The neurofibromin 1 type I isoform predominance characterises female population affected by sporadic breast cancer: preliminary data

AimsNeurofibromin 1 (NF1) as a tumour suppressor gene can give rise to several transcripts by an alternative splicing event, generated at least for CELF cofactors. At present, the NF1 isoforms and CELF splicing transcripts in sporadic breast cancer are unknown. The aim of the authors was to detect N...

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Veröffentlicht in:Journal of clinical pathology 2012-05, Vol.65 (5), p.419-423
Hauptverfasser: Marrero, Daniel, Peralta, Raúl, Valdivia, Alejandra, De la Mora, Antonio, Romero, Pablo, Parra, Miriam, Mendoza, Nayeli, Mendoza, Monica, Rodriguez, Dalila, Camacho, Ernesto, Duarte, Armando, Castelazo, German, Vanegas, Enrique, Garcia, Israel, Vargas, Claudia, Arenas, Diego, Jimenez, Florinda, Salcedo, Mauricio
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container_end_page 423
container_issue 5
container_start_page 419
container_title Journal of clinical pathology
container_volume 65
creator Marrero, Daniel
Peralta, Raúl
Valdivia, Alejandra
De la Mora, Antonio
Romero, Pablo
Parra, Miriam
Mendoza, Nayeli
Mendoza, Monica
Rodriguez, Dalila
Camacho, Ernesto
Duarte, Armando
Castelazo, German
Vanegas, Enrique
Garcia, Israel
Vargas, Claudia
Arenas, Diego
Jimenez, Florinda
Salcedo, Mauricio
description AimsNeurofibromin 1 (NF1) as a tumour suppressor gene can give rise to several transcripts by an alternative splicing event, generated at least for CELF cofactors. At present, the NF1 isoforms and CELF splicing transcripts in sporadic breast cancer are unknown. The aim of the authors was to detect NF1 gene expression, the NF1 isoform ratio and the CELF transcripts present in sporadic breast cancer.MethodsNeurofibromin and RAS expression were analysed on tissue microarrays containing sporadic breast cancer (n=22), benign lesions (n=18, including six fibroadenomas, six fibrocystic changes and six ductal hyperplasias) and normal breast tissue (n=6) by immunohistochemistry assay. NF1 and CELF 3–6 RNA expression was performed by end point reverse transcription-PCR in the breast samples.ResultsNF1 and RAS expression in breast tissues showed no differential expression by immunohistochemistry results. Interestingly, the authors observed a shift transition in the isoform transcripts, from type II in normal breast tissue to type I isoform in breast carcinomas. CELF cofactor expression failed to be related with the shift transition of NF1 in breast tissues.ConclusionsThese data suggest that there is a tendency for an NF1 expression shift transition from type II to type I isoform, which could comprise a significant event in the development and progression of sporadic breast cancer. This shift transition may not be related with CELF cofactors.
doi_str_mv 10.1136/jclinpath-2011-200569
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At present, the NF1 isoforms and CELF splicing transcripts in sporadic breast cancer are unknown. The aim of the authors was to detect NF1 gene expression, the NF1 isoform ratio and the CELF transcripts present in sporadic breast cancer.MethodsNeurofibromin and RAS expression were analysed on tissue microarrays containing sporadic breast cancer (n=22), benign lesions (n=18, including six fibroadenomas, six fibrocystic changes and six ductal hyperplasias) and normal breast tissue (n=6) by immunohistochemistry assay. NF1 and CELF 3–6 RNA expression was performed by end point reverse transcription-PCR in the breast samples.ResultsNF1 and RAS expression in breast tissues showed no differential expression by immunohistochemistry results. Interestingly, the authors observed a shift transition in the isoform transcripts, from type II in normal breast tissue to type I isoform in breast carcinomas. CELF cofactor expression failed to be related with the shift transition of NF1 in breast tissues.ConclusionsThese data suggest that there is a tendency for an NF1 expression shift transition from type II to type I isoform, which could comprise a significant event in the development and progression of sporadic breast cancer. This shift transition may not be related with CELF cofactors.