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      Cytokeratin 17 and Ki-67: Immunohistochemical markers for the differential diagnosis of keratoacanthoma and squamous cell carcinoma

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          Abstract

          The clinical and histopathological distinction between keratoacanthoma (KA) and squamous cell carcinoma (SCC) is essential, but frequently difficult to make. The utility of CK17 and Ki-67 expression in distinguishing between KA and SCC was investigated. Immunohistochemical staining patterns for CK17 and Ki-67 were evaluated in 24 KA and 27 SCC cases. The pattern of staining was evaluated as central, peripheral or diffuse, according to the basal/peripheral and suprabasal/central cell staining of tumor lobules. The sensitivity and specificity of the central CK17 staining pattern in the identification of KA were 92 and 70%, respectively. Additionally, the sensitivity and specificity of the diffuse Ki-67 staining pattern in the identification of SCC were 81 and 100%, respectively. The results of the present study suggest that a diffuse Ki-67 staining pattern may be used to diagnose SCC, while a central CK17 staining pattern indicates KA. However, the KA-like SCC cases exhibited mixed patterns, which limits the effectiveness of these markers.

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          Onset of Keratin 17 Expression Coincides with the Definition of Major Epithelial Lineages during Skin Development

          Kevin M. McGowan, Pierre A. Coulombe (1998)
          The type I keratin 17 (K17) shows a peculiar localization in human epithelial appendages including hair follicles, which undergo a growth cycle throughout adult life. Additionally K17 is induced, along with K6 and K16, early after acute injury to human skin. To gain further insights into its potential function(s), we cloned the mouse K17 gene and investigated its expression during skin development. Synthesis of K17 protein first occurs in a subset of epithelial cells within the single-layered, undifferentiated ectoderm of embryonic day 10.5 mouse fetuses. In the ensuing 48 h, K17-expressing cells give rise to placodes, the precursors of ectoderm-derived appendages (hair, glands, and tooth), and to periderm. During early development, there is a spatial correspondence in the distribution of K17 and that of lymphoid-enhancer factor (lef-1), a DNA-bending protein involved in inductive epithelial–mesenchymal interactions. We demonstrate that ectopic lef-1 expression induces K17 protein in the skin of adult transgenic mice. The pattern of K17 gene expression during development has direct implications for the morphogenesis of skin epithelia, and points to the existence of a molecular relationship between development and wound repair.
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            Keratin 17 modulates hair follicle cycling in a TNFalpha-dependent fashion.

            Xuemei Tong, P Coulombe (2006)
            Mammalian hair follicles cycle between stages of rapid growth (anagen) and metabolic quiescence (telogen) throughout life. Transition from anagen to telogen involves an intermediate stage, catagen, consisting of a swift, apoptosis-driven involution of the lower half of the follicle. How catagen is coordinated, and spares the progenitor cells needed for anagen re-entry, is poorly understood. Keratin 17 (K17)-null mice develop alopecia in the first week post-birth, correlating with hair shaft fragility and untimely apoptosis in the hair bulb. Here we show that this abnormal apoptosis reflects premature entry into catagen. Of the proapoptotic challenges tested, K17-null skin keratinocytes in primary culture are selectively more sensitive to TNFalpha. K17 interacts with TNF receptor 1 (TNFR1)-associated death domain protein (TRADD), a death adaptor essential for TNFR1-dependent signal relay, suggesting a functional link between this keratin and TNFalpha signaling. The activity of NF-kappaB, a downstream target of TNFalpha, is increased in K17-null skin. We also find that TNFalpha is required for a timely anagen-catagen transition in mouse pelage follicles, and that its ablation partially rescues the hair cycling defect of K17-null mice. These findings identify K17 and TNFalpha as two novel and interdependent regulators of hair cycling.
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              Antibody markers of basal cells in complex epithelia.

              J. Jordan Steel, Maureen Lane, Darryl MacKenzie … (1990)
              In the course of immunohistochemical studies it has become apparent that there is a distinct phenotype of keratin expression that is shared by basal epithelial cells in a variety of different tissues. A basal cell can be defined as a cell in contact with a basal lamina but with no free luminal surface; this distinguishes it from a simple epithelial cell, which has a free luminal surface as well as basal lamina contact, and from stratifying suprabasal keratinocytes, which have neither basal lamina contact nor free luminal surface. All basal cells, whether they are in glandular ductal or secretory epithelia, or in stratified squamous epithelia, express the keratin pair K5 and K14. In this paper we describe monoclonal and polyclonal antibodies that are monospecific for both keratins 14 and 5 or are specific for denaturation-sensitive epitopes unique to basal cells, including five new monoclonal antibodies: LL001 and LL002 (to keratin 14), 2.1.D7 (to keratins 5, 6 and 8), and LH6 and LH8 (conformation-specific basal cell markers). These antibodies have been used to monitor the distribution of the basal cell phenotype and to demonstrate the expression of keratins 5 and 14 in this cell type, in both stratified epithelia and mixed epithelial glands. The consistent association of this keratin pair with basal cells suggests a possible specific function for these keratin in reinforcing epithelia under physical stress, whilst expression of these keratins may conflict with the differentiated functions of most simple epithelial cells.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Oncol Lett
                Journal ID (iso-abbrev): Oncol Lett
                Journal ID (publisher-id): OL
                Title: Oncology Letters
                Publisher: D.A. Spandidos
                ISSN (Print): 1792-1074
                ISSN (Electronic): 1792-1082
                Publication date (Print): April 2017
                Publication date (Electronic): 01 March 2017
                Publication date PMC-release: 01 March 2017
                Volume: 13
                Issue: 4
                Pages: 2539-2548
                Affiliations
                [1 ]Department of Pathology, Istanbul Education and Research Hospital, Istanbul 34098, Turkey
                [2 ]Department of Pathology, Erciyes University, School of Medicine, Kayseri 38039, Turkey
                Author notes
                Correspondence to: Dr Cem Leblebici, Department of Pathology, Istanbul Education and Research Hospital, 24 Abdurrahman Nafiz Gürman Street, Istanbul 34098, Turkey, E-mail: cleblebici@ 123456gmail.com
                Article
                Publisher ID: OL-0-0-5793
                DOI: 10.3892/ol.2017.5793
                PMC ID: 5403446
                SO-VID: 0cdfc734-33f9-4aa5-a82a-267fa39eff7b
                Copyright © Copyright: © Leblebici et al.
                License:

                This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

                History
                Date received : 20 May 2016
                Date accepted : 04 November 2016
                Categories
                Subject: Articles

                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: cytokeratin 17,proliferation marker protein ki-67,keratoacanthoma,skin,squamous cell carcinoma
                Data availability:
                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: cytokeratin 17, proliferation marker protein ki-67, keratoacanthoma, skin, squamous cell carcinoma

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