Hidradenocarcinoma: Criteria for Malignancy and Hypothesis of an Apoeccrine Origin
Identifieur interne : 000985 ( Istex/Corpus ); précédent : 000984; suivant : 000986Hidradenocarcinoma: Criteria for Malignancy and Hypothesis of an Apoeccrine Origin
Auteurs : C. Ko ; F. Luo ; A. Cochran ; S. BinderSource :
- Journal of Cutaneous Pathology [ 0303-6987 ] ; 2005-01.
Abstract
The immunohistochemical profile of hidradenocarcinoma, defined here as the malignant counterpart of hidradenoma, has not been well characterised. We evaluated the staining pattern of six cases of hidradenocarcinoma using antibodies to gross cystic disease fluid protein‐15 (GCDFP‐15), carcino‐embryonic antigen (CEA), epithelial membrane antigen (EMA), S‐100 protein, keratin AE1/3, cytokeratin 5/6, p53, bcl‐1, bcl‐2, and Ki67. All tumours were poorly circumscribed with clefting between tumour and stroma, evidence of poroid cells and cuticular cells, decapitation secretion, and increased mitoses with cords of tumour infiltrating through the adjacent desmoplastic stroma. The tumours stained with antibodies to CEA, S‐100 protein, GCDFP‐15, and EMA in no consistent pattern. All tumours studied stained positively for keratin AE1/3 and cytokeratin 5/6. Ki67 and p53 staining were strongly positive in 5 of 6 tumours. Bcl‐1 and bcl‐2 staining were variable. Our study demonstrates that hidradenocarcinomas may have both apocrine and eccrine features within the same tumour and suggests that it may be most accurate to consider that these tumours originate from apoeccrine structures or stem cells with the capacity for pluripotential differentiation.
Url:
DOI: 10.1111/j.0303-6987.2005.320dr.x
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Ko</name><affiliation><mods:affiliation>Department of Pathology, University of California, Los Angeles, Los Angeles, CA, USA</mods:affiliation></affiliation></author><author><name sortKey="Luo, F" sort="Luo, F" uniqKey="Luo F" first="F." last="Luo">F. Luo</name><affiliation><mods:affiliation>Department of Pathology, University of California, Los Angeles, Los Angeles, CA, USA</mods:affiliation></affiliation></author><author><name sortKey="Cochran, A" sort="Cochran, A" uniqKey="Cochran A" first="A." last="Cochran">A. Cochran</name><affiliation><mods:affiliation>Department of Pathology, University of California, Los Angeles, Los Angeles, CA, USA</mods:affiliation></affiliation></author><author><name sortKey="Binder, S" sort="Binder, S" uniqKey="Binder S" first="S." last="Binder">S. Binder</name><affiliation><mods:affiliation>Department of Pathology, University of California, Los Angeles, Los Angeles, CA, USA</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j" type="main">Journal of Cutaneous Pathology</title><title level="j" type="alt">JOURNAL OF CUTANEOUS PATHOLOGY</title><idno type="ISSN">0303-6987</idno><idno type="eISSN">1600-0560</idno><imprint><biblScope unit="vol">32</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="98">98</biblScope><biblScope unit="page" to="98">98</biblScope><biblScope unit="page-count">1</biblScope><publisher>Blackwell Publishing Ltd/Inc.</publisher><pubPlace>Oxford, UK; Malden, USA</pubPlace><date type="published" when="2005-01">2005-01</date></imprint><idno type="ISSN">0303-6987</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0303-6987</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The immunohistochemical profile of hidradenocarcinoma, defined here as the malignant counterpart of hidradenoma, has not been well characterised. We evaluated the staining pattern of six cases of hidradenocarcinoma using antibodies to gross cystic disease fluid protein‐15 (GCDFP‐15), carcino‐embryonic antigen (CEA), epithelial membrane antigen (EMA), S‐100 protein, keratin AE1/3, cytokeratin 5/6, p53, bcl‐1, bcl‐2, and Ki67. All tumours were poorly circumscribed with clefting between tumour and stroma, evidence of poroid cells and cuticular cells, decapitation secretion, and increased mitoses with cords of tumour infiltrating through the adjacent desmoplastic stroma. The tumours stained with antibodies to CEA, S‐100 protein, GCDFP‐15, and EMA in no consistent pattern. All tumours studied stained positively for keratin AE1/3 and cytokeratin 5/6. Ki67 and p53 staining were strongly positive in 5 of 6 tumours. Bcl‐1 and bcl‐2 staining were variable. Our study demonstrates that hidradenocarcinomas may have both apocrine and eccrine features within the same tumour and suggests that it may be most accurate to consider that these tumours originate from apoeccrine structures or stem cells with the capacity for pluripotential 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Ko</name><affiliations><json:string>Department of Pathology, University of California, Los Angeles, Los Angeles, CA, USA</json:string></affiliations></json:item><json:item><name>F. Luo</name><affiliations><json:string>Department of Pathology, University of California, Los Angeles, Los Angeles, CA, USA</json:string></affiliations></json:item><json:item><name>A. Cochran</name><affiliations><json:string>Department of Pathology, University of California, Los Angeles, Los Angeles, CA, USA</json:string></affiliations></json:item><json:item><name>S. Binder</name><affiliations><json:string>Department of Pathology, University of California, Los Angeles, Los Angeles, CA, USA</json:string></affiliations></json:item></author><articleId><json:string>CUP320DR</json:string></articleId><language><json:string>eng</json:string></language><originalGenre><json:string>abstract</json:string></originalGenre><abstract>The immunohistochemical profile of hidradenocarcinoma, defined here as the malignant counterpart of hidradenoma, has not been well characterised. We