</description><identifier>ISSN: 0021-9746</identifier><identifier>EISSN: 1472-4146</identifier><identifier>DOI: 10.1136/jclinpath-2011-200569</identifier><identifier>PMID: 22412049</identifier><identifier>CODEN: JCPAAK</identifier><language>eng</language><publisher>London: BMJ Publishing Group Ltd and Association of Clinical Pathologists</publisher><subject>Aged ; Aged, 80 and over ; Biological and medical sciences ; breast cancer ; Breast Neoplasms - genetics ; Breast Neoplasms - metabolism ; Breast Neoplasms - pathology ; Carcinoma, Ductal, Breast - genetics ; Carcinoma, Ductal, Breast - metabolism ; Carcinoma, Ductal, Breast - pathology ; Carcinoma, Intraductal, Noninfiltrating - genetics ; Carcinoma, Intraductal, Noninfiltrating - metabolism ; Carcinoma, Intraductal, Noninfiltrating - pathology ; CCAAT-Enhancer-Binding Protein-delta - genetics ; CCAAT-Enhancer-Binding Protein-delta - metabolism ; CELFs ; Disease Progression ; expression ; Female ; Fibroadenoma - genetics ; Fibroadenoma - metabolism ; Fibroadenoma - pathology ; Fibrocystic Breast Disease - genetics ; Fibrocystic Breast Disease - metabolism ; Fibrocystic Breast Disease - pathology ; Gene Expression ; Gene Expression Profiling ; Genetic Predisposition to Disease ; Gynecology. Andrology. Obstetrics ; Humans ; Investigative techniques, diagnostic techniques (general aspects) ; isoforms ; Mammary gland diseases ; Medical sciences ; Middle Aged ; Neurofibromin 1 - genetics ; Neurofibromin 1 - metabolism ; NF1 ; Pathology. Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques ; Protein Isoforms ; Tissue Array Analysis ; Tumors ; Young Adult</subject><ispartof>Journal of clinical pathology, 2012-05, Vol.65 (5), p.419-423</ispartof><rights>2012, Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.</rights><rights>2015 INIST-CNRS</rights><rights>Copyright: 2012 (c) 2012, Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-b446t-5dcd9831e641d84c067e053b90e740521e99519eba11709dacddadde49e9987a3</citedby><cites>FETCH-LOGICAL-b446t-5dcd9831e641d84c067e053b90e740521e99519eba11709dacddadde49e9987a3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://jcp.bmj.com/content/65/5/419.full.pdf$$EPDF$$P50$$Gbmj$$H</linktopdf><linktohtml>$$Uhttps://jcp.bmj.com/content/65/5/419.full$$EHTML$$P50$$Gbmj$$H</linktohtml><link.rule.ids>114,115,314,780,784,3196,23571,27924,27925,77600,77631</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&amp;idt=26078831$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22412049$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Marrero, Daniel</creatorcontrib><creatorcontrib>Peralta, Raúl</creatorcontrib><creatorcontrib>Valdivia, Alejandra</creatorcontrib><creatorcontrib>De la Mora, Antonio</creatorcontrib><creatorcontrib>Romero, Pablo</creatorcontrib><creatorcontrib>Parra, Miriam</creatorcontrib><creatorcontrib>Mendoza, Nayeli</creatorcontrib><creatorcontrib>Mendoza, Monica</creatorcontrib><creatorcontrib>Rodriguez, Dalila</creatorcontrib><creatorcontrib>Camacho, Ernesto</creatorcontrib><creatorcontrib>Duarte, Armando</creatorcontrib><creatorcontrib>Castelazo, German</creatorcontrib><creatorcontrib>Vanegas, Enrique</creatorcontrib><creatorcontrib>Garcia, Israel</creatorcontrib><creatorcontrib>Vargas, Claudia</creatorcontrib><creatorcontrib>Arenas, Diego</creatorcontrib><creatorcontrib>Jimenez, Florinda</creatorcontrib><creatorcontrib>Salcedo, Mauricio</creatorcontrib><title>The neurofibromin 1 type I isoform predominance characterises female population affected by sporadic breast cancer: preliminary data</title><title>Journal of clinical pathology</title><addtitle>J Clin Pathol</addtitle><description>AimsNeurofibromin 1 (NF1) as a tumour suppressor gene can give rise to several transcripts by an alternative splicing event, generated at least for CELF cofactors. At present, the NF1 isoforms and CELF splicing transcripts in sporadic breast cancer are unknown. The aim of the authors was to detect NF1 gene expression, the NF1 isoform ratio and the CELF transcripts present in sporadic breast cancer.MethodsNeurofibromin and RAS expression were analysed on tissue microarrays containing sporadic breast