Tyrosine kinase discoidin domain receptors DDR1 and DDR2 are coordinately deregulated in triple-negative breast cancer
Receptor kinases Discoidin Domain Receptors (DDRs) 1 and 2 are emerging as new therapeutic targets in breast cancer (BC). However, the expression of DDR proteins during BC progression and their association with BC subtypes remain poorly defined. Herein we report the first comprehensive immunohistoch...
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| creator | Toy, Kathy A. Valiathan, Rajeshwari R. Núñez, Fernando Kidwell, Kelley M. Gonzalez, Maria E. Fridman, Rafael Kleer, Celina G. |
| description | Receptor kinases Discoidin Domain Receptors (DDRs) 1 and 2 are emerging as new therapeutic targets in breast cancer (BC). However, the expression of DDR proteins during BC progression and their association with BC subtypes remain poorly defined. Herein we report the first comprehensive immunohistochemical analyses of DDR protein expression in a wide range of breast tissues. DDR1 and DDR2 expression was investigated by immunohistochemistry in 218 samples of normal breast (
n
= 10), ductal carcinoma in situ (DCIS,
n
= 10), and invasive carcinomas (
n
= 198), arrayed in tissue microarrays with comprehensive clinical and follow-up information. Staining was evaluated for cell type, subcellular localization, percentage and intensity (scores 1–4), and association with disease subtype and outcome. In normal epithelium and DCIS, DDR1 was highly expressed, while DDR2 was negative in normal epithelium, and in DCIS it localized to cells at the epithelial-stromal interface. Of the 198 invasive carcinomas, DDR1 was high in 87 (44 %) and low in 103 (52 %), and DDR2 was high in 110 (56 %) and low in 87 (44 %). High DDR2 was associated with high tumor grade (
P
= 0.002), triple-negative subtype (TNBC) (
P
|
| doi_str_mv | 10.1007/s10549-015-3285-7 |
| format | Article |
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n
= 10), ductal carcinoma in situ (DCIS,
n
= 10), and invasive carcinomas (
n
= 198), arrayed in tissue microarrays with comprehensive clinical and follow-up information. Staining was evaluated for cell type, subcellular localization, percentage and intensity (scores 1–4), and association with disease subtype and outcome. In normal epithelium and DCIS, DDR1 was highly expressed, while DDR2 was negative in normal epithelium, and in DCIS it localized to cells at the epithelial-stromal interface. Of the 198 invasive carcinomas, DDR1 was high in 87 (44 %) and low in 103 (52 %), and DDR2 was high in 110 (56 %) and low in 87 (44 %). High DDR2 was associated with high tumor grade (
P
= 0.002), triple-negative subtype (TNBC) (
P
< 0.0001), and worse survival (
P
= 0.037). We discovered a novel concordant deregulation of DDR expression, with a DDR1
Low
/DDR2
High
profile significantly associated with TNBC, compared to luminal tumors (
P
= 0.012), and with worse overall survival. In conclusion, DDR2 upregulation occurs in DCIS, before stromal invasion, and may reflect epithelial-stromal cross-talk. A DDR1
Low
/DDR2
High
protein profile is associated with TNBC and may identify invasive carcinomas with worse prognosis.</description><identifier>ISSN: 0167-6806</identifier><identifier>EISSN: 1573-7217</identifier><identifier>DOI: 10.1007/s10549-015-3285-7</identifier><identifier>PMID: 25667101</identifier><identifier>CODEN: BCTRD6</identifier><language>eng</language><publisher>Boston: Springer US</publisher><subject>Adult ; Aged ; Aged, 80 and over ; Analysis ; Breast cancer ; Cancer research ; Cancer therapies ; Carcinoma, Ductal, Breast - genetics ; Carcinoma, Ductal, Breast - metabolism ; Carcinoma, Ductal, Breast - pathology ; Clinical outcomes ; Combined Modality Therapy ; Computer memory ; Discoidin Domain Receptors ; Female ; Gene Expression ; Health aspects ; Humans ; Immunohistochemistry ; Kaplan-Meier Estimate ; Kinases ; Medicine ; Medicine & Public Health ; Middle Aged ; Neoplasm Grading ; Neoplasm Invasiveness ; Oncology ; Preclinical Study ; Prognosis ; Protein Binding ; Proteins ; Receptor Protein-Tyrosine Kinases - genetics ; Receptor Protein-Tyrosine Kinases - metabolism ; Receptors, Mitogen - genetics ; Receptors, Mitogen - metabolism ; Risk Factors ; Triple Negative Breast Neoplasms - genetics ; Triple Negative Breast Neoplasms - metabolism ; Triple Negative Breast Neoplasms - mortality ; Triple Negative Breast Neoplasms - pathology ; Triple Negative Breast Neoplasms - therapy ; Tumor Burden ; Tyrosine</subject><ispartof>Breast cancer research and treatment, 2015-02, Vol.150 (1), p.9-18</ispartof><rights>Springer Science+Business Media New York 2015</rights><rights>COPYRIGHT 2015 Springer</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c638t-58322ca1f41e381a626c4610738356884f5f24852ee7e65139d7b17aaa4433223</citedby><cites>FETCH-LOGICAL-c638t-58322ca1f41e381a626c4610738356884f5f24852ee7e65139d7b17aaa4433223</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s10549-015-3285-7$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s10549-015-3285-7$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>230,314,776,780,881,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25667101$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Toy, Kathy A.</creatorcontrib><creatorcontrib>Valiathan, Rajeshwari R.</creatorcontrib><creatorcontrib>Núñez, Fernando</creatorcontrib><creatorcontrib>Kidwell, Kelley M.</creatorcontrib><creatorcontrib>Gonzalez, Maria E.</creatorcontrib><creatorcontrib>Fridman, Rafael</creatorcontrib><creatorcontrib>Kleer, Celina G.</creatorcontrib><title>Tyrosine kinase discoidin domain receptors DDR1 and DDR2 are coordinately deregulated in triple-negative breast cancer</title><title>Breast cancer research and treatment</title><addtitle>Breast Cancer Res Treat</addtitle><addtitle>Breast Cancer Res Treat</addtitle><description>Receptor kinases Discoidin Domain Receptors (DDRs) 1 and 2 are emerging as new therapeutic targets in breast cancer (BC). However, the expression of DDR proteins during BC progression and their association with BC subtypes remain poorly defined. Herein we report the first comprehensive immunohistochemical analyses of DDR protein expression in a wide range of breast tissues. DDR1 and DDR2 expression was investigated by immunohistochemistry in 218 samples of normal breast (
n
= 10), ductal carcinoma in situ (DCIS,
n
= 10), and invasive carcinomas (
n
= 198), arrayed in tissue microarrays with comprehensive clinical and follow-up information. Staining was evaluated for cell type, subcellular localization, percentage and intensity (scores 1–4), and association with disease subtype and outcome. In normal epithelium and DCIS, DDR1 was highly expressed, while DDR2 was negative in normal epithelium, and in DCIS it localized to cells at the epithelial-stromal interface. Of the 198 invasive carcinomas, DDR1 was high in 87 (44 %) and low in 103 (52 %), and DDR2 was high in 110 (56 %) and low in 87 (44 %). High DDR2 was associated with high tumor grade (
P
= 0.002), triple-negative subtype (TNBC) (
P
< 0.0001), and worse survival (
P
= 0.037). We discovered a novel concordant deregulation of DDR expression, with a DDR1
Low
/DDR2
High
profile significantly associated with TNBC, compared to luminal tumors (
P
= 0.012), and with worse overall survival. In conclusion, DDR2 upregulation occurs in DCIS, before stromal invasion, and may reflect epithelial-stromal cross-talk. A DDR1
Low
/DDR2
High
protein profile is associated with TNBC and may identify invasive carcinomas with worse prognosis.</description><subject>Adult</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Analysis</subject><subject>Breast cancer</subject><subject>Cancer research</subject><subject>Cancer therapies</subject><subject>Carcinoma, Ductal, Breast - genetics</subject><subject>Carcinoma, Ductal, Breast - metabolism</subject><subject>Carcinoma, Ductal, Breast - pathology</subject><subject>Clinical outcomes</subject><subject>Combined Modality Therapy</subject><subject>Computer memory</subject><subject>Discoidin Domain Receptors</subject><subject>Female</subject><subject>Gene Expression</subject><subject>Health aspects</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>Kaplan-Meier Estimate</subject><subject>Kinases</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Middle Aged</subject><subject>Neoplasm Grading</subject><subject>Neoplasm Invasiveness</subject><subject>Oncology</subject><subject>Preclinical Study</subject><subject>Prognosis</subject><subject>Protein Binding</subject><subject>Proteins</subject><subject>Receptor Protein-Tyrosine Kinases - genetics</subject><subject>Receptor Protein-Tyrosine