PARP1 and phospho-p65 protein expression is increased in human HER2-positive breast cancers
Previous studies have shown that basal breast cancers, which may have an inherent “BRCAness” phenotype and sensitivity to inhibitors of poly (ADP-Ribose) polymerase (PARP), express elevated levels of PARP1. Our lab recently reported that HER2+ breast cancers also exhibit sensitivity to PARP inhibito...
Gespeichert in:
| Veröffentlicht in: | Breast cancer research and treatment 2015-04, Vol.150 (3), p.569-579 |
|---|---|
| Hauptverfasser: | , , , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 579 |
|---|---|
| container_issue | 3 |
| container_start_page | 569 |
| container_title | Breast cancer research and treatment |
| container_volume | 150 |
| creator | Stanley, Jennifer Klepczyk, Lisa Keene, Kimberly Wei, Shi Li, Yufeng Forero, Andres Grizzle, William Wielgos, Monica Brazelton, Jason LoBuglio, Albert F. Yang, Eddy S. |
| description | Previous studies have shown that basal breast cancers, which may have an inherent “BRCAness” phenotype and sensitivity to inhibitors of poly (ADP-Ribose) polymerase (PARP), express elevated levels of PARP1. Our lab recently reported that HER2+ breast cancers also exhibit sensitivity to PARP inhibitors (PARPi) by attenuating the NF-κB pathway. In this study, we assessed PARP1 and phospho-p65, a marker of activated NF-κB levels in human breast cancer tissues. PARP1 and PARP2 copy number, mRNA, and protein expression was assessed by interrogating the PAM-50 defined breast cancer patient set from the TCGA using cBioPortal. PARP1 and phospho-p65 immunohistochemistry and correlation to clinical parameters was conducted using 307 primary breast cancer specimens (132 basal, 82 luminal, 93 HER2+) through univariate and multivariate analyses. In the PAM50 breast cancer data set, PARP1 and 2 expression was altered in 24/58 (41 %) HER2+, 32/81 (40 %) basal, and 75/324 (23 %) luminal A/B breast cancer patients. This correlated with a statistically significant increase in PARP1 protein levels in HER2+ and basal but not luminal breast cancers (
p
= 0.003,
p
= 0.027,
p
= 0.289, respectively). No change in PARP2 protein level was observed. Interestingly, using breast cancer specimens from 307 patients, HER2 positivity correlated with elevated PARP1 expression (
p
|
| doi_str_mv | 10.1007/s10549-015-3359-6 |
| format | Article |
| fullrecord | <record><control><sourceid>gale_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_4396624</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A430343247</galeid><sourcerecordid>A430343247</sourcerecordid><originalsourceid>FETCH-LOGICAL-c568t-fbbb68f5499273211de48832650b081f327786b8abb943cac6ecca588d4cada93</originalsourceid><addsrcrecordid>eNp1kt9r1TAUx4so7jr9A3yRgCC-ZOZHk6YvwmVMJwwcQ598CGl6epvRJjVph_73ptw57xUlhIScz_km5-RbFC8pOaOEVO8SJaKsMaECcy5qLB8VGyoqjitGq8fFhlBZYamIPCmepXRLCKkrUj8tTphQnDNKN8W36-3NNUXGt2jqQ8oTT1KgKYYZnEfwY4qQkgseuYSctxFMgjbvUL-MxqPLixuGp5Dc7O4ANWt4RtZ4CzE9L550Zkjw4n49Lb5-uPhyfomvPn_8dL69wlZINeOuaRqpulxJzar1VS2USnEmBWmIoh1nVaVko0zT1CW3xkqw1gil2tKa1tT8tHi_152WZoTWgp-jGfQU3WjiTx2M08cR73q9C3e65LWUrMwCb-8FYvi-QJr16JKFYTAewpI0lbJWnApFM_r6L_Q2LNHn8jKVCyBMcPaH2pkBtPNdyPfaVVRvS054yVlZZersH1QeLYzOBg-dy-dHCW8OEnoww9ynMCxz_p90DNI9aGNIKUL30AxK9GodvbeOztbRq3W0zDmvDrv4kPHbKxlgeyDlkN9BPCj9v6q_AEu6zBU</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1699202532</pqid></control><display><type>article</type><title>PARP1 and phospho-p65 protein expression is increased in human HER2-positive breast cancers</title><source>MEDLINE</source><source>SpringerLink Journals - AutoHoldings</source><creator>Stanley, Jennifer ; Klepczyk, Lisa ; Keene, Kimberly ; Wei, Shi ; Li, Yufeng ; Forero, Andres ; Grizzle, William ; Wielgos, Monica ; Brazelton, Jason ; LoBuglio, Albert F. ; Yang, Eddy S.