cancer (n=22), benign lesions (n=18, including six fibroadenomas, six fibrocystic changes and six ductal hyperplasias) and normal breast tissue (n=6) by immunohistochemistry assay. NF1 and CELF 3–6 RNA expression was performed by end point reverse transcription-PCR in the breast samples.ResultsNF1 and RAS expression in breast tissues showed no differential expression by immunohistochemistry results. Interestingly, the authors observed a shift transition in the isoform transcripts, from type II in normal breast tissue to type I isoform in breast carcinomas. CELF cofactor expression failed to be related with the shift transition of NF1 in breast tissues.ConclusionsThese data suggest that there is a tendency for an NF1 expression shift transition from type II to type I isoform, which could comprise a significant event in the development and progression of sporadic breast cancer. This shift transition may not be related with CELF cofactors.</description><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Biological and medical sciences</subject><subject>breast cancer</subject><subject>Breast Neoplasms - genetics</subject><subject>Breast Neoplasms - metabolism</subject><subject>Breast Neoplasms - pathology</subject><subject>Carcinoma, Ductal, Breast - genetics</subject><subject>Carcinoma, Ductal, Breast - metabolism</subject><subject>Carcinoma, Ductal, Breast - pathology</subject><subject>Carcinoma, Intraductal, Noninfiltrating - genetics</subject><subject>Carcinoma, Intraductal, Noninfiltrating - metabolism</subject><subject>Carcinoma, Intraductal, Noninfiltrating - pathology</subject><subject>CCAAT-Enhancer-Binding Protein-delta - genetics</subject><subject>CCAAT-Enhancer-Binding Protein-delta - metabolism</subject><subject>CELFs</subject><subject>Disease Progression</subject><subject>expression</subject><subject>Female</subject><subject>Fibroadenoma - genetics</subject><subject>Fibroadenoma - metabolism</subject><subject>Fibroadenoma - pathology</subject><subject>Fibrocystic Breast Disease - genetics</subject><subject>Fibrocystic Breast Disease - metabolism</subject><subject>Fibrocystic Breast Disease - pathology</subject><subject>Gene Expression</subject><subject>Gene Expression Profiling</subject><subject>Genetic Predisposition to Disease</subject><subject>Gynecology. Andrology. Obstetrics</subject><subject>Humans</subject><subject>Investigative techniques, diagnostic techniques (general aspects)</subject><subject>isoforms</subject><subject>Mammary gland diseases</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Neurofibromin 1 - genetics</subject><subject>Neurofibromin 1 - metabolism</subject><subject>NF1</subject><subject>Pathology. Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques</subject><subject>Protein Isoforms</subject><subject>Tissue Array Analysis</subject><subject>Tumors</subject><subject>Young Adult</subject><issn>0021-9746</issn><issn>1472-4146</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqNkb2O1DAURi0EYoeFRwBZQkg0Ad_EiWM6dpafFSMoWLa1HPtG4yGJg51ITM-D4yjDIFHR2MV37pF9P0KeAnsFUFSvD6Zzw6infZYzgHSwspL3yAa4yDMOvLpPNozlkEnBqwvyKMYDY1AIKB6SizznkDMuN-TX7R7pgHPwrWuC791AgU7HEekNddG3PvR0DGiXRA8GqdnroM2EwUWMtMVed0hHP86dnpwfqG5bTLGlzZHG0QdtnaFNQB0nahZDeLMIO7cIw5FaPenH5EGru4hPTvcl-fb-3e32Y7b78uFm-3aXNZxXU1ZaY2VdAFYcbM0NqwSysmgkQ8FZmQNKWYLERgMIJq021mprkcsU1EIXl-Tl6h2D_zFjnFTvosGu0wP6OSpgTJZFXQqR0Of_oAc_hyG9ToGogfHE5okqV8oEH2PAVo3B9elbSaWWmtS5JrXUpNaa0tyzk31uerTnqT-9JODFCdDR6K4NaXMu_uUqJuq0icRlK-fihD_PuQ7fVSUKUarPd1vFr652Xz9dX6u7xLOVb_rDf771NzZ_vcE</recordid><startdate>20120501</startdate><enddate>20120501</enddate><creator>Marrero, Daniel</creator><creator>Peralta, Raúl</creator><creator>Valdivia, Alejandra</creator><creator>De la Mora, Antonio</creator><creator>Romero, Pablo</creator><creator>Parra, Miriam</creator><creator>Mendoza, Nayeli</creator><creator>Mendoza, Monica</creator><creator>Rodriguez, Dalila</creator><creator>Camacho, Ernesto</creator><creator>Duarte, Armando</creator><creator>Castelazo, German</creator><creator>Vanegas, Enrique</creator><creator>Garcia, Israel</creator><creator>Vargas, Claudia</creator><creator>Arenas, Diego</creator><creator>Jimenez, Florinda</creator><creator>Salcedo, Mauricio</creator><general>BMJ Publishing Group Ltd and Association of Clinical Pathologists</general><general>BMJ Publishing Group</general><general>BMJ Publishing Group LTD</general><scope>BSCLL</scope><scope>IQODW</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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</scope><scope>8AF</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>BTHHO</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope></search><sort><creationdate>20120501</creationdate><title>The neurofibromin 1 type I isoform predominance characterises female population affected by sporadic breast cancer: preliminary data</title><author>Marrero, Daniel ; Peralta, Raúl ; Valdivia, Alejandra ; De la Mora, Antonio ; Romero, Pablo ; Parra, Miriam ; Mendoza, Nayeli ; Mendoza, Monica ; Rodriguez, Dalila ; Camacho, Ernesto ; Duarte, Armando ; Castelazo, German ; Vanegas, Enrique ; Garcia, Israel ; Vargas, Claudia ; Arenas, Diego ; Jimenez, Florinda ; Salcedo, Mauricio</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b446t-5dcd9831e641d84c067e053b90e740521e99519eba11709dacddadde49e9987a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Biological and medical sciences</topic><topic>breast cancer</topic><topic>Breast Neoplasms - genetics</topic><topic>Breast Neoplasms - metabolism</topic><topic>Breast Neoplasms - pathology</topic><topic>Carcinoma, Ductal, Breast - genetics</topic><topic>Carcinoma, Ductal, Breast - metabolism</topic><topic>Carcinoma, Ductal, Breast - pathology</topic><topic>Carcinoma, Intraductal, Noninfiltrating - genetics</topic><topic>Carcinoma, Intraductal, Noninfiltrating - metabolism</topic><topic>Carcinoma, Intraductal, Noninfiltrating - pathology</topic><topic>CCAAT-Enhancer-Binding Protein-delta - genetics</topic><topic>CCAAT-Enhancer-Binding Protein-delta - metabolism</topic><topic>CELFs</topic><topic>Disease Progression</topic><topic>expression</topic><topic>Female</topic><topic>Fibroadenoma - genetics</topic><topic>Fibroadenoma - metabolism</topic><topic>Fibroadenoma - pathology</topic><topic>Fibrocystic Breast Disease - genetics</topic><topic>Fibrocystic Breast Disease - metabolism</topic><topic>Fibrocystic Breast Disease - pathology</topic><topic>Gene Expression</topic><topic>Gene Expression Profiling</topic><topic>Genetic Predisposition to Disease</topic><topic>Gynecology. Andrology. Obstetrics</topic><topic>Humans</topic><topic>Investigative techniques, diagnostic techniques (general aspects)</topic><topic>isoforms</topic><topic>Mammary gland diseases</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Neurofibromin 1 - genetics</topic><topic>Neurofibromin 1 - metabolism</topic><topic>NF1</topic><topic>Pathology. Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques</topic><topic>Protein Isoforms</topic><topic>Tissue Array Analysis</topic><topic>Tumors</topic><topic>Young Adult</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Marrero, Daniel</creatorcontrib><creatorcontrib>Peralta, Raúl</creatorcontrib><creatorcontrib>Valdivia, Alejandra</creatorcontrib><creatorcontrib>De la Mora, Antonio</creatorcontrib><creatorcontrib>Romero, Pablo</creatorcontrib><creatorcontrib>Parra, Miriam</creatorcontrib><creatorcontrib>Mendoza, Nayeli</creatorcontrib><creatorcontrib>Mendoza, Monica</creatorcontrib><creatorcontrib>Rodriguez, Dalila</creatorcontrib><creatorcontrib>Camacho, Ernesto</creatorcontrib><creatorcontrib>Duarte, Armando</creatorcontrib><creatorcontrib>Castelazo, German</creatorcontrib><creatorcontrib>Vanegas, Enrique</creatorcontrib><creatorcontrib>Garcia, Israel</creatorcontrib><creatorcontrib>Vargas, Claudia</creatorcontrib><creatorcontrib>Arenas, Diego</creatorcontrib><creatorcontrib>Jimenez, Florinda</creatorcontrib><creatorcontrib>Salcedo, Mauricio</creatorcontrib><collection>Istex</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>ProQuest_Health &amp; Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>STEM Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>BMJ Journals</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health &amp; Medical Complete (Alumni)</collection><collection>Health &amp; Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</collection><collection>ProQuest