Abnormal Differentiation of Human Papillomavirus-Induced Laryngeal Papillomas

Steinberg, Bettie M.; Meade, Raymond P.; Kalinowski, Stephen; Abramson, Allan L.

doi:10.1001/archotol.1990.01870100061013

Cited by 42 publications

(26 citation statements)

References 32 publications

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“…Papilloma cells proliferate more slowly than normal laryngeal epithelial cells (26), in accord with the elevated level of p21 CIP1/WAF1 reported here. Overexpression of p21…”

supporting

confidence: 89%

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Increased p50/p50 NF-κB Activation in Human Papillomavirus Type 6- or Type 11-Induced Laryngeal Papilloma Tissue

Vancurova¹,

Miskolci³

et al. 2002

J Virol

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We have observed elevated NF-B DNA-binding activity in nuclear extracts from human papillomavirus type 6-and 11-infected laryngeal papilloma tissues. The predominant DNA-binding species is the p50/p50 homodimer. The elevated NF-B activity could be correlated with a reduced level of cytoplasmic IB␤ and could be associated with the overexpression of p21 CIP1/WAF1 in papilloma cells. Increased NF-B activity and cytoplasmic accumulation of p21 CIP1/WAF1 might counteract death-promoting effects elicited by overexpressed PTEN and reduced activation of Akt and STAT3 previously noted in these tissues.

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“…Papilloma cells proliferate more slowly than normal laryngeal epithelial cells (26), in accord with the elevated level of p21 CIP1/WAF1 reported here. Overexpression of p21…”

supporting

confidence: 89%

“…could also lead to disruption of normal epithelial differentiation programming previously observed in papilloma tissue (26,29). This hypothesis is supported by the finding that expression of p21 CIP1/WAF1 in keratinocytes inhibits expression of differentiation markers such as keratin 1, involucrin, and filaggrin (9).…”

Section: Cip1/waf1mentioning

confidence: 88%

Increased p50/p50 NF-κB Activation in Human Papillomavirus Type 6- or Type 11-Induced Laryngeal Papilloma Tissue

Vancurova¹,

Miskolci³

et al. 2002

J Virol

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“…Lin et al (34) reported that COX-2 expression and/or PGE 2 activated PI3K, and PI3K inhibition reduced COX-2 levels. Thus, activation of PI3K via PGE 2 receptors, in addition to the EGFR, might play a role in the proposed feedback loop in our cells. COX-2 -derived prostaglandins have been reported to increase cell proliferation and Research.…”

Section: Discussionmentioning

confidence: 90%

Epidermal Growth Factor–Induced Cyclooxygenase-2 Expression Is Mediated through Phosphatidylinositol-3 Kinase, Not Mitogen-Activated Protein/Extracellular Signal-Regulated Kinase Kinase, in Recurrent Respiratory Papillomas

Abramson

Shikowitz

et al. 2005

Clinical Cancer Research

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Purpose: Recurrent respiratory papillomas, caused by human papillomaviruses, are premalignant tumors that overexpress the epidermal growth factor receptor (EGFR). The goals of this study were as follows: (a) to evaluate the expression of cyclooxygenase-2 (COX-2) in papillomas, (b) to investigate the role of EGFR signaling in COX-2 expression, and (c) to determine whether COX-2 activity is important for the growth of papilloma cells. Experimental Design: Immunohistochemistry, Western blotting, and real-time PCR were used to determine levels of COX-2 in papilloma and normal laryngeal tissue. Explant cultures of both normal laryngeal and papilloma cells were used to define the signaling pathways that regulate COX-2 expression and investigate the potential of targeting COX-2 as a strategy to suppress papilloma growth. Results: COX-2 levels were markedly increased in papillomas. In vitro studies suggested that overexpression in papillomas reflected activation of EGFR!phosphatidylinositol 3-kinase signaling. Treatment with prostaglandin E 2 (PGE 2 ) induced COX-2, whereas celecoxib, a selective COX-2 inhibitor, suppressed levels of COX-2, suggesting a positive feedback loop. Moreover, treatment with PGE 2 stimulated papilloma cell growth, whereas celecoxib suppressed proliferation and induced apoptosis. Conclusions: Overexpression of COX-2 in papillomas seems to be a consequence of enhanced EGFR!phosphatidylinositol 3-kinase signaling. We propose a positive feedback loop for COX-2 expression, with induction of COX-2 resulting in enhanced PGE 2 synthesis and further expression of COX-2 that contributes to the growth of papillomas in vivo.These data strengthen the rationale for evaluating whether nonsteroidal anti-inflammatory drugs, prototypic COX inhibitors, will be useful in the management of respiratory papillomas.

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“…Our data showed that three cases exhibited a few cells with koilocytic features, but were not detected HPV DNA by HPV ISH (Table 1). How HPV induces cellular proliferation is not well understood [17].…”

Section: Discussionmentioning

confidence: 99%

Papillomas of the External Ear Canal: Report of Ten cases in Chinese Patients with HPV In Situ Hybridization

Wang

Yee

Wen

et al. 2009

Head and Neck Pathol

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Squamous papilloma is a benign exophytic proliferation which can occur occasionally in the external ear canal. It is widely assumed that the Human Papilloma Virus (HPV) is an etiologic factor of papillomas. Available techniques for detection of HPV genomes include immunohistochemistry, Southern blot hybridization, in situ hybridization (ISH), and polymerase chain reaction. To our knowledge, HPV typing has not been reported on tissue sections of papillomas in the external ear canal. We report HPV ISH analysis in ten cases of papillomas, involving the external ear canal in Chinese patients. These papilloma excrescences were less than 1 cm in diameter, and were benign morphologically. Automated HPV ISH analysis was performed for the hybridization of DNA probes, including both low-risk and high-risk HPV subtypes. HPV ISH results revealed that seven out of ten cases were positive for low-risk HPV (6, 11), three cases demonstrated no hybridization for low-risk HPV probe, and none of the cases revealed any detection of high-risk HPV (16, 18, 31, 33, 35, 39, 51, 52, 56, 58, and 66). On follow-up after 18-29 months (average 24.5 months), eight patients were doing well, with no local recurrence after excision. Two patients were lost to follow-up. Our results confirm that benign papillomas of the external ear canal are associated with low-risk HPV infection with benign behavior and neither recurrence nor high grade dysplasia.

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Abnormal Differentiation of Human Papillomavirus-Induced Laryngeal Papillomas

Cited by 42 publications

References 32 publications

Increased p50/p50 NF-κB Activation in Human Papillomavirus Type 6- or Type 11-Induced Laryngeal Papilloma Tissue

Increased p50/p50 NF-κB Activation in Human Papillomavirus Type 6- or Type 11-Induced Laryngeal Papilloma Tissue

Epidermal Growth Factor–Induced Cyclooxygenase-2 Expression Is Mediated through Phosphatidylinositol-3 Kinase, Not Mitogen-Activated Protein/Extracellular Signal-Regulated Kinase Kinase, in Recurrent Respiratory Papillomas

Papillomas of the External Ear Canal: Report of Ten cases in Chinese Patients with HPV In Situ Hybridization

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