title: Epidermal growth factor receptors in idiopathic and virally induced skin diseases.
abstract: 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.
authors.affiliation: Department of Plastic Surgery, Vanderbilt University, Nashville, TN 37232.
authors.forename: L B
authors.initials: LB
authors.lastname: Nanney
authors.forename: D L
authors.initials: DL
authors.lastname: Ellis
authors.forename: J
authors.initials: J
authors.lastname: Levine
authors.forename: L E
authors.initials: LE
authors.lastname: King
mesh_terms: D002455:Cell Division; D012628:Dermatitis, Seborrheic / Q000378:metabolism / Q000473:pathology; D066246:ErbB Receptors / Q000378:metabolism*; D006801:Humans; D007642:Keratosis / Q000378:metabolism / Q000473:pathology; D012016:Reference Values; D012871:Skin Diseases / Q000378:metabolism* / Q000382:microbiology / Q000473:pathology; D014777:Virus Diseases / Q000150:complications*
chemical_list: D066246:ErbB Receptors