Estrogen Receptor Expression Is Associated with DNA Repair Capacity in Breast Cancer
Estrogen-receptor-positive (ER+) tumors employ complex signaling that engages in crosstalk with multiple pathways through genomic and non-genomic regulation. A greater understanding of these pathways is important for developing improved biomarkers that can better determine treatment choices, risk of...
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| Veröffentlicht in: | PloS one 2016-03, Vol.11 (3), p.e0152422 |
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| creator | Matta, Jaime Morales, Luisa Ortiz, Carmen Adams, Damian Vargas, Wanda Casbas, Patricia Dutil, Julie Echenique, Miguel Suárez, Erick |
| description | Estrogen-receptor-positive (ER+) tumors employ complex signaling that engages in crosstalk with multiple pathways through genomic and non-genomic regulation. A greater understanding of these pathways is important for developing improved biomarkers that can better determine treatment choices, risk of recurrence and cancer progression. Deficiencies in DNA repair capacity (DRC) is a hallmark of breast cancer (BC); therefore, in this work we tested whether ER signaling influences DRC. We analyzed the association between ER positivity (% receptor activation) and DRC in 270 BC patients, then further stratified our analysis by HER2 receptor status. Our results show that among HER2 negative, the likelihood of having low DRC values among ER- women is 1.92 (95% CI: 1.03, 3.57) times the likelihood of having low DRC values among ER+ women, even adjusting for different potential confounders (p |
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A greater understanding of these pathways is important for developing improved biomarkers that can better determine treatment choices, risk of recurrence and cancer progression. Deficiencies in DNA repair capacity (DRC) is a hallmark of breast cancer (BC); therefore, in this work we tested whether ER signaling influences DRC. We analyzed the association between ER positivity (% receptor activation) and DRC in 270 BC patients, then further stratified our analysis by HER2 receptor status. Our results show that among HER2 negative, the likelihood of having low DRC values among ER- women is 1.92 (95% CI: 1.03, 3.57) times the likelihood of having low DRC values among ER+ women, even adjusting for different potential confounders (p<0.05); however, a contrary pattern was observed among HER2 positives women. In conclusion, there is an association between DRC levels and ER status, and this association is modified by HER2 receptor status. Adding a DNA repair capacity test to hormone receptor testing may provide new information on defective DNA repair phenotypes, which could better stratify BC patients who have ER+ tumors. ER+/HER2- tumors are heterogeneous, incompletely defined, and clinically challenging to treat; the addition of a DRC test could better characterize and classify these patients as well as help clinicians select optimal therapies, which could improve outcomes and reduce recurrences.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0152422</identifier><identifier>PMID: 27032101</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Adult ; Aged ; Biochemistry ; Biology ; Biology and life sciences ; Biomarkers ; Biomarkers, Tumor - metabolism ; Breast cancer ; Breast Neoplasms - metabolism ; Breast Neoplasms - pathology ; Cancer ; Care and treatment ; Cellular signal transduction ; Crosstalk ; Deoxyribonucleic acid ; DNA ; DNA damage ; DNA Repair ; Epidemiology ; ErbB-2 protein ; Estrogen receptors ; Estrogens ; Female ; Gene expression ; Health risks ; Health sciences ; Humans ; Logistic Models ; Lymphocytes ; Medicine ; Medicine and Health Sciences ; Middle Aged ; Mutation ; Neoplasm Staging ; Patients ; Pharmacology ; Phenotype ; Public health ; Receptor mechanisms ; Receptor, ErbB-2 - metabolism ; Receptors, Estrogen - genetics ; Receptors, Estrogen - metabolism ; Receptors, Progesterone - metabolism ; Repair ; Signal transduction ; Signaling ; Skin cancer ; Toxicology ; Tumors ; Womens health</subject><ispartof>PloS one, 2016-03, Vol.11 (3), p.e0152422</ispartof><rights>COPYRIGHT 2016 Public Library of Science</rights><rights>2016 Matta et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2016 Matta et al 2016 Matta et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c725t-f8170282d172588aa3683cd6debd53b6fe618b5c420f4d035663c8528aaea13f3</citedby><cites>FETCH-LOGICAL-c725t-f8170282d172588aa3683cd6debd53b6fe618b5c420f4d035663c8528aaea13f3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4816515/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4816515/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,2102,2928,23866,27924,27925,53791,53793,79600,79601</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27032101$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Coleman, William B.