Molecular apocrine tumours in EORTC 10994/BIG 1-00 phase III study: pathological response after neoadjuvant chemotherapy and clinical outcomes

Background We explored, within the EORTC10994 study, the outcomes for patients with molecular apocrine (MA) breast cancer, and defined immunohistochemistry (IHC) as androgen-receptor (AR) positive, oestrogen (ER) and progesterone (PR) negative. We also assessed the concordance between IHC and gene e...

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Veröffentlicht in:British journal of cancer 2019-04, Vol.120 (9), p.913-921
Hauptverfasser: Bonnefoi, Hervé, MacGrogan, Gaetan, Poncet, Coralie, Iggo, Richard, Pommeret, Fanny, Grellety, Thomas, Larsimont, Denis, Bécette, Véronique, Kerdraon, Olivier, Bibeau, Frédéric, Ghnassia, Jean-Pierre, Picquenot, Jean-Michel, Thomas, Jeremy, Tille, Jean-Christophe, Slaets, Leen, Bodmer, Alexandre, Bergh, Jonas, Cameron, David
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container_end_page 921
container_issue 9
container_start_page 913
container_title British journal of cancer
container_volume 120
creator Bonnefoi, Hervé
MacGrogan, Gaetan
Poncet, Coralie
Iggo, Richard
Pommeret, Fanny
Grellety, Thomas
Larsimont, Denis
Bécette, Véronique
Kerdraon, Olivier
Bibeau, Frédéric
Ghnassia, Jean-Pierre
Picquenot, Jean-Michel
Thomas, Jeremy
Tille, Jean-Christophe
Slaets, Leen
Bodmer, Alexandre
Bergh, Jonas
Cameron, David
description Background We explored, within the EORTC10994 study, the outcomes for patients with molecular apocrine (MA) breast cancer, and defined immunohistochemistry (IHC) as androgen-receptor (AR) positive, oestrogen (ER) and progesterone (PR) negative. We also assessed the concordance between IHC and gene expression arrays (GEA) in the identification of MA cancers. Methods Centrally assessed biopsies for AR, ER, PR, HER2 and Ki67 by IHC were classified into six subtypes: MA, triple-negative (TN) basal-like, luminal A, luminal B HER2 negative, luminal B HER2 positive and “other”. The two main objectives were the pCR rates and survival outcomes in the overall MA subtype (and further divided by HER2 status) and the remaining five subtypes. Results IHC subtyping was obtained in 846 eligible patients. Ninety-three (11%) tumours were classified as the MA subtype. Both IHC and GEA data were available for 64 patients. In this subset, IHC concordance was 88.3% in identifying MA tumours compared with GEA. Within the MA subtype, pCR was observed in 33.3% of the patients (95% CI: 29.4–43.9) and the 5-year recurrence-free interval was 59.2% (95% CI: 48.2–68.6). Patients with MA and TN basal-like tumours have lower survival outcomes. Conclusions Irrespective of their HER2 status, the prognosis for MA tumours remains poor and adjuvant trials evaluating anti-androgens should be considered.
