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Relationship between ER expression by IHC or mRNA with Ki67 response to aromatase inhibition: a POETIC study
In clinical practice, oestrogen receptor (ER) analysis is almost entirely by immunohistochemistry (IHC). ASCO/CAP recommends cut-offs of
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| Published in: | Breast cancer research : BCR 2022-09, Vol.24 (1), p.61-61, Article 61 |
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| creator | Lopez-Knowles, Elena Detre, Simone Hills, Margaret Schuster, Eugene F Cheang, Maggie C U Tovey, Holly Kilburn, Lucy S Bliss, Judith M Robertson, John Mallon, Elizabeth Skene, Anthony Evans, Abigail Smith, Ian Dowsett, Mitch |
| description | In clinical practice, oestrogen receptor (ER) analysis is almost entirely by immunohistochemistry (IHC). ASCO/CAP recommends cut-offs of |
| doi_str_mv | 10.1186/s13058-022-01556-6 |
| format | article |
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Cases were selected from the aromatase inhibitor treatment group of POETIC. We selected the 15% with the poorest Ki67 response (PR, < 40% Ki67 suppression, n = 230) and a random 30% of the remainder categorised as intermediate (IR, 40-79% Ki67 suppression, n = 150) and good-responders (GR, ≥ 80% Ki67 suppression, n = 230) from HER2 - group. All HER2 + cases available were selected irrespective of their response category (n = 317). ER expression was measured by IHC and qPCR.
ER IHC was available from 515 HER2 - and 186 HER2 + tumours and ER qPCR from 367 HER2 - and 171 HER2 + tumours. Ninety-one percentage of patients with ER IHC < 10% were PRs with similar rates in HER2 - and HER2 + cases. At or above ER IHC 10% substantial numbers of patients showed IR or GR. Similar proportions of patients were defined by cut-points of ER IHC < 10% and ER mRNA < 5 units. In addition, loss of PgR expression altered ER anti-proliferation response with 92% of PgR - cases with ER IHC < 40% being PRs.
There was little responsiveness at IHC < 10% and no distinction between < 1% and 1-10% cells positive. Similar separation of PRs from IR/GRs was achieved by IHC and mRNA.]]></description><identifier>ISSN: 1465-542X</identifier><identifier>ISSN: 1465-5411</identifier><identifier>EISSN: 1465-542X</identifier><identifier>DOI: 10.1186/s13058-022-01556-6</identifier><identifier>PMID: 36096872</identifier><language>eng</language><publisher>England: BioMed Central Ltd</publisher><subject>Analysis ; Aromatase ; Aromatase inhibitors ; Aromatase Inhibitors - pharmacology ; Aromatase Inhibitors - therapeutic use ; Breast cancer ; Breast Neoplasms - drug therapy ; Breast Neoplasms - genetics ; Cancer therapies ; Cloning ; Endocrine therapy ; ErbB-2 protein ; ESR1 ; Estrogen ; Female ; Gene expression ; Humans ; Immunohistochemistry ; Ki-67 Antigen - genetics ; Ki-67 Antigen - metabolism ; Ki67 ; Messenger RNA ; mRNA ; Patients ; PgR ; Proteins ; Receptor, ErbB-2 - genetics ; Receptor, ErbB-2 - metabolism ; Receptors, Estrogen - genetics ; Receptors, Estrogen - metabolism ; Receptors, Progesterone - metabolism ; RNA, Messenger - genetics ; Tumors</subject><ispartof>Breast cancer research : BCR, 2022-09, Vol.24 (1), p.61-61, Article 61</ispartof><rights>2022. The Author(s).</rights><rights>COPYRIGHT 2022 BioMed Central Ltd.</rights><rights>2022. This work is licensed under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>The Author(s) 2022</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c563t-71a9ab96ba0ac2a78fccc5ea443fb0f90efc94c64790ee0fe2d0ebad6fb7b9623</citedby><cites>FETCH-LOGICAL-c563t-71a9ab96ba0ac2a78fccc5ea443fb0f90efc94c64790ee0fe2d0ebad6fb7b9623</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/PMC9466340/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/2715510098?