</creator><creatorcontrib>Stanley, Jennifer ; Klepczyk, Lisa ; Keene, Kimberly ; Wei, Shi ; Li, Yufeng ; Forero, Andres ; Grizzle, William ; Wielgos, Monica ; Brazelton, Jason ; LoBuglio, Albert F. ; Yang, Eddy S.</creatorcontrib><description>Previous studies have shown that basal breast cancers, which may have an inherent “BRCAness” phenotype and sensitivity to inhibitors of poly (ADP-Ribose) polymerase (PARP), express elevated levels of PARP1. Our lab recently reported that HER2+ breast cancers also exhibit sensitivity to PARP inhibitors (PARPi) by attenuating the NF-κB pathway. In this study, we assessed PARP1 and phospho-p65, a marker of activated NF-κB levels in human breast cancer tissues. PARP1 and PARP2 copy number, mRNA, and protein expression was assessed by interrogating the PAM-50 defined breast cancer patient set from the TCGA using cBioPortal. PARP1 and phospho-p65 immunohistochemistry and correlation to clinical parameters was conducted using 307 primary breast cancer specimens (132 basal, 82 luminal, 93 HER2+) through univariate and multivariate analyses. In the PAM50 breast cancer data set, PARP1 and 2 expression was altered in 24/58 (41 %) HER2+, 32/81 (40 %) basal, and 75/324 (23 %) luminal A/B breast cancer patients. This correlated with a statistically significant increase in PARP1 protein levels in HER2+ and basal but not luminal breast cancers (
p
= 0.003,
p
= 0.027,
p
= 0.289, respectively). No change in PARP2 protein level was observed. Interestingly, using breast cancer specimens from 307 patients, HER2 positivity correlated with elevated PARP1 expression (
p
< 0.0001) and was three times more likely than HER2 negative breast cancers to exhibit high PARP1 levels. No significant differences were noted between race, ER status, or PR status for PARP1 expression. Additionally, we found a significant correlation between HER2 status and phospho-p65 expression (
p
< 0.0001). Lastly, a direct correlation between PARP1 and phospho-p65 (
p
< 0.0001) was noted. These results indicate a potential connection between HER2, PARP1, and phospho-p65. Furthermore, these data suggest that the PARPi sensitivity we previously observed in HER2+ breast cancer cells may be due to elevated PARP1 expression.</description><identifier>ISSN: 0167-6806</identifier><identifier>EISSN: 1573-7217</identifier><identifier>DOI: 10.1007/s10549-015-3359-6</identifier><identifier>PMID: 25833211</identifier><identifier>CODEN: BCTRD6</identifier><language>eng</language><publisher>Boston: Springer US</publisher><subject>Adult ; Aged ; Aged, 80 and over ; Analysis ; Breast cancer ; Breast Neoplasms - genetics ; Breast Neoplasms - metabolism ; Breast Neoplasms - pathology ; Cancer research ; Cancer therapies ; Female ; Genetic markers ; Humans ; Immunohistochemistry ; Medicine ; Medicine & Public Health ; Middle Aged ; Oncology ; Phosphorylation ; Poly (ADP-Ribose) Polymerase-1 ; Poly(ADP-ribose) Polymerases - genetics ; Poly(ADP-ribose) Polymerases - metabolism ; Preclinical Study ; Protein expression ; Receptor, ErbB-2 - metabolism ; RNA ; Signal Transduction ; Transcription Factor RelA - metabolism ; Young Adult</subject><ispartof>Breast cancer research and treatment, 2015-04, Vol.150 (3), p.569-579</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-c568t-fbbb68f5499273211de48832650b081f327786b8abb943cac6ecca588d4cada93</citedby><cites>FETCH-LOGICAL-c568t-fbbb68f5499273211de48832650b081f327786b8abb943cac6ecca588d4cada93</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/s10549-015-3359-6$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s10549-015-3359-6$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>230,314,780,784,885,27923,27924,41487,42556,51318</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25833211$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Stanley, Jennifer</creatorcontrib><creatorcontrib>Klepczyk, Lisa</creatorcontrib><creatorcontrib>Keene, Kimberly</creatorcontrib><creatorcontrib>Wei, Shi</creatorcontrib><creatorcontrib>Li, Yufeng</creatorcontrib><creatorcontrib>Forero, Andres</creatorcontrib><creatorcontrib>Grizzle, William</creatorcontrib><creatorcontrib>Wielgos, Monica</creatorcontrib><creatorcontrib>Brazelton, Jason</creatorcontrib><creatorcontrib>LoBuglio, Albert F.