doi_str_mv 10.1038/s41416-019-0420-y
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We also assessed the concordance between IHC and gene expression arrays (GEA) in the identification of MA cancers. Methods Centrally assessed biopsies for AR, ER, PR, HER2 and Ki67 by IHC were classified into six subtypes: MA, triple-negative (TN) basal-like, luminal A, luminal B HER2 negative, luminal B HER2 positive and “other”. The two main objectives were the pCR rates and survival outcomes in the overall MA subtype (and further divided by HER2 status) and the remaining five subtypes. Results IHC subtyping was obtained in 846 eligible patients. Ninety-three (11%) tumours were classified as the MA subtype. Both IHC and GEA data were available for 64 patients. In this subset, IHC concordance was 88.3% in identifying MA tumours compared with GEA. Within the MA subtype, pCR was observed in 33.3% of the patients (95% CI: 29.4–43.9) and the 5-year recurrence-free interval was 59.2% (95% CI: 48.2–68.6). Patients with MA and TN basal-like tumours have lower survival outcomes. Conclusions Irrespective of their HER2 status, the prognosis for MA tumours remains poor and adjuvant trials evaluating anti-androgens should be considered.</description><identifier>ISSN: 0007-0920</identifier><identifier>ISSN: 1532-1827</identifier><identifier>EISSN: 1532-1827</identifier><identifier>DOI: 10.1038/s41416-019-0420-y</identifier><identifier>PMID: 30899086</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>631/67/1347 ; Androgen receptors ; Androgens ; Antineoplastic Combined Chemotherapy Protocols - therapeutic use ; Biomedical and Life Sciences ; Biomedicine ; Breast cancer ; Breast Neoplasms - drug therapy ; Breast Neoplasms - genetics ; Breast Neoplasms - metabolism ; Breast Neoplasms - surgery ; Cancer ; Cancer Research ; Chemotherapy ; Chemotherapy, Adjuvant ; Clinical trials ; Disease-Free Survival ; Drug Resistance ; Epidemiology ; ErbB Receptors - metabolism ; ErbB-2 protein ; Estrogens ; Female ; Gene expression ; Gene Expression Profiling ; Humans ; Immunohistochemistry ; Life Sciences ; Medical prognosis ; Medicin och hälsovetenskap ; Molecular Medicine ; Oncology ; Pharmaceutical sciences ; Pharmacology ; Progesterone ; Receptor, ErbB-2 - metabolism ; Receptors, Androgen - metabolism ; Receptors, Estrogen - metabolism ; Receptors, Progesterone - metabolism ; Survival ; Survival Rate ; Treatment Outcome ; Tumors</subject><ispartof>British journal of cancer, 2019-04, Vol.120 (9), p.913-921</ispartof><rights>Cancer Research UK 2019</rights><rights>This work is published under https://creativecommons.org/licenses/by/4.0/ (the “License”). 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We also assessed the concordance between IHC and gene expression arrays (GEA) in the identification of MA cancers. Methods Centrally assessed biopsies for AR, ER, PR, HER2 and Ki67 by IHC were classified into six subtypes: MA, triple-negative (TN) basal-like, luminal A, luminal B HER2 negative, luminal B HER2 positive and “other”. The two main objectives were the pCR rates and survival outcomes in the overall MA subtype (and further divided by HER2 status) and the remaining five subtypes. Results IHC subtyping was obtained in 846 eligible patients. Ninety-three (11%) tumours were classified as the MA subtype. Both IHC and GEA data were available for 64 patients. In this subset, IHC concordance was 88.3% in identifying MA tumours compared with GEA. Within the MA subtype, pCR was observed in 33.3% of the patients (95% CI: 29.4–43.9) and the 5-year recurrence-free interval was 59.2% (95% CI: 48.2–68.6). Patients with MA and TN basal-like tumours have lower survival outcomes. Conclusions Irrespective of their HER2 status, the prognosis for MA tumours remains poor and adjuvant trials evaluating anti-androgens should be considered.