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World J Urol. 2015 Dec;33(12):2145-51. doi: 10.1007/s00345-015-1539-y. Epub 2015 Mar 19.

Low prevalence of HPV detection and genotyping in non-muscle invasive bladder cancer using single-step PCR followed by reverse line blot.

Author information

1
Division of Experimental Urology, Department of Urology, Medical University of Innsbruck, Innsbruck, Austria.
2
Section of Virology, Department of Hygiene, Microbiology and Social Medicine, Innsbruck, Austria.
3
Division of General Pathology, Department of Pathology, Medical University Innsbruck, Innsbruck, Austria.
4
Department of Medical Statistics, Informatics and Health Economics, Müllerstrasse 44A-6020, Innsbruck, Austria.
5
Division of General Pathology, Department of Pathology, Medical University Innsbruck, Innsbruck, Austria. Andrea.Brunner@i-med.ac.at.

Abstract

PURPOSE:

To clarify the role of human papillomavirus (HPV) in non-muscle invasive bladder cancer, HPV-DNA was scrutinized in formalin-fixed, paraffin-embedded (FFPE) bladder cancer tissue using single-step PCR (HPV L1) for HPV detection, followed by reverse line blot (RLB) for genotyping.

METHODS:

A total of 186 patients who underwent transurethral resection of the bladder due to primary, non-muscle invasive bladder cancer from 2006 to 2009 were reviewed. A positive control group of 22 cervical tissues with cervical carcinoma was included.

RESULTS:

Histology confirmed urothelial carcinoma in all patients: primary CIS, pTa, pT1 and pTa + pT1 in 14 (7.5 %), 134 (72 %), 36 (19.4 %) and two (1.1 %) patients, respectively. A total of 119 (63.9 %) of them were classified as low-risk, while 67 (36.1 %) were high-risk cancers. Tumor recurrence and progression (≥pT2) were seen in 79 and 11 patients (mean follow-up 45 months). The presence of HPV-DNA by single-step PCR was detected in four (2.2 %) patients. HPV 16 and HPV 6 were positive in two (1.1 %) and one (0.6 %) patient, respectively In one case, no HPV genotype listed on the RLB assay could be identified. In the control group, the HPV infection rate was 100 %: HPV 16 in 12 (54.6 %) patients, HPV 16/18 in four (18.3 %) patients, HPV 18 in two (9.1 %) patients, HPV 16/45 in one patient (4.5 %), HPV 18/33 in one (4.5 %) patient, HPV 16/33 in one (4.5 %) patient and HPV 33 in one (4.5 %) patient.

CONCLUSIONS:

Our study demonstrates low prevalence of HPV infection in FFPE bladder cancer tissue, arguing against the etiological role of HPV in non-muscle urothelial carcinogenesis.

KEYWORDS:

Bladder cancer; Carcinogenesis; Human papillomavirus; Hybridization; Infection; PCR

PMID:
25786709
DOI:
10.1007/s00345-015-1539-y
[Indexed for MEDLINE]

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