Hostname: page-component-cd9895bd7-q99xh Total loading time: 0 Render date: 2024-12-27T13:56:13.160Z Has data issue: false hasContentIssue false

Constitutive (HO-2) and inducible (HO-1) haem oxygenase in pleomorphic adenomas of the human parotid: an immunocytochemical study

Published online by Cambridge University Press:  08 March 2006

Stephen Lo
Affiliation:
Department of Otolaryngology, St George’s Hospital Medical School, London, UK.
Silvana Di Palma
Affiliation:
Department of Pathology, Queen Alexandra Hospital, Portsmouth, UK.
Hafsa Yusuf
Affiliation:
Department of Otolaryngology, Frimley Park Hospital, Surrey, UK.
Andrew W McCombe
Affiliation:
Department of Otolaryngology, Frimley Park Hospital, Surrey, UK.

Abstract

This study examines the expression HO-1 and HO-2 isozymes in human parotid pleomorphic adenomas. They are members of the heat shock protein family, and are thought to play a role in the regulation of tumoral blood flow. Immunocytochemistry using antibodies specific for HO-1 and HO-2 were undertaken in 12 pleomorphic adenoma specimens, all sections of which contained adjacent normal salivary tissue. Normal salivary gland acini and ducts displayed significantly stronger immunoreactivity for HO-2 compared to tumour cells (p < 0.001). Expression for HO-1 was minimal in both normal salivary gland acini and tumour cells with no difference (p = 1.000). However, positive staining for HO-1 was seen in normal salivary ducts and in pleomorphic adenomas showing ductal differentiation. In conclusion, this is the first study to examine the expression of HO-1 and HO-2 within normal salivary glands and pleomorphic adenomas. Our findings suggest that HO may be implicated in the pathogenesis of salivary pleomorphic adenomas.

Type
Research Article
Copyright
© 2005 Royal Society of Medicine Press

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)