</creatorcontrib><creatorcontrib>Yang, Eddy S.</creatorcontrib><title>PARP1 and phospho-p65 protein expression is increased in human HER2-positive breast cancers</title><title>Breast cancer research and treatment</title><addtitle>Breast Cancer Res Treat</addtitle><addtitle>Breast Cancer Res Treat</addtitle><description>Previous studies have shown that basal breast cancers, which may have an inherent “BRCAness” phenotype and sensitivity to inhibitors of poly (ADP-Ribose) polymerase (PARP), express elevated levels of PARP1. Our lab recently reported that HER2+ breast cancers also exhibit sensitivity to PARP inhibitors (PARPi) by attenuating the NF-κB pathway. In this study, we assessed PARP1 and phospho-p65, a marker of activated NF-κB levels in human breast cancer tissues. PARP1 and PARP2 copy number, mRNA, and protein expression was assessed by interrogating the PAM-50 defined breast cancer patient set from the TCGA using cBioPortal. PARP1 and phospho-p65 immunohistochemistry and correlation to clinical parameters was conducted using 307 primary breast cancer specimens (132 basal, 82 luminal, 93 HER2+) through univariate and multivariate analyses. In the PAM50 breast cancer data set, PARP1 and 2 expression was altered in 24/58 (41 %) HER2+, 32/81 (40 %) basal, and 75/324 (23 %) luminal A/B breast cancer patients. This correlated with a statistically significant increase in PARP1 protein levels in HER2+ and basal but not luminal breast cancers (
p
= 0.003,
p
= 0.027,
p
= 0.289, respectively). No change in PARP2 protein level was observed. Interestingly, using breast cancer specimens from 307 patients, HER2 positivity correlated with elevated PARP1 expression (
p
< 0.0001) and was three times more likely than HER2 negative breast cancers to exhibit high PARP1 levels. No significant differences were noted between race, ER status, or PR status for PARP1 expression. Additionally, we found a significant correlation between HER2 status and phospho-p65 expression (
p
< 0.0001). Lastly, a direct correlation between PARP1 and phospho-p65 (
p
< 0.0001) was noted. These results indicate a potential connection between HER2, PARP1, and phospho-p65. Furthermore, these data suggest that the PARPi sensitivity we previously observed in HER2+ breast cancer cells may be due to elevated PARP1 expression.</description><subject>Adult</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Analysis</subject><subject>Breast cancer</subject><subject>Breast Neoplasms - genetics</subject><subject>Breast Neoplasms - metabolism</subject><subject>Breast Neoplasms - pathology</subject><subject>Cancer research</subject><subject>Cancer therapies</subject><subject>Female</subject><subject>Genetic markers</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Middle Aged</subject><subject>Oncology</subject><subject>Phosphorylation</subject><subject>Poly (ADP-Ribose) Polymerase-1</subject><subject>Poly(ADP-ribose) Polymerases - genetics</subject><subject>Poly(ADP-ribose) Polymerases - metabolism</subject><subject>Preclinical Study</subject><subject>Protein expression</subject><subject>Receptor, ErbB-2 - metabolism</subject><subject>RNA</subject><subject>Signal Transduction</subject><subject>Transcription Factor RelA - metabolism</subject><subject>Young