evaluated the staining pattern of six cases of hidradenocarcinoma using antibodies to gross cystic disease fluid protein‐15 (GCDFP‐15), carcino‐embryonic antigen (CEA), epithelial membrane antigen (EMA), S‐100 protein, keratin AE1/3, cytokeratin 5/6, p53, bcl‐1, bcl‐2, and Ki67. All tumours were poorly circumscribed with clefting between tumour and stroma, evidence of poroid cells and cuticular cells, decapitation secretion, and increased mitoses with cords of tumour infiltrating through the adjacent desmoplastic stroma. The tumours stained with antibodies to CEA, S‐100 protein, GCDFP‐15, and EMA in no consistent pattern. All tumours studied stained positively for keratin AE1/3 and cytokeratin 5/6. Ki67 and p53 staining were strongly positive in 5 of 6 tumours. Bcl‐1 and bcl‐2 staining were variable. Our study demonstrates that hidradenocarcinomas may have both apocrine and eccrine features within the same tumour and suggests that it may be most accurate to consider that these tumours originate from apoeccrine structures or stem cells with the capacity for pluripotential differentiation.</abstract><qualityIndicators><score>7.1</score><pdfVersion>1.3</pdfVersion><pdfPageSize>595 x 782 pts</pdfPageSize><refBibsNative>false</refBibsNative><abstractCharCount>1253</abstractCharCount><pdfWordCount>46669</pdfWordCount><pdfCharCount>312307</pdfCharCount><pdfPageCount>53</pdfPageCount><abstractWordCount>175</abstractWordCount></qualityIndicators><title>Hidradenocarcinoma: Criteria for Malignancy and Hypothesis of an Apoeccrine Origin</title><genre><json:string>abstract</json:string></genre><host><title>Journal of Cutaneous Pathology</title><language><json:string>unknown</json:string></language><doi><json:string>10.1111/(ISSN)1600-0560</json:string></doi><issn><json:string>0303-6987</json:string></issn><eissn><json:string>1600-0560</json:string></eissn><publisherId><json:string>CUP</json:string></publisherId><volume>32</volume><issue>1</issue><pages><first>98</first><last>98</last><total>1</total></pages><genre><json:string>journal</json:string></genre></host><categories><wos><json:string>science</json:string><json:string>pathology</json:string><json:string>dermatology</json:string></wos><scienceMetrix><json:string>health sciences</json:string><json:string>clinical medicine</json:string><json:string>dermatology & venereal diseases</json:string></scienceMetrix><inist><json:string>sciences appliquees, technologies et medecines</json:string><json:string>sciences biologiques et medicales</json:string><json:string>sciences medicales</json:string><json:string>dermatologie</json:string></inist></categories><publicationDate>2005</publicationDate><copyrightDate>2005</copyrightDate><doi><json:string>10.1111/j.0303-6987.2005.320dr.x</json:string></doi><id>1511BD1AA122799F1A375CF6CBD4507113BA322D</id><score>1</score><fulltext><json:item><extension>pdf</extension><original>true</original><mimetype>application/pdf</mimetype><uri>https://api.istex.fr/document/1511BD1AA122799F1A375CF6CBD4507113BA322D/fulltext/pdf</uri></json:item><json:item><extension>zip</extension><original>false</original><mimetype>application/zip</mimetype><uri>https://api.istex.fr/document/1511BD1AA122799F1A375CF6CBD4507113BA322D/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/1511BD1AA122799F1A375CF6CBD4507113BA322D/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main">Hidradenocarcinoma: Criteria for Malignancy and Hypothesis of an Apoeccrine Origin</title></titleStmt><publicationStmt><publisher>Blackwell Publishing Ltd/Inc.</publisher><pubPlace>Oxford, UK; 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We evaluated the staining pattern of six cases of hidradenocarcinoma using antibodies to gross cystic disease fluid protein‐15 (GCDFP‐15), carcino‐embryonic antigen (CEA), epithelial membrane antigen (EMA), S‐100 protein, keratin AE1/3, cytokeratin 5/6, p53, bcl‐1, bcl‐2, and Ki67. All tumours were poorly circumscribed with clefting between tumour and stroma, evidence of poroid cells and cuticular cells, decapitation secretion, and increased mitoses with cords of tumour infiltrating through the adjacent desmoplastic stroma. The tumours stained with antibodies to CEA, S‐100 protein, GCDFP‐15, and EMA in no consistent pattern. All tumours studied stained positively for keratin AE1/3 and cytokeratin 5/6. Ki67 and p53 staining were strongly positive in 5 of 6 tumours. Bcl‐1 and bcl‐2 staining were variable. Our study demonstrates that hidradenocarcinomas may have both apocrine and eccrine features within the same tumour and suggests that it may be most accurate to consider that these tumours originate from apoeccrine structures or stem cells with the capacity for pluripotential differentiation.</abstract><relatedItem type="host"><titleInfo><title>Journal of Cutaneous Pathology</title></titleInfo><genre type="journal">journal</genre><identifier type="ISSN">0303-6987</identifier><identifier type="eISSN">1600-0560</identifier><identifier type="DOI">10.1111/(ISSN)1600-0560</identifier><identifier type="PublisherID">CUP</identifier><part><date>2005</date><detail type="volume"><caption>vol.</caption><number>32</number></detail><detail type="issue"><caption>no.</caption><number>1</number></detail><extent unit="pages"><start>98</start><end>98</end><total>1</total></extent></part></relatedItem><identifier type="istex">1511BD1AA122799F1A375CF6CBD4507113BA322D</identifier><identifier type="DOI">10.1111/j.0303-6987.2005.320dr.x</identifier><identifier type="ArticleID">CUP320DR</identifier><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Blackwell Publishing Ltd/Inc.</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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