</description><subject>631/67/1347</subject><subject>Androgen receptors</subject><subject>Androgens</subject><subject>Antineoplastic Combined Chemotherapy Protocols - therapeutic use</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Breast cancer</subject><subject>Breast Neoplasms - drug therapy</subject><subject>Breast Neoplasms - genetics</subject><subject>Breast Neoplasms - metabolism</subject><subject>Breast Neoplasms - surgery</subject><subject>Cancer</subject><subject>Cancer Research</subject><subject>Chemotherapy</subject><subject>Chemotherapy, Adjuvant</subject><subject>Clinical trials</subject><subject>Disease-Free Survival</subject><subject>Drug Resistance</subject><subject>Epidemiology</subject><subject>ErbB Receptors - metabolism</subject><subject>ErbB-2 protein</subject><subject>Estrogens</subject><subject>Female</subject><subject>Gene expression</subject><subject>Gene Expression Profiling</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>Life Sciences</subject><subject>Medical prognosis</subject><subject>Medicin och hälsovetenskap</subject><subject>Molecular Medicine</subject><subject>Oncology</subject><subject>Pharmaceutical sciences</subject><subject>Pharmacology</subject><subject>Progesterone</subject><subject>Receptor, ErbB-2 - metabolism</subject><subject>Receptors, Androgen - metabolism</subject><subject>Receptors, Estrogen - metabolism</subject><subject>Receptors, Progesterone - metabolism</subject><subject>Survival</subject><subject>Survival Rate</subject><subject>Treatment Outcome</subject><subject>Tumors</subject><issn>0007-0920</issn><issn>1532-1827</issn><issn>1532-1827</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><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>D8T</sourceid><recordid>eNp1Uk1v1DAQjRCIbgs_gAuyxAUOoWPHcWwOSGVV2pUWVULlbDmOs8mS2MFOFu2f6G_G2922tFJPHs-8N58vSd5h-Iwh46eBYopZClikQAmk2xfJDOcZSTEnxctkBgBFCoLAUXIcwjp-BfDidXKUARfRZLPk5ofrjJ465ZEanPatNWicejf5gFqLzq9-Xs8RBiHo6bfFBcIpABoaFQxaLBYojFO1_YIGNTauc6tWqw55EwZnI0DVo_HIGqeq9bRRdkS6Mb0bG-PVsEXKVkh3rb0luWnUrjfhTfKqVl0wbw_vSfLr-_n1_DJdXl0s5mfLVOeCjGmcuix5JYoaBOOKYJVnTFeCckJBs0LUhaGiypgpBQeis7rUGc8x4JJUlcDZSZLu84a_ZphKOfi2V34rnWrlwfU7WkZSHofnES-exQ_eVQ-kOyKmwIEySiP3654bAb2ptLGjV93jFI8itm3kym0kKzLK8l3xT_sEzRPa5dlS7nxACCc5Z5vdYB8Pxbz7M5kwyr4N2nSdioeYgiRYsDz2dtvXhyfQdTy7jWuXhOCC5jxneUThPUp7F4I39X0HGOROhXKvQhlVKHcqlNvIef__xPeMO9lFADmsM4bsyviH0s9n_QdKvukp</recordid><startdate>20190430</startdate><enddate>20190430</enddate><creator>Bonnefoi, Hervé</creator><creator>MacGrogan, Gaetan</creator><creator>Poncet, Coralie</creator><creator>Iggo, Richard</creator><creator>Pommeret, Fanny</creator><creator>Grellety, Thomas</creator><creator>Larsimont, Denis</creator><creator>Bécette, Véronique</creator><creator>Kerdraon, Olivier</creator><creator>Bibeau, Frédéric</creator><creator>Ghnassia, Jean-Pierre</creator><creator>Picquenot, Jean-Michel</creator><creator>Thomas, Jeremy</creator><creator>Tille, Jean-Christophe</creator><creator>Slaets, Leen</creator><creator>Bodmer, Alexandre</creator><creator>Bergh, Jonas</creator><creator>Cameron, David</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><general>Cancer Research UK</general><scope>C6C</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>7RV</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB0</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>1XC</scope><scope>VOOES</scope><scope>5PM</scope><scope>ADTPV</scope><scope>AOWAS</scope><scope>D8T</scope><scope>ZZAVC</scope></search><sort><creationdate>20190430</creationdate><title>Molecular apocrine tumours in EORTC 10994/BIG 1-00 phase III study: pathological response after neoadjuvant chemotherapy and clinical outcomes</title><author>Bonnefoi, Hervé ; MacGrogan, Gaetan ; Poncet, Coralie ; Iggo, Richard ; Pommeret, Fanny ; Grellety, Thomas ; Larsimont, Denis ; Bécette, Véronique ; Kerdraon, Olivier ; Bibeau, Frédéric ; Ghnassia, Jean-Pierre ; Picquenot, Jean-Michel ; Thomas, Jeremy ; Tille, Jean-Christophe ; Slaets, Leen ; Bodmer, Alexandre ; Bergh, Jonas ; Cameron, David</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c592t-416bb8d97f0968a21a536cd948240c679f7e49d36eb9802c3fbc385101b2dd913</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>631/67/1347</topic><topic>Androgen receptors</topic><topic>Androgens</topic><topic>Antineoplastic Combined Chemotherapy Protocols - therapeutic use</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Breast cancer</topic><topic>Breast Neoplasms - drug therapy</topic><topic>Breast Neoplasms - genetics</topic><topic>Breast Neoplasms - metabolism</topic><topic>Breast Neoplasms - surgery</topic><topic>Cancer</topic><topic>Cancer Research</topic><topic>Chemotherapy</topic><topic>Chemotherapy, Adjuvant</topic><topic>Clinical trials</topic><topic>Disease-Free Survival</topic><topic>Drug Resistance</topic><topic>Epidemiology</topic><topic>ErbB Receptors - metabolism</topic><topic>ErbB-2 protein</topic><topic>Estrogens</topic><topic>Female</topic><topic>Gene expression</topic><topic>Gene Expression Profiling</topic><topic>Humans</topic><topic>Immunohistochemistry</topic><topic>Life Sciences</topic><topic>Medical prognosis</topic><topic>Medicin och hälsovetenskap</topic><topic>Molecular Medicine</topic><topic>Oncology</topic><topic>Pharmaceutical sciences</topic><topic>Pharmacology</topic><topic>Progesterone</topic><topic>Receptor, ErbB-2 - metabolism</topic><topic>Receptors, Androgen - metabolism</topic><topic>Receptors, Estrogen - metabolism</topic><topic>Receptors, Progesterone - metabolism</topic><topic>Survival</topic><topic>Survival Rate</topic><topic>Treatment Outcome</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Bonnefoi, Hervé</creatorcontrib><creatorcontrib>MacGrogan, Gaetan</creatorcontrib><creatorcontrib>Poncet, Coralie</creatorcontrib><creatorcontrib>Iggo, Richard</creatorcontrib><creatorcontrib>Pommeret, Fanny</creatorcontrib><creatorcontrib>Grellety, Thomas</creatorcontrib><creatorcontrib>Larsimont, Denis</creatorcontrib><creatorcontrib>Bécette, Véronique</creatorcontrib><creatorcontrib>Kerdraon, Olivier</creatorcontrib><creatorcontrib>Bibeau, Frédéric</creatorcontrib><creatorcontrib>Ghnassia, Jean-Pierre</creatorcontrib><creatorcontrib>Picquenot, Jean-Michel</creatorcontrib><creatorcontrib>Thomas, Jeremy</creatorcontrib><creatorcontrib>Tille, Jean-Christophe</creatorcontrib><creatorcontrib>Slaets, Leen</creatorcontrib><creatorcontrib>Bodmer, Alexandre</creatorcontrib><creatorcontrib>Bergh, Jonas</creatorcontrib><creatorcontrib>Cameron, David</creatorcontrib><creatorcontrib>EORTC 10994/BIG 1-00 study investigators</creatorcontrib><creatorcontrib>and on behalf of the EORTC 10994/BIG 1-00 study investigators</creatorcontrib><collection>SpringerOpen</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 Nursing and Allied Health Journals</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>ProQuest Health &amp; 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Medical Complete (Alumni)</collection><collection>Nursing &amp; Allied Health Database (Alumni Edition)</collection><collection>Biological Sciences</collection><collection>Health &amp; Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</collection><collection>Biological Science Database</collection><collection>Nursing &amp; Allied Health Premium</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>Hyper Article en Ligne (HAL)</collection><collection>Hyper Article en Ligne (HAL) (Open Access)</collection><collection>PubMed Central (Full Participant titles)</collection><collection>SwePub</collection><collection>SwePub Articles</collection><collection>SWEPUB Freely available online</collection><collection>SwePub Articles full text</collection><jtitle>British journal of