Adult</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>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNp1kt9r1TAUx4so7jr9A3yRgCC-ZOZHk6YvwmVMJwwcQ598CGl6epvRJjVph_73ptw57xUlhIScz_km5-RbFC8pOaOEVO8SJaKsMaECcy5qLB8VGyoqjitGq8fFhlBZYamIPCmepXRLCKkrUj8tTphQnDNKN8W36-3NNUXGt2jqQ8oTT1KgKYYZnEfwY4qQkgseuYSctxFMgjbvUL-MxqPLixuGp5Dc7O4ANWt4RtZ4CzE9L550Zkjw4n49Lb5-uPhyfomvPn_8dL69wlZINeOuaRqpulxJzar1VS2USnEmBWmIoh1nVaVko0zT1CW3xkqw1gil2tKa1tT8tHi_152WZoTWgp-jGfQU3WjiTx2M08cR73q9C3e65LWUrMwCb-8FYvi-QJr16JKFYTAewpI0lbJWnApFM_r6L_Q2LNHn8jKVCyBMcPaH2pkBtPNdyPfaVVRvS054yVlZZersH1QeLYzOBg-dy-dHCW8OEnoww9ynMCxz_p90DNI9aGNIKUL30AxK9GodvbeOztbRq3W0zDmvDrv4kPHbKxlgeyDlkN9BPCj9v6q_AEu6zBU</recordid><startdate>20150401</startdate><enddate>20150401</enddate><creator>Stanley, Jennifer</creator><creator>Klepczyk, Lisa</creator><creator>Keene, Kimberly</creator><creator>Wei, Shi</creator><creator>Li, Yufeng</creator><creator>Forero, Andres</creator><creator>Grizzle, William</creator><creator>Wielgos, Monica</creator><creator>Brazelton, Jason</creator><creator>LoBuglio, Albert F.</creator><creator>Yang, Eddy S.</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>20150401</creationdate><title>PARP1 and phospho-p65 protein expression is increased in human HER2-positive breast cancers</title><author>Stanley, Jennifer ; Klepczyk, Lisa ; Keene, Kimberly ; Wei, Shi ; Li, Yufeng ; Forero, Andres ; Grizzle, William ; Wielgos, Monica ; Brazelton, Jason ; LoBuglio, Albert F. ; Yang, Eddy S.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c568t-fbbb68f5499273211de48832650b081f327786b8abb943cac6ecca588d4cada93</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>Breast Neoplasms - genetics</topic><topic>Breast Neoplasms - metabolism</topic><topic>Breast Neoplasms - pathology</topic><topic>Cancer research</topic><topic>Cancer therapies</topic><topic>Female</topic><topic>Genetic markers</topic><topic>Humans</topic><topic>Immunohistochemistry</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Middle Aged</topic><topic>Oncology</topic><topic>Phosphorylation</topic><topic>Poly (ADP-Ribose) Polymerase-1</topic><topic>Poly(ADP-ribose) Polymerases - genetics</topic><topic>Poly(ADP-ribose) Polymerases - metabolism</topic><topic>Preclinical Study</topic><topic>Protein expression</topic><topic>Receptor, ErbB-2 - metabolism</topic><topic>RNA</topic><topic>Signal Transduction</topic><topic>Transcription Factor RelA - metabolism</topic><topic>Young Adult</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Stanley, Jennifer</creatorcontrib><creatorcontrib>Klepczyk, Lisa</creatorcontrib><creatorcontrib>Keene, Kimberly</creatorcontrib><creatorcontrib>Wei, Shi</creatorcontrib><creatorcontrib>Li, Yufeng</creatorcontrib><creatorcontrib>Forero, Andres</creatorcontrib><creatorcontrib>Grizzle, William</creatorcontrib><creatorcontrib>Wielgos, Monica</creatorcontrib><creatorcontrib>Brazelton, Jason</creatorcontrib><creatorcontrib>LoBuglio, Albert F.</creatorcontrib><creatorcontrib>Yang, Eddy S.</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>Stanley, Jennifer</au><au>Klepczyk, Lisa</au><au>Keene, Kimberly</au><au>Wei, Shi</au><au>Li, Yufeng</au><au>Forero, Andres</au><au>Grizzle, William</au><au>Wielgos, Monica</au><au>Brazelton, Jason</au><au>LoBuglio, Albert F.</au><au>Yang, Eddy S.