Kinases - metabolism</subject><subject>Receptors, Mitogen - genetics</subject><subject>Receptors, Mitogen - metabolism</subject><subject>Risk Factors</subject><subject>Triple Negative Breast Neoplasms - genetics</subject><subject>Triple Negative Breast Neoplasms - metabolism</subject><subject>Triple Negative Breast Neoplasms - mortality</subject><subject>Triple Negative Breast Neoplasms - pathology</subject><subject>Triple Negative Breast Neoplasms - therapy</subject><subject>Tumor Burden</subject><subject>Tyrosine</subject><issn>0167-6806</issn><issn>1573-7217</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNp1kl1rFDEUhoModrv6A7yRgCDeTE0yk2TmRiitVaEgSL0O2cyZ2dSZZE1mFvbfe5atdVc0gXyd5z0hJy8hrzi74Izp95kzWTUF47IoRS0L_YQsuNRloQXXT8mCcaULVTN1Rs5zvmeMNZo1z8mZkEppzviCbO92KWYfgP7wwWagrc8u-tYH2sbR4pTAwWaKKdPr62-c2tDuF4LaBNTFmBC1Eww72kKCfh5w01LUTclvBigC9HbyW6CrBDZP1NngIL0gzzo7ZHj5MC_J95uPd1efi9uvn75cXd4WTpX1VMi6FMJZ3lUcyppbJZSrFGe6rEup6rrqZCeqWgoADUrysmn1imtrbVWVKC2X5MMh72ZejdA6CFOyg9kkP9q0M9F6cxoJfm36uDWS4d3YluTdQ4IUf86QJzNigWAYbIA4Z8OVYkzUQjWIvvkLvY9zCvg8pJpGMIHDH6q3Axgfuoj3un1Sc1mJRjHBNEPq4h8U9hZG72KAzuP5ieDtkWANdpjWOQ7z5GPIpyA_gA7_PSfoHovBmdm7yhxcZdBVZu8qo1Hz-riKj4rfNkJAHICModBDOnr6f7P-AtXX1Rk</recordid><startdate>20150201</startdate><enddate>20150201</enddate><creator>Toy, Kathy A.</creator><creator>Valiathan, Rajeshwari R.</creator><creator>Núñez, Fernando</creator><creator>Kidwell, Kelley M.</creator><creator>Gonzalez, Maria E.</creator><creator>Fridman, Rafael</creator><creator>Kleer, Celina G.</creator><general>Springer US</general><general>Springer</general><general>Springer Nature B.V</general><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>7TO</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>K9-</scope><scope>K9.</scope><scope>M0R</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20150201</creationdate><title>Tyrosine kinase discoidin domain receptors DDR1 and DDR2 are coordinately deregulated in triple-negative breast cancer</title><author>Toy, Kathy A. ; Valiathan, Rajeshwari R. ; Núñez, Fernando ; Kidwell, Kelley M. ; Gonzalez, Maria E. ; Fridman, Rafael ; Kleer, Celina G.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c638t-58322ca1f41e381a626c4610738356884f5f24852ee7e65139d7b17aaa4433223</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Analysis</topic><topic>Breast cancer</topic><topic>Cancer research</topic><topic>Cancer therapies</topic><topic>Carcinoma, Ductal, Breast - genetics</topic><topic>Carcinoma, Ductal, Breast - metabolism</topic><topic>Carcinoma, Ductal, Breast - pathology</topic><topic>Clinical outcomes</topic><topic>Combined Modality Therapy</topic><topic>Computer memory</topic><topic>Discoidin Domain Receptors</topic><topic>Female</topic><topic>Gene Expression</topic><topic>Health aspects</topic><topic>Humans</topic><topic>Immunohistochemistry</topic><topic>Kaplan-Meier Estimate</topic><topic>Kinases</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Middle Aged</topic><topic>Neoplasm Grading</topic><topic>Neoplasm Invasiveness</topic><topic>Oncology</topic><topic>Preclinical Study</topic><topic>Prognosis</topic><topic>Protein Binding</topic><topic>Proteins</topic><topic>Receptor Protein-Tyrosine Kinases - genetics</topic><topic>Receptor Protein-Tyrosine Kinases - metabolism</topic><topic>Receptors, Mitogen - genetics</topic><topic>Receptors, Mitogen - metabolism</topic><topic>Risk Factors</topic><topic>Triple Negative Breast Neoplasms - genetics</topic><topic>Triple Negative Breast Neoplasms - metabolism</topic><topic>Triple Negative Breast Neoplasms - mortality</topic><topic>Triple Negative Breast Neoplasms - pathology</topic><topic>Triple Negative Breast Neoplasms - therapy</topic><topic>Tumor Burden</topic><topic>Tyrosine</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Toy, Kathy A.</creatorcontrib><creatorcontrib>Valiathan, Rajeshwari R.</creatorcontrib><creatorcontrib>Núñez, Fernando</creatorcontrib><creatorcontrib>Kidwell, Kelley M.</creatorcontrib><creatorcontrib>Gonzalez, Maria E.</creatorcontrib><creatorcontrib>Fridman, Rafael</creatorcontrib><creatorcontrib>Kleer, Celina G.