cancer</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Bonnefoi, Hervé</au><au>MacGrogan, Gaetan</au><au>Poncet, Coralie</au><au>Iggo, Richard</au><au>Pommeret, Fanny</au><au>Grellety, Thomas</au><au>Larsimont, Denis</au><au>Bécette, Véronique</au><au>Kerdraon, Olivier</au><au>Bibeau, Frédéric</au><au>Ghnassia, Jean-Pierre</au><au>Picquenot, Jean-Michel</au><au>Thomas, Jeremy</au><au>Tille, Jean-Christophe</au><au>Slaets, Leen</au><au>Bodmer, Alexandre</au><au>Bergh, Jonas</au><au>Cameron, David</au><aucorp>EORTC 10994/BIG 1-00 study investigators</aucorp><aucorp>and on behalf of the EORTC 10994/BIG 1-00 study investigators</aucorp><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Molecular apocrine tumours in EORTC 10994/BIG 1-00 phase III study: pathological response after neoadjuvant chemotherapy and clinical outcomes</atitle><jtitle>British journal of cancer</jtitle><stitle>Br J Cancer</stitle><addtitle>Br J Cancer</addtitle><date>2019-04-30</date><risdate>2019</risdate><volume>120</volume><issue>9</issue><spage>913</spage><epage>921</epage><pages>913-921</pages><issn>0007-0920</issn><issn>1532-1827</issn><eissn>1532-1827</eissn><abstract>Background We explored, within the EORTC10994 study, the outcomes for patients with molecular apocrine (MA) breast cancer, and defined immunohistochemistry (IHC) as androgen-receptor (AR) positive, oestrogen (ER) and progesterone (PR) negative. We also assessed the concordance between IHC and gene expression arrays (GEA) in the identification of MA cancers. Methods Centrally assessed biopsies for AR, ER, PR, HER2 and Ki67 by IHC were classified into six subtypes: MA, triple-negative (TN) basal-like, luminal A, luminal B HER2 negative, luminal B HER2 positive and “other”. The two main objectives were the pCR rates and survival outcomes in the overall MA subtype (and further divided by HER2 status) and the remaining five subtypes. Results IHC subtyping was obtained in 846 eligible patients. Ninety-three (11%) tumours were classified as the MA subtype. Both IHC and GEA data were available for 64 patients. In this subset, IHC concordance was 88.3% in identifying MA tumours compared with GEA. Within the MA subtype, pCR was observed in 33.3% of the patients (95% CI: 29.4–43.9) and the 5-year recurrence-free interval was 59.2% (95% CI: 48.2–68.6). Patients with MA and TN basal-like tumours have lower survival outcomes. Conclusions Irrespective of their HER2 status, the prognosis for MA tumours remains poor and adjuvant trials evaluating anti-androgens should be considered.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>30899086</pmid><doi>10.1038/s41416-019-0420-y</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record>
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identifier ISSN: 0007-0920
ispartof British journal of cancer, 2019-04, Vol.120 (9), p.913-921
issn 0007-0920
1532-1827
1532-1827
language eng
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source PubMed (Medline); MEDLINE; SpringerLink; SWEPUB Freely available online; EZB Electronic Journals Library
subjects 631/67/1347
Androgen receptors
Androgens
Antineoplastic Combined Chemotherapy Protocols - therapeutic use
Biomedical and Life Sciences
Biomedicine
Breast cancer
Breast Neoplasms - drug therapy
Breast Neoplasms - genetics
Breast Neoplasms - metabolism
Breast Neoplasms - surgery
Cancer
Cancer Research
Chemotherapy
Chemotherapy, Adjuvant
Clinical trials
Disease-Free Survival
Drug Resistance
Epidemiology
ErbB Receptors - metabolism
ErbB-2 protein
Estrogens
Female
Gene expression
Gene Expression Profiling
Humans
Immunohistochemistry
Life Sciences
Medical prognosis
Medicin och hälsovetenskap
Molecular Medicine
Oncology
Pharmaceutical sciences
Pharmacology
Progesterone
Receptor, ErbB-2 - metabolism
Receptors, Androgen - metabolism
Receptors, Estrogen - metabolism
Receptors, Progesterone - metabolism
Survival
Survival Rate
Treatment Outcome
Tumors
title Molecular apocrine tumours in EORTC 10994/BIG 1-00 phase III study: pathological response after neoadjuvant chemotherapy and clinical outcomes
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