The expression of cancerous inhibitor protein phosphatase 2A in chronic rhinosinusitis with nasal polyps

Abstract

Conclusion: The study suggests that cancerous inhibitor of protein phosphatase 2A (CIP2A) expression and eosinophilia associate with chronic rhinosinusitis with nasal polyps with aspirin exacerbated respiratory disease (CRSwNP + AERD). Further studies with a larger sample size are needed to evaluate further the role of CIP2A and related pathways in CRSwNP + AERD.

Objectives: Low prostaglandin E2 levels putatively associate with CRSwNP + AERD and decreased c-Myc levels. The aim of this study was to evaluate the expression and revision-predictive role of oncoprotein CIP2A, another c-Myc modulator, in CRSwNP with/without AERD, and in antrochoanal polyps.

Method: Ninety retrospective archival objective glasses of nasal polyp tissue from CRSwNP or ACP patients were used for assessing mucosal eosinophilia. Of this population, 90 archival nasal polyp specimens were available for immunohistochemical staining with a polyclonal anti-CIP2A antibody, together with 19 control nasal mucosa specimens. CIP2A staining intensity and tissue eosinophilia were assessed by two blinded observers with a light microscope. Subject characteristics from 90 patients and 19 controls were obtained from patient records and additionally by a questionnaire from controls. The follow-up data was available from patient records of 84 patients and 16 controls.

Results: The expression of epithelial CIP2A was detected both in control inferior turbinate mucosa and nasal polyps. The expression was significantly lower in the CRSwNP + AERD group compared to controls and CRSwNP without AERD (p < 0.01). High mucosal eosinophilia associated with CRSwNP (p < 0.01). Neither CIP2A nor eosinophilia predicted the need for revision surgery (p > 0.05), whereas previous surgery, allergic rhinitis, and use of corticosteroids did predict the need for revision surgery (p < 0.05).

Keywords:

• Aspirin exacerbated respiratory disease
• cancerous inhibitor of protein phosphatase 2A
• immunohistochemistry
• nasal polyp
• sinusitis

Acknowledgements

We thank Eini Eskola, Marja-Leena Oksanen, Marja-Leena Koskinen, Raija Hukkila, Markus Rautiainen, Arto Ranta, Hannu Raitiola, Mikko Suvinen and Teemu Honkanen for excellent assistance.

The study was supported in part by the Competitive Research Funding of the Tampere Medical Research Fund of Tampere University Hospital, and in part by research grants from the Finnish Medical Foundation, Finnish Association of Otorhinolaryngology and Head and Neck Surgery, Jane and Aatos Erkko Foundation, Paulo Foundation, the Finnish Cultural Foundation, the Tampere Tuberculosis Foundation, Väinö and Laina Kivi Foundation, Minerva Foundation, Yrjö Jahnsson Foundation, and Dentists of Helsinki Region.

Disclosure statement

The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.