</creatorcontrib><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>Oncogenes and Growth Factors Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Consumer Health Database (Alumni Edition)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Consumer Health Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Research Library (Corporate)</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><collection>PubMed Central (Full Participant titles)</collection><jtitle>Breast cancer research and treatment</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Toy, Kathy A.</au><au>Valiathan, Rajeshwari R.</au><au>Núñez, Fernando</au><au>Kidwell, Kelley M.</au><au>Gonzalez, Maria E.</au><au>Fridman, Rafael</au><au>Kleer, Celina G.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Tyrosine kinase discoidin domain receptors DDR1 and DDR2 are coordinately deregulated in triple-negative breast cancer</atitle><jtitle>Breast cancer research and treatment</jtitle><stitle>Breast Cancer Res Treat</stitle><addtitle>Breast Cancer Res Treat</addtitle><date>2015-02-01</date><risdate>2015</risdate><volume>150</volume><issue>1</issue><spage>9</spage><epage>18</epage><pages>9-18</pages><issn>0167-6806</issn><eissn>1573-7217</eissn><coden>BCTRD6</coden><abstract>Receptor kinases Discoidin Domain Receptors (DDRs) 1 and 2 are emerging as new therapeutic targets in breast cancer (BC). However, the expression of DDR proteins during BC progression and their association with BC subtypes remain poorly defined. Herein we report the first comprehensive immunohistochemical analyses of DDR protein expression in a wide range of breast tissues. DDR1 and DDR2 expression was investigated by immunohistochemistry in 218 samples of normal breast (
n
= 10), ductal carcinoma in situ (DCIS,
n
= 10), and invasive carcinomas (
n
= 198), arrayed in tissue microarrays with comprehensive clinical and follow-up information. Staining was evaluated for cell type, subcellular localization, percentage and intensity (scores 1–4), and association with disease subtype and outcome. In normal epithelium and DCIS, DDR1 was highly expressed, while DDR2 was negative in normal epithelium, and in DCIS it localized to cells at the epithelial-stromal interface. Of the 198 invasive carcinomas, DDR1 was high in 87 (44 %) and low in 103 (52 %), and DDR2 was high in 110 (56 %) and low in 87 (44 %). High DDR2 was associated with high tumor grade (
P
= 0.002), triple-negative subtype (TNBC) (
P
< 0.0001), and worse survival (
P
= 0.037). We discovered a novel concordant deregulation of DDR expression, with a DDR1
Low
/DDR2
High
profile significantly associated with TNBC, compared to luminal tumors (
P
= 0.012), and with worse overall survival. In conclusion, DDR2 upregulation occurs in DCIS, before stromal invasion, and may reflect epithelial-stromal cross-talk. A DDR1
Low
/DDR2
High
protein profile is associated with TNBC and may identify invasive carcinomas with worse prognosis.</abstract><cop>Boston</cop><pub>Springer US</pub><pmid>25667101</pmid><doi>10.1007/s10549-015-3285-7</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
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| ispartof | Breast cancer research and treatment, 2015-02, Vol.150 (1), p.9-18 |
| issn | 0167-6806 1573-7217 |
| language | eng |
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| source | MEDLINE; SpringerLink Journals - AutoHoldings |
| subjects | Adult Aged Aged, 80 and over Analysis Breast cancer Cancer research Cancer therapies Carcinoma, Ductal, Breast - genetics Carcinoma, Ductal, Breast - metabolism Carcinoma, Ductal, Breast - pathology Clinical outcomes Combined Modality Therapy Computer memory Discoidin Domain Receptors Female Gene Expression Health aspects Humans Immunohistochemistry Kaplan-Meier Estimate Kinases Medicine Medicine & Public Health Middle Aged Neoplasm Grading Neoplasm Invasiveness Oncology Preclinical Study Prognosis Protein Binding Proteins Receptor Protein-Tyrosine Kinases - genetics Receptor Protein-Tyrosine Kinases - metabolism Receptors, Mitogen - genetics Receptors, Mitogen - metabolism Risk Factors Triple Negative Breast Neoplasms - genetics Triple Negative Breast Neoplasms - metabolism Triple Negative Breast Neoplasms - mortality Triple Negative Breast Neoplasms - pathology Triple Negative Breast Neoplasms - therapy Tumor Burden Tyrosine |
| title | Tyrosine kinase discoidin domain receptors DDR1 and DDR2 are coordinately deregulated in triple-negative breast cancer |
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