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,25753,27924,27925,37012,37013,44590,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/36096872$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lopez-Knowles, Elena</creatorcontrib><creatorcontrib>Detre, Simone</creatorcontrib><creatorcontrib>Hills, Margaret</creatorcontrib><creatorcontrib>Schuster, Eugene F</creatorcontrib><creatorcontrib>Cheang, Maggie C U</creatorcontrib><creatorcontrib>Tovey, Holly</creatorcontrib><creatorcontrib>Kilburn, Lucy S</creatorcontrib><creatorcontrib>Bliss, Judith M</creatorcontrib><creatorcontrib>Robertson, John</creatorcontrib><creatorcontrib>Mallon, Elizabeth</creatorcontrib><creatorcontrib>Skene, Anthony</creatorcontrib><creatorcontrib>Evans, Abigail</creatorcontrib><creatorcontrib>Smith, Ian</creatorcontrib><creatorcontrib>Dowsett, Mitch</creatorcontrib><title>Relationship between ER expression by IHC or mRNA with Ki67 response to aromatase inhibition: a POETIC study</title><title>Breast cancer research : BCR</title><addtitle>Breast Cancer Res</addtitle><description><![CDATA[In clinical practice, oestrogen receptor (ER) analysis is almost entirely by immunohistochemistry (IHC). ASCO/CAP recommends cut-offs of < 1% (negative) and 1-10% (low) cells positive. There is uncertainty whether patients with ER low tumours benefit from endocrine therapy. We aimed to assess IHC and mRNA cut-points for ER versus biological response of primary breast cancer to 2 weeks' aromatase inhibitor treatment as measured by change in Ki67.
Cases were selected from the aromatase inhibitor treatment group of POETIC. We selected the 15% with the poorest Ki67 response (PR, < 40% Ki67 suppression, n = 230) and a random 30% of the remainder categorised as intermediate (IR, 40-79% Ki67 suppression, n = 150) and good-responders (GR, ≥ 80% Ki67 suppression, n = 230) from HER2 - group. All HER2 + cases available were selected irrespective of their response category (n = 317). ER expression was measured by IHC and qPCR.
ER IHC was available from 515 HER2 - and 186 HER2 + tumours and ER qPCR from 367 HER2 - and 171 HER2 + tumours. Ninety-one percentage of patients with ER IHC < 10% were PRs with similar rates in HER2 - and HER2 + cases. At or above ER IHC 10% substantial numbers of patients showed IR or GR. Similar proportions of patients were defined by cut-points of ER IHC < 10% and ER mRNA < 5 units. In addition, loss of PgR expression altered ER anti-proliferation response with 92% of PgR - cases with ER IHC < 40% being PRs.
There was little responsiveness at IHC < 10% and no distinction between < 1% and 1-10% cells positive. Similar separation of PRs from IR/GRs was achieved by IHC and mRNA.]]></description><subject>Analysis</subject><subject>Aromatase</subject><subject>Aromatase inhibitors</subject><subject>Aromatase Inhibitors - pharmacology</subject><subject>Aromatase Inhibitors - therapeutic use</subject><subject>Breast cancer</subject><subject>Breast Neoplasms - drug therapy</subject><subject>Breast Neoplasms - genetics</subject><subject>Cancer therapies</subject><subject>Cloning</subject><subject>Endocrine therapy</subject><subject>ErbB-2 protein</subject><subject>ESR1</subject><subject>Estrogen</subject><subject>Female</subject><subject>Gene expression</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>Ki-67 Antigen - genetics</subject><subject>Ki-67 Antigen - metabolism</subject><subject>Ki67</subject><subject>Messenger RNA</subject><subject>mRNA</subject><subject>Patients</subject><subject>PgR</subject><subject>Proteins</subject><subject>Receptor, ErbB-2 - genetics</subject><subject>Receptor, ErbB-2 - metabolism</subject><subject>Receptors, Estrogen - genetics</subject><subject>Receptors, Estrogen - metabolism</subject><subject>Receptors, Progesterone - metabolism</subject><subject>RNA, Messenger - genetics</subject><subject>Tumors</subject><issn>1465-542X</issn><issn>1465-5411</issn><issn>1465-542X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><sourceid>DOA</sourceid><recordid>eNptkktvEzEUhUcIREvhD7BAltiwmeLH-MUCKYoCjagoiorEzrI9nsTRzDi1Zyj593iaUhqEvLB9fc5n3atTFK8RPEdIsPcJEUhFCTEuIaKUlexJcYoqRkta4R9PH51PihcpbSFEXFDxvDghDEomOD4t2pVr9eBDnzZ-B4wbbp3rwWIF3K9ddCnlF2D2YHkxByGCbvV1Bm79sAFfPOMgC3bZ6cAQgI6h04POF99vvPET8wPQ4NvV4no5B2kY6_3L4lmj2-Re3e9nxfdPi-v5RXl59Xk5n12WljIylBxpqY1kRkNtseaisdZSp6uKNAY2ErrGysqyiuejg43DNXRG16wxPNswOSuWB24d9Fbtou903KugvborhLhWOg7etk4ZJi2kVkjS4EoSqgmBWBBrLEeC1yKzPh5Yu9F0rrauH6Juj6DHL73fqHX4qWTFGKlgBry7B8RwM7o0qM4n69pW9y6MSWGOKsiQhJP07T_SbRhjn0c1qShFEErxV7XWuQHfNyH_ayeomnHEsWCETqzz_6jyql3nbehd43P9yIAPBhtDStE1Dz0iqKa8qUPeVM6busubYtn05vF0Hix_AkZ-AwBbz4k</recordid><startdate>20220912</startdate><enddate>20220912</enddate><creator>Lopez-Knowles, Elena</creator><creator>Detre, Simone</creator><creator>Hills, Margaret</creator><creator>Schuster, Eugene F</creator><creator>Cheang, Maggie C U</creator><creator>Tovey, Holly</creator><creator>Kilburn, Lucy S</creator><creator>Bliss, Judith M</creator><creator>Robertson, John</creator><creator>Mallon, Elizabeth</creator><creator>Skene, Anthony</creator><creator>Evans, Abigail</creator><creator>Smith, Ian</creator><creator>Dowsett, Mitch</creator><general>BioMed Central Ltd</general><general>BioMed Central</general><general>BMC</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>8FI</scope><scope>8FJ</scope><scope>8FK</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>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20220912</creationdate><title>Relationship between ER expression by IHC or mRNA with Ki67 response to aromatase inhibition: a POETIC study</title><author>Lopez-Knowles, Elena ; Detre, Simone ; Hills, Margaret ; Schuster, Eugene F ; Cheang, Maggie C U ; Tovey, Holly ; Kilburn, Lucy S ; Bliss, Judith M ; Robertson, John ; Mallon, Elizabeth ; Skene, Anthony ; Evans, Abigail ; Smith, Ian ; Dowsett, Mitch</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c563t-71a9ab96ba0ac2a78fccc5ea443fb0f90efc94c64790ee0fe2d0ebad6fb7b9623</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Analysis</topic><topic>Aromatase</topic><topic>Aromatase inhibitors</topic><topic>Aromatase Inhibitors - pharmacology</topic><topic>Aromatase Inhibitors - therapeutic use</topic><topic>Breast cancer</topic><topic>Breast Neoplasms - drug therapy</topic><topic>Breast Neoplasms - genetics</topic><topic>Cancer therapies</topic><topic>Cloning</topic><topic>Endocrine therapy</topic><topic>ErbB-2 protein</topic><topic>ESR1</topic><topic>Estrogen</topic><topic>Female</topic><topic>Gene expression</topic><topic>Humans</topic><topic>Immunohistochemistry</topic><topic>Ki-67 Antigen - genetics</topic><topic>Ki-67 Antigen - metabolism</topic><topic>Ki67</topic><topic>Messenger RNA</topic><topic>mRNA</topic><topic>Patients</topic><topic>PgR</topic><topic>Proteins</topic><topic>Receptor, ErbB-2 - genetics</topic><topic>Receptor, ErbB-2 - metabolism</topic><topic>Receptors, Estrogen - genetics</topic><topic>Receptors, Estrogen - metabolism</topic><topic>Receptors, Progesterone - metabolism</topic><topic>RNA, Messenger - genetics</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lopez-Knowles, Elena</creatorcontrib><creatorcontrib>Detre, Simone</creatorcontrib><creatorcontrib>Hills, Margaret</creatorcontrib><creatorcontrib>Schuster, Eugene F</creatorcontrib><creatorcontrib>Cheang, Maggie C U</creatorcontrib><creatorcontrib>Tovey, Holly</creatorcontrib><creatorcontrib>Kilburn, Lucy S</creatorcontrib><creatorcontrib>Bliss, Judith M</creatorcontrib><creatorcontrib>Robertson, John</creatorcontrib><creatorcontrib>Mallon, Elizabeth</creatorcontrib><creatorcontrib>Skene, Anthony</creatorcontrib><creatorcontrib>Evans, Abigail</creatorcontrib><creatorcontrib>Smith, Ian</creatorcontrib><creatorcontrib>Dowsett, Mitch</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>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>AUTh