Keratoacanthoma: a distinct entity?
Keratoacanthoma (KA) are common but exceptional benign tumors, often appearing on sun‐exposed areas of light skinned people and showing spontaneous resolution. The goal of this study was to review existing literature, to point out the etiological complexity of KA biology and to answer the controvers...
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Veröffentlicht in: | Experimental dermatology 2016-02, Vol.25 (2), p.85-91 |
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description | Keratoacanthoma (KA) are common but exceptional benign tumors, often appearing on sun‐exposed areas of light skinned people and showing spontaneous resolution. The goal of this study was to review existing literature, to point out the etiological complexity of KA biology and to answer the controversial debate if or not KA is a distinct entity or a variant of squamous cell carcinoma (SCC). Relying on recent results, we highlight that KA is an individual lesion with a unique molecular signature caused by alterations in the TGFβ signalling pathway. These recent findings will help to understand the nature of KA and to develop new reliable diagnostic tools, simplifying the discrimination of the histologically similar KA and SCC. |
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The goal of this study was to review existing literature, to point out the etiological complexity of KA biology and to answer the controversial debate if or not KA is a distinct entity or a variant of squamous cell carcinoma (SCC). Relying on recent results, we highlight that KA is an individual lesion with a unique molecular signature caused by alterations in the TGFβ signalling pathway. These recent findings will help to understand the nature of KA and to develop new reliable diagnostic tools, simplifying the discrimination of the histologically similar KA and SCC.</description><identifier>ISSN: 0906-6705</identifier><identifier>EISSN: 1600-0625</identifier><identifier>DOI: 10.1111/exd.12880</identifier><identifier>PMID: 26476131</identifier><language>eng</language><publisher>Denmark: Blackwell Publishing Ltd</publisher><subject>Carcinoma, Squamous Cell - diagnosis ; Cell Transformation, Neoplastic - genetics ; Cell Transformation, Neoplastic - radiation effects ; Comparative Genomic Hybridization ; Diagnosis, Differential ; Disease Progression ; Genetic Predisposition to Disease ; Humans ; keratoacanthoma ; Keratoacanthoma - diagnosis ; Keratoacanthoma - etiology ; Keratoacanthoma - genetics ; Keratoacanthoma - metabolism ; Keratoacanthoma - pathology ; Neoplasm Proteins - genetics ; Neoplasm Proteins - physiology ; Neoplasms, Radiation-Induced - chemistry ; Neoplasms, Radiation-Induced - diagnosis ; Neoplasms, Radiation-Induced - genetics ; Neoplasms, Radiation-Induced - pathology ; paradoxical activation ; Protein-Serine-Threonine Kinases - deficiency ; Protein-Serine-Threonine Kinases - genetics ; Protein-Serine-Threonine Kinases - physiology ; Receptors, Transforming Growth Factor beta - deficiency ; Receptors, Transforming Growth Factor beta - genetics ; Receptors, Transforming Growth Factor beta - physiology ; Signal Transduction ; Skin Diseases - diagnosis ; Skin Diseases - etiology ; Skin Diseases - genetics ; Skin Diseases - metabolism ; Skin Diseases - pathology ; Skin Neoplasms - diagnosis ; squamous cell carcinoma ; Sunlight - adverse effects ; TGF β ; TGFβ ; Transforming Growth Factor beta - physiology ; tumor ; Ultraviolet Rays - adverse effects</subject><ispartof>Experimental dermatology, 2016-02, Vol.25 (2), p.85-91</ispartof><rights>2015 John Wiley & Sons A/S. 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Published by John Wiley & Sons Ltd.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3980-6aa3162c0725f6b192303fe126ca5012740410dbd9dcb701f749a700053694a73</citedby><cites>FETCH-LOGICAL-c3980-6aa3162c0725f6b192303fe126ca5012740410dbd9dcb701f749a700053694a73</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fexd.12880$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fexd.12880$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26476131$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Gleich, Tobias</creatorcontrib><creatorcontrib>Chiticariu, Elena</creatorcontrib><creatorcontrib>Huber, Marcel</creatorcontrib><creatorcontrib>Hohl, Daniel</creatorcontrib><title>Keratoacanthoma: a distinct entity?