV 18 DNA, we used specific primer sequences F-GAATTCACTCTATGTGCAG and R-TAGTTGTT GCCTGTAGGTG as published by Riethdorf et al 17 The products were analyzed by electrophoresis on polyacrylamide gels and detected by silver staining.…”