Library subscriptions: 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>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Publicly Available Content Database</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>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>Breast cancer research : BCR</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lopez-Knowles, Elena</au><au>Detre, Simone</au><au>Hills, Margaret</au><au>Schuster, Eugene F</au><au>Cheang, Maggie C U</au><au>Tovey, Holly</au><au>Kilburn, Lucy S</au><au>Bliss, Judith M</au><au>Robertson, John</au><au>Mallon, Elizabeth</au><au>Skene, Anthony</au><au>Evans, Abigail</au><au>Smith, Ian</au><au>Dowsett, Mitch</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Relationship between ER expression by IHC or mRNA with Ki67 response to aromatase inhibition: a POETIC study</atitle><jtitle>Breast cancer research : BCR</jtitle><addtitle>Breast Cancer Res</addtitle><date>2022-09-12</date><risdate>2022</risdate><volume>24</volume><issue>1</issue><spage>61</spage><epage>61</epage><pages>61-61</pages><artnum>61</artnum><issn>1465-542X</issn><issn>1465-5411</issn><eissn>1465-542X</eissn><abstract><![CDATA[In clinical practice, oestrogen receptor (ER) analysis is almost entirely by immunohistochemistry (IHC). ASCO/CAP recommends cut-offs of < 1% (negative) and 1-10% (low) cells positive. There is uncertainty whether patients with ER low tumours benefit from endocrine therapy. We aimed to assess IHC and mRNA cut-points for ER versus biological response of primary breast cancer to 2 weeks' aromatase inhibitor treatment as measured by change in Ki67.
Cases were selected from the aromatase inhibitor treatment group of POETIC. We selected the 15% with the poorest Ki67 response (PR, < 40% Ki67 suppression, n = 230) and a random 30% of the remainder categorised as intermediate (IR, 40-79% Ki67 suppression, n = 150) and good-responders (GR, ≥ 80% Ki67 suppression, n = 230) from HER2 - group. All HER2 + cases available were selected irrespective of their response category (n = 317). ER expression was measured by IHC and qPCR.
ER IHC was available from 515 HER2 - and 186 HER2 + tumours and ER qPCR from 367 HER2 - and 171 HER2 + tumours. Ninety-one percentage of patients with ER IHC < 10% were PRs with similar rates in HER2 - and HER2 + cases. At or above ER IHC 10% substantial numbers of patients showed IR or GR. Similar proportions of patients were defined by cut-points of ER IHC < 10% and ER mRNA < 5 units. In addition, loss of PgR expression altered ER anti-proliferation response with 92% of PgR - cases with ER IHC < 40% being PRs.
There was little responsiveness at IHC < 10% and no distinction between < 1% and 1-10% cells positive. Similar separation of PRs from IR/GRs was achieved by IHC and mRNA.]]></abstract><cop>England</cop><pub>BioMed Central Ltd</pub><pmid>36096872</pmid><doi>10.1186/s13058-022-01556-6</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Analysis Aromatase Aromatase inhibitors Aromatase Inhibitors - pharmacology Aromatase Inhibitors - therapeutic use Breast cancer Breast Neoplasms - drug therapy Breast Neoplasms - genetics Cancer therapies Cloning Endocrine therapy ErbB-2 protein ESR1 Estrogen Female Gene expression Humans Immunohistochemistry Ki-67 Antigen - genetics Ki-67 Antigen - metabolism Ki67 Messenger RNA mRNA Patients PgR Proteins Receptor, ErbB-2 - genetics Receptor, ErbB-2 - metabolism Receptors, Estrogen - genetics Receptors, Estrogen - metabolism Receptors, Progesterone - metabolism RNA, Messenger - genetics Tumors |
| title | Relationship between ER expression by IHC or mRNA with Ki67 response to aromatase inhibition: a POETIC study |
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