Human‐papillomavirus DNA in cholesteatomas

Bergmann, Krister; Hoppe, Florian; He, Yukai; Helms, J.; Müller-Hermelink, H. K.; Stremlau, A.; Villiers, E.-M. de

doi:10.1002/ijc.2910590405

Cited by 20 publications

(22 citation statements)

References 23 publications

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“…They applied PCR and in situ hybridization with an HPV-6-or HPV-11-specific probe, claiming a sensitivity of 0.1 viral copy/cell. With a prevalence of 3% (1/32 specimen positive for HPV-6 DNA), this result sig- nificantly differed from the results of Bergmann et al [10] . The results of our study again demonstrate a low prevalence (3%) of HPV DNA in cholesteatoma specimens.…”

Section: Discussioncontrasting

confidence: 57%

“…This assumption has led to several studies investigating the role of HPV infections in the development of acquired cholesteatoma. Bergmann et al [10] detected HPV-11 DNA in 36% (16/45) of cholesteatoma specimens using a PCR with degenerate primers for L1 ORF, with a protocol similar to the PCR protocol applied in this study except for the nested PCR. Only the hybridization of the amplified products with an HPV-11-specific radiolabelled probe resulted in positive signals in 36% of the samples; the use of a probe designed to cover all papillomaviruses had resulted in 1 positive signal.…”

Section: Discussionmentioning

confidence: 99%

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Prevalence of Human Papillomavirus DNA in Cholesteatomas

Franz

Teschendorf²,

Wohlschläger³

et al. 2007

ORL

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Cholesteatomas show histomorphological features like papillary growth and koilocytosis, which are characteristic of lesions induced by human papillomaviruses (HPV). Two previous studies investigating the possible role of HPV in the development of cholesteatoma had detected HPV-6 and HPV-11 DNA with a prevalence differing from 3 to 36%. The aim of the presented study was to evaluate the prevalence of different HPV types in cholesteatomas using a sensitive detection system for HPV DNA. Twenty-nine biopsies from cholesteatomas were screened for HPV DNA with a 2-step broad-spectrum PCR (PCR and nested PCR). HPV-positive products were directly sequenced by means of a cycle sequencing approach. Sensitivity of the applied broad-spectrum PCR was 0.1 copy/genome. One out of 29 biopsies showed a positive signal on the nested PCR level. Considering the low prevalence (1/29 biopsies) of detected HPV DNA in cholesteatomas, infections with common HPV types are unlikely to be a causative factor.

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Section: Discussioncontrasting

confidence: 57%

Section: Discussionmentioning

confidence: 99%

Prevalence of Human Papillomavirus DNA in Cholesteatomas

Franz

Teschendorf²,

Wohlschläger³

et al. 2007

ORL

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“…The E6/E7 oncogenes of certain human papilloma viruses (HPV) such as HPV16 and HPV18 appear to be essential causative factors for the majority of cervical cancers (Campo, 1998;zur Hausen, 2000) and for a significant fraction of neoplasms in humans at specific other sites, particularly anogenital, head-neck (oropharyngeal) (Gillison et al, 2000;Klussmann et al, 2001;Ringstrom et al, 2002), eye (conjunctival) (Scott et al, 2002) and ear (middle ear) (Bergmann et al, 1994;Jin et al, 1997;Tsai et al, 1997). These types of cancers are typically preceded by clinically detectable premalignant, that is, noninvasive lesions that usually arise in epithelial transition zones where cell types are changing.…”

Section: Introductionmentioning

confidence: 99%

Strong synergy between mutant ras and HPV16 E6/E7 in the development of primary tumors

et al. 2004

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E6/E7 oncogenes of high-risk human papilloma virus (HPV) subtypes are essential for the development of certain types of cancers. However, these oncogenes are insufficient to transform normal cells into an immortalized or malignant state. Mutant Ha-ras cooperates with E6/E7 of HPV subtype 16 in transformation of cells in vitro and may contribute to some HPV-associated cancers in humans. This study investigates whether HPV16 E6/E7 and v-Ha-ras synergize in vivo. FVB/n mice transgenic for v-Ha-ras gene (R þ ) were crossed with transgenic C57BL/ 6 mice that harbor E6/E7 of HPV16 (E þ ). Beginning at about 3 months of age, the bitransgenic E þ R þ (C57BL/ 6 Â FVB/n) F1 mice developed mouth, eye and ear tumors. By 6 months, the prevalence of these types of mouth, eye and ear tumors was 100, 71 and 79% respectively in the E þ R þ mice. Most tumors grew progressively until the mice had to be killed. The median times for the appearance of the first mouth, eye and ear tumor were 3.6, 4.3 and 4.2 months, respectively. For the two singly transgenic groups of mice, the prevalence of mouth, eye and ear tumors was 0, 0 and 6% (E À R þ ) and 0, 0 and 0% (E þ R À ), respectively, and the median time to first tumor was greater than 12 months for singly transgenic mice (E À R þ , E þ R À ). Thus, a remarkable synergy occurred between the v-Ha-ras and HPV16 E6/E7 oncogenes in the development of primary tumors in mice.

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“…The sensitivity of this method is about 0.1 viral copy/cell, which is higher than the 10-20 copies/cell detection limit of in situ hybridization (Fujinaga et al, 1991;Okagaki, 1992;Yousem et al, 1992). One investigator has identified HPV DNA in 36% of middle-ear cholesteatomas by PCR (Bergmann et al, 1994). A previous report has noted a high association of cholesteatoma with cancer of the middle ear (Lewis, 1960).…”

Section: Resultsmentioning

confidence: 98%

“…This suggests that the stimulation of chronic inflammation and possible infection may be causally important for the subsequent development of middle-ear carcinoma. A recent study using the polymerase chain reaction (PCR) method revealed that 36% (16/45) of cholesteatomas contained papillomavirus DNA (Bergmann et al, 1994). This study was therefore designed to determine whether the high-risk types of HPV could be detected in archival paraffin-embedded tissues of middle-ear carcinoma using PCR.…”

mentioning

confidence: 99%

High prevalence of human papillomavirus types 16 and 18 in middle-ear carcinomas

Tsai

Jin

et al. 1997

Int. J. Cancer

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Chronic suppurative otitis media, averaging 20 or more years of duration, has been associated with cancer in this region in 40%-80% of cases. Although human papillomaviruses (HPV) have been implicated in many human squamouscell neoplasms, their role in the pathogenesis of middle-ear malignancies remains unexplored. In this study, we investigated the presence and subtypes of HPV in middle-ear carcinomas. Formalin-fixed and paraffin-embedded tumor tissues were sampled for DNA extraction. PCR was done with consensus primers, capable of detecting HPV 16, 18, 31, 33, 52b and 58. Typing of the products generated by consensus primers was performed with restriction enzyme digestion. It was found that a resulting 89% (8/9) of the middle-ear carcinomas contained HPV DNA. Coexistence of HPV 16 and 18 was detected in 3 squamous-cell carcinomas. HPV 16 was detected in 4 squamous-cell carcinomas and 1 adenocarcinoma. The high prevalence of high-risk-type HPV in carcinomas of the middle ear suggests that viral infection may be an important etiologic component in the carcinogenic process.

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Human‐papillomavirus DNA in cholesteatomas

Cited by 20 publications

References 23 publications

Prevalence of Human Papillomavirus DNA in Cholesteatomas

Prevalence of Human Papillomavirus DNA in Cholesteatomas

Strong synergy between mutant ras and HPV16 E6/E7 in the development of primary tumors

High prevalence of human papillomavirus types 16 and 18 in middle-ear carcinomas

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