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>PARP1 and phospho-p65 protein expression is increased in human HER2-positive breast cancers</atitle><jtitle>Breast cancer research and treatment</jtitle><stitle>Breast Cancer Res Treat</stitle><addtitle>Breast Cancer Res Treat</addtitle><date>2015-04-01</date><risdate>2015</risdate><volume>150</volume><issue>3</issue><spage>569</spage><epage>579</epage><pages>569-579</pages><issn>0167-6806</issn><eissn>1573-7217</eissn><coden>BCTRD6</coden><abstract>Previous studies have shown that basal breast cancers, which may have an inherent “BRCAness” phenotype and sensitivity to inhibitors of poly (ADP-Ribose) polymerase (PARP), express elevated levels of PARP1. Our lab recently reported that HER2+ breast cancers also exhibit sensitivity to PARP inhibitors (PARPi) by attenuating the NF-κB pathway. In this study, we assessed PARP1 and phospho-p65, a marker of activated NF-κB levels in human breast cancer tissues. PARP1 and PARP2 copy number, mRNA, and protein expression was assessed by interrogating the PAM-50 defined breast cancer patient set from the TCGA using cBioPortal. PARP1 and phospho-p65 immunohistochemistry and correlation to clinical parameters was conducted using 307 primary breast cancer specimens (132 basal, 82 luminal, 93 HER2+) through univariate and multivariate analyses. In the PAM50 breast cancer data set, PARP1 and 2 expression was altered in 24/58 (41 %) HER2+, 32/81 (40 %) basal, and 75/324 (23 %) luminal A/B breast cancer patients. This correlated with a statistically significant increase in PARP1 protein levels in HER2+ and basal but not luminal breast cancers (
p
= 0.003,
p
= 0.027,
p
= 0.289, respectively). No change in PARP2 protein level was observed. Interestingly, using breast cancer specimens from 307 patients, HER2 positivity correlated with elevated PARP1 expression (
p
< 0.0001) and was three times more likely than HER2 negative breast cancers to exhibit high PARP1 levels. No significant differences were noted between race, ER status, or PR status for PARP1 expression. Additionally, we found a significant correlation between HER2 status and phospho-p65 expression (
p
< 0.0001). Lastly, a direct correlation between PARP1 and phospho-p65 (
p
< 0.0001) was noted. These results indicate a potential connection between HER2, PARP1, and phospho-p65. Furthermore, these data suggest that the PARPi sensitivity we previously observed in HER2+ breast cancer cells may be due to elevated PARP1 expression.</abstract><cop>Boston</cop><pub>Springer US</pub><pmid>25833211</pmid><doi>10.1007/s10549-015-3359-6</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0167-6806 |
| ispartof | Breast cancer research and treatment, 2015-04, Vol.150 (3), p.569-579 |
| issn | 0167-6806 1573-7217 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_4396624 |
| source | MEDLINE; SpringerLink Journals - AutoHoldings |
| subjects | Adult Aged Aged, 80 and over Analysis Breast cancer Breast Neoplasms - genetics Breast Neoplasms - metabolism Breast Neoplasms - pathology Cancer research Cancer therapies Female Genetic markers Humans Immunohistochemistry Medicine Medicine & Public Health Middle Aged Oncology Phosphorylation Poly (ADP-Ribose) Polymerase-1 Poly(ADP-ribose) Polymerases - genetics Poly(ADP-ribose) Polymerases - metabolism Preclinical Study Protein expression Receptor, ErbB-2 - metabolism RNA Signal Transduction Transcription Factor RelA - metabolism Young Adult |
| title | PARP1 and phospho-p65 protein expression is increased in human HER2-positive breast cancers |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-13T05%3A24%3A00IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=PARP1%20and%20phospho-p65%20protein%20expression%20is%20increased%20in%20human%20HER2-positive%20breast%20cancers&rft.jtitle=Breast%20cancer%20research%20and%20treatment&rft.au=Stanley,%20Jennifer&rft.date=2015-04-01&rft.volume=150&rft.issue=3&rft.spage=569&rft.epage=579&rft.pages=569-579&rft.issn=0167-6806&rft.eissn=1573-7217&rft.coden=BCTRD6&rft_id=info:doi/10.1007/s10549-015-3359-6&rft_dat=%3Cgale_pubme%3EA430343247%3C/gale_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1699202532&rft_id=info:pmid/25833211&rft_galeid=A430343247&rfr_iscdi=true |