</contributor><creatorcontrib>Matta, Jaime</creatorcontrib><creatorcontrib>Morales, Luisa</creatorcontrib><creatorcontrib>Ortiz, Carmen</creatorcontrib><creatorcontrib>Adams, Damian</creatorcontrib><creatorcontrib>Vargas, Wanda</creatorcontrib><creatorcontrib>Casbas, Patricia</creatorcontrib><creatorcontrib>Dutil, Julie</creatorcontrib><creatorcontrib>Echenique, Miguel</creatorcontrib><creatorcontrib>Suárez, Erick</creatorcontrib><title>Estrogen Receptor Expression Is Associated with DNA Repair Capacity in Breast Cancer</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Estrogen-receptor-positive (ER+) tumors employ complex signaling that engages in crosstalk with multiple pathways through genomic and non-genomic regulation. A greater understanding of these pathways is important for developing improved biomarkers that can better determine treatment choices, risk of recurrence and cancer progression. Deficiencies in DNA repair capacity (DRC) is a hallmark of breast cancer (BC); therefore, in this work we tested whether ER signaling influences DRC. We analyzed the association between ER positivity (% receptor activation) and DRC in 270 BC patients, then further stratified our analysis by HER2 receptor status. Our results show that among HER2 negative, the likelihood of having low DRC values among ER- women is 1.92 (95% CI: 1.03, 3.57) times the likelihood of having low DRC values among ER+ women, even adjusting for different potential confounders (p<0.05); however, a contrary pattern was observed among HER2 positives women. In conclusion, there is an association between DRC levels and ER status, and this association is modified by HER2 receptor status. Adding a DNA repair capacity test to hormone receptor testing may provide new information on defective DNA repair phenotypes, which could better stratify BC patients who have ER+ tumors. ER+/HER2- tumors are heterogeneous, incompletely defined, and clinically challenging to treat; the addition of a DRC test could better characterize and classify these patients as well as help clinicians select optimal therapies, which could improve outcomes and reduce recurrences.</description><subject>Adult</subject><subject>Aged</subject><subject>Biochemistry</subject><subject>Biology</subject><subject>Biology and life sciences</subject><subject>Biomarkers</subject><subject>Biomarkers, Tumor - metabolism</subject><subject>Breast cancer</subject><subject>Breast Neoplasms - metabolism</subject><subject>Breast Neoplasms - pathology</subject><subject>Cancer</subject><subject>Care and treatment</subject><subject>Cellular signal transduction</subject><subject>Crosstalk</subject><subject>Deoxyribonucleic acid</subject><subject>DNA</subject><subject>DNA damage</subject><subject>DNA Repair</subject><subject>Epidemiology</subject><subject>ErbB-2 protein</subject><subject>Estrogen receptors</subject><subject>Estrogens</subject><subject>Female</subject><subject>Gene expression</subject><subject>Health risks</subject><subject>Health sciences</subject><subject>Humans</subject><subject>Logistic Models</subject><subject>Lymphocytes</subject><subject>Medicine</subject><subject>Medicine and Health Sciences</subject><subject>Middle Aged</subject><subject>Mutation</subject><subject>Neoplasm Staging</subject><subject>Patients</subject><subject>Pharmacology</subject><subject>Phenotype</subject><subject>Public health</subject><subject>Receptor mechanisms</subject><subject>Receptor, ErbB-2 - metabolism</subject><subject>Receptors, Estrogen - genetics</subject><subject>Receptors, Estrogen - metabolism</subject><subject>Receptors, Progesterone - metabolism</subject><subject>Repair</subject><subject>Signal transduction</subject><subject>Signaling</subject><subject>Skin cancer</subject><subject>Toxicology</subject><subject>Tumors</subject><subject>Womens