Science Journals</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of clinical pathology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Marrero, Daniel</au><au>Peralta, Raúl</au><au>Valdivia, Alejandra</au><au>De la Mora, Antonio</au><au>Romero, Pablo</au><au>Parra, Miriam</au><au>Mendoza, Nayeli</au><au>Mendoza, Monica</au><au>Rodriguez, Dalila</au><au>Camacho, Ernesto</au><au>Duarte, Armando</au><au>Castelazo, German</au><au>Vanegas, Enrique</au><au>Garcia, Israel</au><au>Vargas, Claudia</au><au>Arenas, Diego</au><au>Jimenez, Florinda</au><au>Salcedo, Mauricio</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The neurofibromin 1 type I isoform predominance characterises female population affected by sporadic breast cancer: preliminary data</atitle><jtitle>Journal of clinical pathology</jtitle><addtitle>J Clin Pathol</addtitle><date>2012-05-01</date><risdate>2012</risdate><volume>65</volume><issue>5</issue><spage>419</spage><epage>423</epage><pages>419-423</pages><issn>0021-9746</issn><eissn>1472-4146</eissn><coden>JCPAAK</coden><abstract>AimsNeurofibromin 1 (NF1) as a tumour suppressor gene can give rise to several transcripts by an alternative splicing event, generated at least for CELF cofactors. At present, the NF1 isoforms and CELF splicing transcripts in sporadic breast cancer are unknown. The aim of the authors was to detect NF1 gene expression, the NF1 isoform ratio and the CELF transcripts present in sporadic breast cancer.MethodsNeurofibromin and RAS expression were analysed on tissue microarrays containing sporadic breast cancer (n=22), benign lesions (n=18, including six fibroadenomas, six fibrocystic changes and six ductal hyperplasias) and normal breast tissue (n=6) by immunohistochemistry assay. NF1 and CELF 3–6 RNA expression was performed by end point reverse transcription-PCR in the breast samples.ResultsNF1 and RAS expression in breast tissues showed no differential expression by immunohistochemistry results. Interestingly, the authors observed a shift transition in the isoform transcripts, from type II in normal breast tissue to type I isoform in breast carcinomas. CELF cofactor expression failed to be related with the shift transition of NF1 in breast tissues.ConclusionsThese data suggest that there is a tendency for an NF1 expression shift transition from type II to type I isoform, which could comprise a significant event in the development and progression of sporadic breast cancer. This shift transition may not be related with CELF cofactors.</abstract><cop>London</cop><pub>BMJ Publishing Group Ltd and Association of Clinical Pathologists</pub><pmid>22412049</pmid><doi>10.1136/jclinpath-2011-200569</doi><tpages>5</tpages></addata></record>
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subjects Aged
Aged, 80 and over
Biological and medical sciences
breast cancer
Breast Neoplasms - genetics
Breast Neoplasms - metabolism
Breast Neoplasms - pathology
Carcinoma, Ductal, Breast - genetics
Carcinoma, Ductal, Breast - metabolism
Carcinoma, Ductal, Breast - pathology
Carcinoma, Intraductal, Noninfiltrating - genetics
Carcinoma, Intraductal, Noninfiltrating - metabolism
Carcinoma, Intraductal, Noninfiltrating - pathology
CCAAT-Enhancer-Binding Protein-delta - genetics
CCAAT-Enhancer-Binding Protein-delta - metabolism
CELFs
Disease Progression
expression
Female
Fibroadenoma - genetics
Fibroadenoma - metabolism
Fibroadenoma - pathology
Fibrocystic Breast Disease - genetics
Fibrocystic Breast Disease - metabolism
Fibrocystic Breast Disease - pathology
Gene Expression
Gene Expression Profiling
Genetic Predisposition to Disease
Gynecology. Andrology. Obstetrics
Humans
Investigative techniques, diagnostic techniques (general aspects)
isoforms
Mammary gland diseases
Medical sciences
Middle Aged
Neurofibromin 1 - genetics
Neurofibromin 1 - metabolism
NF1
Pathology. Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques
Protein Isoforms
Tissue Array Analysis
Tumors
Young Adult
title The neurofibromin 1 type I isoform predominance characterises female population affected by sporadic breast cancer: preliminary data
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