23 research outputs found

    Age distribution of antrochoanal- and nasal polyps.

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    <p>The Boxplot shows high significant difference in age distribution of antrochoanal polyps (ACP) in comparison to nasal polyps (NP). Asterisks symbolize significance levels of multiple comparison rank analysis (* p < 0.05; ** p < 0.01; *** p < 0.001).</p

    HPV Immunohistochemistry.

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    <p>IHC Overview of a representative HPV-positive antrochoanal polyp with HPV16 staining (A). HPV16 E6 protein staining of a representative HPV-positive antrochoanal polyp, relevant epithelial region shown (B) with corresponding negative control (C). HPV16 E6 protein staining of a representative HPV-positive nasal polyp, relevant epithelial region shown and subepithelial stained cells (D) with corresponding negative control (E). Discontinuous epithelial cell clusters stained positive in HPV-positive antrochoanal- and nasal polyps.</p

    GP5+/6+ PCR.

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    <p>Representative extraction of broad spectrum PCR with GP5+/6+ primer. Three of twelve antrochoanal polyps (ACP) are showing clear bands, and three further weak bands. No bands are visible in negative controls (NK) and the most intense band is present in oropharyngeal carcinoma (OPC) as positive control.</p

    Human Papillomavirus (HPV) Prevalence in Nasal and Antrochoanal Polyps and Association with Clinical Data

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    <div><p>Objectives</p><p>The pathogenesis of sinonasal polyposis remains unclear, in spite of several investigative approaches. Antrochoanal polyps, a subgroup of sinonasal polyposis along with allergic- and chronic-inflammatory nasal polyps, mostly originate from the maxillary sinus and develop as a unilateral, pedunculated mass towards the nasopharynx. The human papillomavirus (HPV) is discussed as a possible causative and influencing factor in development and progression of sinonasal polyposis. This study aims to elucidate HPV frequency in nasal polyps and antrochoanal polyps.</p><p>Materials and Methods</p><p>Genomic DNA from 257 tissue specimens (166 nasal polyps, 39 antrochoanal polyps and 52 nasal turbinates) was subjected to three different established HPV- polymerase chain reaction assays, testing for 37 low- and high-risk HPV. In addition, immunohistochemical analyses for HPV16 were carried out, as well as immunohistochemistry and western blots of p16, a biomarker for HPV induced cancer.</p><p>Results</p><p>HPV-DNA was detected in 53.8% of antrochoanal polyps, 15.1% of nasal polyps, and 5.8% of nasal turbinates. HPV16 was the predominant type with a detection rate of 76% in nasal polyps and 62% in antrochoanal polyps. Immunohistochemically, HPV positive tissues stained positive for HPV16 antigens and p16 in epithelial cell layers. No significant p16 overexpression was traceable in antrochoanal polyps, nasal polyps and nasal turbinates by western blot. There was no correlation of HPV-status with sex, age, smoking, alcohol consumption or allergic background.</p><p>Conclusion</p><p>The present study shows a significant frequency of high-risk type HPV16 in antrochoanal polyps. Absence of oncogenic transformation or correlation of the HPV-status with clinical data suggests a latent superinfection, possibly because of anatomical proximity to the oropharynx.</p></div

    P16 Immunohistochemistry.

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    <p>Immunohistochemistry of p16 protein expression in representative HPV-positive antrochoanal polyp (A) and corresponding negative control (B). Weak irregular spread epithelial p16-IHC staining in strong HPV-DNA positive samples. Detected signals were dominantly intranuclear.</p

    P16 Western Blot.

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    <p>Representative p16 western blot of HPV-positive and -negative antrochoanal polyps (ACP), nasal polyps (NP), nasal turbinates (NT) and oropharyngeal carcinoma (OPC). Two HPV-positive carcinomas are showing strong p16 bands. Three of four HPV-positive.</p

    SOX2 FISH and SOX2 IHC.

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    <p>Above: representative FISH images of sinonasal squamous cell carcinoma samples without <i>SOX2</i> amplification (A), <i>SOX2</i> low level amplification (B) and <i>SOX2</i> high level amplification (C). Below: representative immunohistochemical stains of weak nuclear SOX2 expression in case of wildtype <i>SOX2</i> (D) and strong nuclear SOX2 expression in case harbouring <i>SOX2</i> amplification (E).</p
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