</title><title>Experimental dermatology</title><addtitle>Exp Dermatol</addtitle><description>Keratoacanthoma (KA) are common but exceptional benign tumors, often appearing on sun‐exposed areas of light skinned people and showing spontaneous resolution. The goal of this study was to review existing literature, to point out the etiological complexity of KA biology and to answer the controversial debate if or not KA is a distinct entity or a variant of squamous cell carcinoma (SCC). Relying on recent results, we highlight that KA is an individual lesion with a unique molecular signature caused by alterations in the TGFβ signalling pathway. These recent findings will help to understand the nature of KA and to develop new reliable diagnostic tools, simplifying the discrimination of the histologically similar KA and SCC.</description><subject>Carcinoma, Squamous Cell - diagnosis</subject><subject>Cell Transformation, Neoplastic - genetics</subject><subject>Cell Transformation, Neoplastic - radiation effects</subject><subject>Comparative Genomic Hybridization</subject><subject>Diagnosis, Differential</subject><subject>Disease Progression</subject><subject>Genetic Predisposition to Disease</subject><subject>Humans</subject><subject>keratoacanthoma</subject><subject>Keratoacanthoma - diagnosis</subject><subject>Keratoacanthoma - etiology</subject><subject>Keratoacanthoma - genetics</subject><subject>Keratoacanthoma - metabolism</subject><subject>Keratoacanthoma - pathology</subject><subject>Neoplasm Proteins - genetics</subject><subject>Neoplasm Proteins - physiology</subject><subject>Neoplasms, Radiation-Induced - chemistry</subject><subject>Neoplasms, Radiation-Induced - diagnosis</subject><subject>Neoplasms, Radiation-Induced - genetics</subject><subject>Neoplasms, Radiation-Induced - pathology</subject><subject>paradoxical activation</subject><subject>Protein-Serine-Threonine Kinases - deficiency</subject><subject>Protein-Serine-Threonine Kinases - genetics</subject><subject>Protein-Serine-Threonine Kinases - physiology</subject><subject>Receptors, Transforming Growth Factor beta - deficiency</subject><subject>Receptors, Transforming Growth Factor beta - genetics</subject><subject>Receptors, Transforming Growth Factor beta - physiology</subject><subject>Signal Transduction</subject><subject>Skin Diseases - diagnosis</subject><subject>Skin Diseases - etiology</subject><subject>Skin Diseases - genetics</subject><subject>Skin Diseases - metabolism</subject><subject>Skin Diseases - pathology</subject><subject>Skin Neoplasms - diagnosis</subject><subject>squamous cell carcinoma</subject><subject>Sunlight - adverse effects</subject><subject>TGF β</subject><subject>TGFβ</subject><subject>Transforming Growth Factor beta - physiology</subject><subject>tumor</subject><subject>Ultraviolet Rays - adverse effects</subject><issn>0906-6705</issn><issn>1600-0625</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kD1PwzAQQC0EoqUw8AdQJRYY0t7Zid2wIFTagohgAdHNchxHBPJR4lS0_x6XtN245ZZ3T7pHyDnCAN0MzSoZIB2N4IB0kQN4wGlwSLoQAve4gKBDTqz9BEDBRHBMOpT7giPDLrl8MrVqKqVV2XxUhbrpq36S2SYrddM3ZZM169tTcpSq3Jqz7e6Rt-nkdfzgRS-zx_Fd5GkWjsDjSjHkVIOgQcpjDCkDlhqkXKsAkAoffIQkTsJExwIwFX6oBAAEjIe-EqxHrlrvoq6-l8Y2ssisNnmuSlMtrUTBwT3JwXfodYvqurK2Nqlc1Fmh6rVEkJsm0jWRf00ce7HVLuPCJHtyF8EBwxb4yXKz_t8kJ_P7ndJrL1wps9pfqPpL8k1i-f48kzilc4gwkhH7BSX9dqA</recordid><startdate>201602</startdate><enddate>201602</enddate><creator>Gleich, Tobias</creator><creator>Chiticariu, Elena</creator><creator>Huber, Marcel</creator><creator>Hohl, Daniel</creator><general>Blackwell Publishing Ltd</general><scope>BSCLL</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>201602</creationdate><title>Keratoacanthoma: a distinct entity?</title><author>Gleich, Tobias ; Chiticariu, Elena ; Huber, Marcel ; Hohl, Daniel</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3980-6aa3162c0725f6b192303fe126ca5012740410dbd9dcb701f749a700053694a73</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Carcinoma, Squamous Cell - diagnosis</topic><topic>Cell Transformation, Neoplastic - genetics</topic><topic>Cell Transformation, Neoplastic - radiation effects</topic><topic>Comparative Genomic Hybridization</topic><topic>Diagnosis, Differential</topic><topic>Disease Progression</topic><topic>Genetic Predisposition to Disease</topic><topic>Humans</topic><topic>keratoacanthoma</topic><topic>Keratoacanthoma - diagnosis</topic><topic>Keratoacanthoma - etiology</topic><topic>Keratoacanthoma - genetics</topic><topic>Keratoacanthoma - metabolism</topic><topic>Keratoacanthoma - pathology</topic><topic>Neoplasm Proteins - genetics</topic><topic>Neoplasm Proteins - physiology</topic><topic>Neoplasms, Radiation-Induced - chemistry</topic><topic>Neoplasms, Radiation-Induced - diagnosis</topic><topic>Neoplasms, Radiation-Induced - genetics</topic><topic>Neoplasms, Radiation-Induced - pathology</topic><topic>paradoxical activation</topic><topic>Protein-Serine-Threonine Kinases - deficiency</topic><topic>Protein-Serine-Threonine Kinases - genetics</topic><topic>Protein-Serine-Threonine Kinases - physiology</topic><topic>Receptors, Transforming Growth Factor beta - deficiency</topic><topic>Receptors, Transforming Growth Factor beta - genetics</topic><topic>Receptors, Transforming Growth Factor beta - physiology</topic><topic>Signal Transduction</topic><topic>Skin Diseases - diagnosis</topic><topic>Skin Diseases - etiology</topic><topic>Skin Diseases - genetics</topic><topic>Skin Diseases - metabolism</topic><topic>Skin Diseases - pathology</topic><topic>Skin Neoplasms - diagnosis</topic><topic>squamous cell carcinoma</topic><topic>Sunlight - adverse effects</topic><topic>TGF β</topic><topic>TGFβ</topic><topic>Transforming Growth Factor beta - physiology</topic><topic>tumor</topic><topic>Ultraviolet Rays - adverse effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Gleich, Tobias</creatorcontrib><creatorcontrib>Chiticariu, Elena</creatorcontrib><creatorcontrib>Huber, Marcel</creatorcontrib><creatorcontrib>Hohl, Daniel</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Experimental dermatology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Gleich, Tobias</au><au>Chiticariu, Elena</au><au>Huber, Marcel</au><au>Hohl, Daniel</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Keratoacanthoma: a distinct entity?</atitle><jtitle>Experimental dermatology</jtitle><addtitle>Exp Dermatol</addtitle><date>2016-02</date><risdate>2016</risdate><volume>25</volume><issue>2</issue><spage>85</spage><epage>91</epage><pages>85-91</pages><issn>0906-6705</issn><eissn>1600-0625</eissn><abstract>Keratoacanthoma (KA) are common but exceptional benign tumors, often appearing on sun‐exposed areas of light skinned people and showing spontaneous resolution. The goal of this study was to review existing literature, to point out the etiological complexity of KA biology and to answer the controversial debate if or not KA is a distinct entity or a variant of squamous cell carcinoma (SCC). Relying on recent results, we highlight that KA is an individual lesion with a unique molecular signature caused by alterations in the TGFβ signalling pathway. These recent findings will help to understand the nature of KA and to develop new reliable diagnostic tools, simplifying the discrimination of the histologically similar KA and SCC.</abstract><cop>Denmark</cop><pub>Blackwell Publishing Ltd</pub><pmid>26476131</pmid><doi>10.1111/exd.12880</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Carcinoma, Squamous Cell - diagnosis Cell Transformation, Neoplastic - genetics Cell Transformation, Neoplastic - radiation effects Comparative Genomic Hybridization Diagnosis, Differential Disease Progression Genetic Predisposition to Disease Humans keratoacanthoma Keratoacanthoma - diagnosis Keratoacanthoma - etiology Keratoacanthoma - genetics Keratoacanthoma - metabolism Keratoacanthoma - pathology Neoplasm Proteins - genetics Neoplasm Proteins - physiology Neoplasms, Radiation-Induced - chemistry Neoplasms, Radiation-Induced - diagnosis Neoplasms, Radiation-Induced - genetics Neoplasms, Radiation-Induced - pathology paradoxical activation Protein-Serine-Threonine Kinases - deficiency Protein-Serine-Threonine Kinases - genetics Protein-Serine-Threonine Kinases - physiology Receptors, Transforming Growth Factor beta - deficiency Receptors, Transforming Growth Factor beta - genetics Receptors, Transforming Growth Factor beta - physiology Signal Transduction Skin Diseases - diagnosis Skin Diseases - etiology Skin Diseases - genetics Skin Diseases - metabolism Skin Diseases - pathology Skin Neoplasms - diagnosis squamous cell carcinoma Sunlight - adverse effects TGF β TGFβ Transforming Growth Factor beta - physiology tumor Ultraviolet Rays - adverse effects |
title | Keratoacanthoma: a distinct entity? |
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