help button home button Am J Pathol ASIP 2008 Summer Academy, Molecular Methcanisms of Human Disease: Injury, Inflammation, and Tissue Repair
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS

This Article
Right arrow Order Full text via Infotrieve
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Nanney, L. B.
Right arrow Articles by King, L. E.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Nanney, L. B.
Right arrow Articles by King, L. E.

American Journal of Pathology, Vol 140, 915-925, Copyright © 1992 by American Society for Investigative Pathology

REGULAR ARTICLES

Epidermal growth factor receptors in idiopathic and virally induced skin diseases

LB Nanney, DL Ellis, J Levine and LE King
Department of Plastic Surgery, Vanderbilt University, Nashville, TN 37232.

The altered distribution of epidermal growth factor receptors (EGF-R) in hyperproliferative skin lesions such as psoriasis vulgaris, seborrheic keratoses, acanthosis nigricans, ichthyosis, and others implies aberrant control of growth/proliferation by epidermal growth factor (EGF), transforming growth factor alpha (TGF alpha), and other growth factors/cytokines. Whether overexpression of EGF-R: 1) correlates with epidermal proliferation, 2) serves as a hallmark of specific dermatoses, or 3) is due to modulation by multiple growth factors remains unclear. To correlate distributions of EGF-R with in vivo proliferative status, two benign diseases of unknown etiology, seborrheic keratoses and acrochordons (skin tags), were examined using EGF-R immunolocalization and 125I-EGF binding techniques. Lesions documented as growing by clinical criteria or 5-bromodeoxyuridine incorporation (a measure of cell proliferation) were compared to nongrowing lesions of the same type. To correlate distributions of EGF- R to specific dermatoses, skin diseases of viral etiology (verruca vulgaris and molluscum contagiosum) were also probed by EGF-R immunolocalization and 125I-EGF binding. Elevated immunostaining for EGF-R and 125I-EGF binding sites were associated with actively growing seborrheic keratoses and skin tags whereas normal patterns of immunostaining and 125I-EGF binding were seen in nongrowing seborrheic keratoses and skin tags. Viral diseases showed unique patterns. No EGF- R were detected in verruca vulgaris. Molluscum contagiosum lesions showed intense EGF-R in basal keratinocytes and no EGF-R in virally infected cells. Thus elevations in EGF-R show a positive in vivo correlation with proliferation in at least two differing benign diseases of the epidermis. The decreased levels of EGF-R in virally infected lesions suggests that EGF-R may show unique patterns for specific dermatoses and are not universally elevated in benign hyperproliferative skin disorders.


This article has been cited by other articles:


Home page
 Circ. Res.Home page
C. J. Pastore, J. M. Isner, P. A. Bacha, M. Kearney, and J. G. Pickering
Epidermal Growth Factor Receptor–Targeted Cytotoxin Inhibits Neointimal Hyperplasia In Vivo : Results of Local Versus Systemic Administration
Circ. Res., September 1, 1995; 77(3): 519 - 529.
[Abstract] [Full Text]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1992 by the American Society for Investigative Pathology.