Gene-Expression Signatures of Nasal Polyps Associated With Chronic Rhinosinusitis and Aspirin-Sensitive Asthma

Michael Platt; Ralph Metson; Konstantina Stankovic

Disclosures

Curr Opin Allergy Clin Immunol. 2009;9(1):23-28. 

In This Article

Abstract and Introduction

Abstract

Purpose of Review: The purpose of this review is to highlight recent advances in gene-expression profiling of nasal polyps in patients with chronic rhinosinusitis and aspirin-sensitive asthma.
Recent Findings: Gene-expression profiling has allowed simultaneous interrogation of thousands of genes, including the entire genome, to better understand distinct biological and clinical phenotypes associated with nasal polyps. The genes with altered expression in nasal polyps are involved in many cellular processes, including growth and development, immune functions, and signal transduction. The wide-ranging and typically nonoverlapping results reported in the published studies reflect methodological and demographic differences. The identified genes present possible novel therapeutic targets for nasal polyps associated with chronic rhinosinusitis and aspirin-sensitive asthma.
Summary: Gene-expression profiling is a powerful technology that allows definition of expression signatures to characterize patient subgroups, predict response to treatment, and offer novel therapies. Although the ability to interpret the meaning of the individual gene in these signatures remains a challenge, integrated analysis of a large number of these signatures with other genome-scale data sets and more traditional targeted approaches has a potential to revolutionarize understanding and treatment of chronic rhinosinusitis and aspirin-sensitive asthma.

Introduction

Sinusitis is one of the most commonly diagnosed and economically taxing diseases in the United States.[1,2,3] Patients with chronic rhinosinusitis (CRS) who are most refractory to treatment develop sinonasal polyps. A subset of these patients has aspirin-sensitive asthma (ASA, i.e. triad asthma or Samter's triad) distinguished by the presence of nasal polyps, asthma, and aspirin allergy. Sinonasal polyps are histologically characterized by numerous changes in the mucosal epithelium and underlying stroma,[4] suggesting altered expression of multiple genes. We review studies that have applied microarray technology to sinonasal polyps to monitor expression of thousands of genes, and thereby gain insights into putative mechanisms of and novel targets for sinonasal polyposis, CRS, and asthma.

Comments

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