health</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</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><sourceid>DOA</sourceid><recordid>eNqNkl1v0zAUhiMEYmPwDxBEQkJw0eKP2HFvkEopUGli0hjcWo5z3LpK42A7sP17XJpNDdoFyoXj4-e8x-f4zbLnGE0xLfG7ret9q5pp51qYIsxIQciD7BTPKJlwgujDo_-T7EkIW4QYFZw_zk5IiSjBCJ9mV8sQvVtDm1-Chi46ny-vOw8hWNfmq5DPQ3Daqgh1_tvGTf7x6zyhnbI-X6hOaRtvctvmHzyoEFOo1eCfZo-MagI8G9az7Pun5dXiy-T84vNqMT-f6JKwODECl4gIUuO0FUIpygXVNa-hqhmtuAGORcV0QZApakQZ51QLRhIJClNDz7KXB92ucUEOAwkSl2XJKOWIJmJ1IGqntrLzdqf8jXTKyr8B59dS-Wh1A3JWIV6kYbESqwJzELMZ0sYIWpdVSQ1KWu-Han21g1pDG71qRqLjk9Zu5Nr9koXAnGGWBN4MAt797CFEubNBQ9OoFly_v3dqjlJE97Ve_YPe391ArVVqwLbGpbp6LyrnBaMFw1zwRE3vodJXw87q5B5jU3yU8HaUkJgI13Gt-hDk6tvl_7MXP8bs6yN2A6qJm-CaPiarhTFYHEDtXQgezN2QMZJ7899OQ-7NLwfzp7QXxw90l3TrdvoHhZz8gg</recordid><startdate>20160331</startdate><enddate>20160331</enddate><creator>Matta, Jaime</creator><creator>Morales, Luisa</creator><creator>Ortiz, Carmen</creator><creator>Adams, Damian</creator><creator>Vargas, Wanda</creator><creator>Casbas, Patricia</creator><creator>Dutil, Julie</creator><creator>Echenique, Miguel</creator><creator>Suárez, Erick</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</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>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20160331</creationdate><title>Estrogen Receptor Expression Is Associated with DNA Repair Capacity in Breast Cancer</title><author>Matta, Jaime ; Morales, Luisa ; Ortiz, Carmen ; Adams, Damian ; Vargas, Wanda ; Casbas, Patricia ; Dutil, Julie ; Echenique, Miguel ; Suárez, Erick</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c725t-f8170282d172588aa3683cd6debd53b6fe618b5c420f4d035663c8528aaea13f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Biochemistry</topic><topic>Biology</topic><topic>Biology and life sciences</topic><topic>Biomarkers</topic><topic>Biomarkers, Tumor - 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A greater understanding of these pathways is important for developing improved biomarkers that can better determine treatment choices, risk of recurrence and cancer progression. Deficiencies in DNA repair capacity (DRC) is a hallmark of breast cancer (BC); therefore, in this work we tested whether ER signaling influences DRC. We analyzed the association between ER positivity (% receptor activation) and DRC in 270 BC patients, then further stratified our analysis by HER2 receptor status. Our results show that among HER2 negative, the likelihood of having low DRC values among ER- women is 1.92 (95% CI: 1.03, 3.57) times the likelihood of having low DRC values among ER+ women, even adjusting for different potential confounders (p<0.05); however, a contrary pattern was observed among HER2 positives women. In conclusion, there is an association between DRC levels and ER status, and this association is modified by HER2 receptor status. Adding a DNA repair capacity test to hormone receptor testing may provide new information on defective DNA repair phenotypes, which could better stratify BC patients who have ER+ tumors. ER+/HER2- tumors are heterogeneous, incompletely defined, and clinically challenging to treat; the addition of a DRC test could better characterize and classify these patients as well as help clinicians select optimal therapies, which could improve outcomes and reduce recurrences.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>27032101</pmid><doi>10.1371/journal.pone.0152422</doi><oa>free_for_read</oa></addata></record> |
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| subjects | Adult Aged Biochemistry Biology Biology and life sciences Biomarkers Biomarkers, Tumor - metabolism Breast cancer Breast Neoplasms - metabolism Breast Neoplasms - pathology Cancer Care and treatment Cellular signal transduction Crosstalk Deoxyribonucleic acid DNA DNA damage DNA Repair Epidemiology ErbB-2 protein Estrogen receptors Estrogens Female Gene expression Health risks Health sciences Humans Logistic Models Lymphocytes Medicine Medicine and Health Sciences Middle Aged Mutation Neoplasm Staging Patients Pharmacology Phenotype Public health Receptor mechanisms Receptor, ErbB-2 - metabolism Receptors, Estrogen - genetics Receptors, Estrogen - metabolism Receptors, Progesterone - metabolism Repair Signal transduction Signaling Skin cancer Toxicology Tumors Womens health |
| title | Estrogen Receptor Expression Is Associated with DNA Repair Capacity in Breast Cancer |
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