BluePrint breast cancer molecular subtyping recognizes single and dual subtype tumors with implications for therapeutic guidance
Purpose BluePrint (BP) is an 80-gene molecular subtyping test that classifies early-stage breast cancer (EBC) into Basal, Luminal, and HER2 subtypes. In most cases, breast tumors have one dominant subtype, representative of a single activated pathway. However, some tumors show a statistically equal...
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| Veröffentlicht in: | Breast cancer research and treatment 2022-10, Vol.195 (3), p.263-274 |
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| creator | Kuilman, Midas M. Ellappalayam, Architha Barcaru, Andrei Haan, Josien C. Bhaskaran, Rajith Wehkamp, Diederik Menicucci, Andrea R. Audeh, William M. Mittempergher, Lorenza Glas, Annuska M. |
| description | Purpose
BluePrint (BP) is an 80-gene molecular subtyping test that classifies early-stage breast cancer (EBC) into Basal, Luminal, and HER2 subtypes. In most cases, breast tumors have one dominant subtype, representative of a single activated pathway. However, some tumors show a statistically equal representation of more than one subtype, referred to as dual subtype. This study aims to identify and examine dual subtype tumors by BP to understand their biology and possible implications for treatment guidance.
Methods
The BP scores of over 15,000 tumor samples from EBC patients were analyzed, and the differences between the highest and the lowest scoring subtypes were calculated. Based upon the distribution of the differences between BP scores, a threshold was determined for each subtype to identify dual versus single subtypes.
Results
Approximately 97% of samples had one single activated BluePrint molecular subtype, whereas ~ 3% of samples were classified as BP dual subtype. The most frequently occurring dual subtypes were the Luminal-Basal-type and Luminal-HER2-type. Luminal-Basal-type displays a distinct biology from the Luminal single type and Basal single type. Burstein’s classification of the single and dual Basal samples showed that the Luminal-Basal-type is mostly classified as ‘luminal androgen receptor’ and ‘mesenchymal’ subtypes, supporting molecular evidence of AR activation in the Luminal-Basal-type tumors. Tumors classified as Luminal-HER2-type resemble features of both Luminal-single-type and HER2-single-type. However, patients with dual Luminal-HER2-type have a lower pathological complete response after receiving HER2-targeted therapies in addition to chemotherapy in comparison with patients with a HER2-single-type.
Conclusion
This study demonstrates that BP identifies tumors with two active functional pathways (dual subtype) with specific transcriptional characteristics and highlights the added value of distinguishing BP dual from single subtypes as evidenced by distinct treatment response rates. |
| doi_str_mv | 10.1007/s10549-022-06698-x |
| format | Article |
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BluePrint (BP) is an 80-gene molecular subtyping test that classifies early-stage breast cancer (EBC) into Basal, Luminal, and HER2 subtypes. In most cases, breast tumors have one dominant subtype, representative of a single activated pathway. However, some tumors show a statistically equal representation of more than one subtype, referred to as dual subtype. This study aims to identify and examine dual subtype tumors by BP to understand their biology and possible implications for treatment guidance.
Methods
The BP scores of over 15,000 tumor samples from EBC patients were analyzed, and the differences between the highest and the lowest scoring subtypes were calculated. Based upon the distribution of the differences between BP scores, a threshold was determined for each subtype to identify dual versus single subtypes.
Results
Approximately 97% of samples had one single activated BluePrint molecular subtype, whereas ~ 3% of samples were classified as BP dual subtype. The most frequently occurring dual subtypes were the Luminal-Basal-type and Luminal-HER2-type. Luminal-Basal-type displays a distinct biology from the Luminal single type and Basal single type. Burstein’s classification of the single and dual Basal samples showed that the Luminal-Basal-type is mostly classified as ‘luminal androgen receptor’ and ‘mesenchymal’ subtypes, supporting molecular evidence of AR activation in the Luminal-Basal-type tumors. Tumors classified as Luminal-HER2-type resemble features of both Luminal-single-type and HER2-single-type. However, patients with dual Luminal-HER2-type have a lower pathological complete response after receiving HER2-targeted therapies in addition to chemotherapy in comparison with patients with a HER2-single-type.
Conclusion
This study demonstrates that BP identifies tumors with two active functional pathways (dual subtype) with specific transcriptional characteristics and highlights the added value of distinguishing BP dual from single subtypes as evidenced by distinct treatment response rates.</description><identifier>ISSN: 0167-6806</identifier><identifier>ISSN: 1573-7217</identifier><identifier>EISSN: 1573-7217</identifier><identifier>DOI: 10.1007/s10549-022-06698-x</identifier><identifier>PMID: 35984580</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Analysis ; Androgen receptors ; Biomarkers, Tumor - genetics ; Biomarkers, Tumor - metabolism ; Breast cancer ; Breast Neoplasms - drug therapy ; Breast Neoplasms - therapy ; Cancer ; Cancer research ; Care and treatment ; Chemotherapy ; ErbB-2 protein ; Female ; Humans ; Medicine ; Medicine & Public Health ; Mesenchyme ; Oncology ; Patients ; Preclinical Study ; Receptor, ErbB-2 - genetics ; Receptor, ErbB-2 - metabolism ; Receptors, Progesterone - metabolism ; Tumors</subject><ispartof>Breast cancer research and treatment, 2022-10, Vol.195 (3), p.263-274</ispartof><rights>The Author(s) 2022</rights><rights>2022. The Author(s).</rights><rights>COPYRIGHT 2022 Springer</rights><rights>The Author(s) 2022. This work is published 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><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c572t-40f628134646838b3bf30340b3b6f4c558a397d8e26d15bb9d077b4a8cba3fce3</citedby><cites>FETCH-LOGICAL-c572t-40f628134646838b3bf30340b3b6f4c558a397d8e26d15bb9d077b4a8cba3fce3</cites><orcidid>0000-0002-0775-138X ; 0000-0003-3425-3965</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s10549-022-06698-x$$EPDF$$P50$$Gspringer$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s10549-022-06698-x$$EHTML$$P50$$Gspringer$$Hfree_for_read</linktohtml><link.rule.ids>230,314,780,784,885,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/35984580$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kuilman, Midas M.</creatorcontrib><creatorcontrib>Ellappalayam, Architha</creatorcontrib><creatorcontrib>Barcaru, Andrei</creatorcontrib><creatorcontrib>Haan, Josien C.</creatorcontrib><creatorcontrib>Bhaskaran, Rajith</creatorcontrib><creatorcontrib>Wehkamp, Diederik</creatorcontrib><creatorcontrib>Menicucci, Andrea R.</creatorcontrib><creatorcontrib>Audeh, William M.</creatorcontrib><creatorcontrib>Mittempergher, Lorenza</creatorcontrib><creatorcontrib>Glas, Annuska M.</creatorcontrib><title>BluePrint breast cancer molecular subtyping recognizes single and dual subtype tumors with implications for therapeutic guidance</title><title>Breast cancer research and treatment</title><addtitle>Breast Cancer Res Treat</addtitle><addtitle>Breast Cancer Res Treat</addtitle><description>Purpose
BluePrint (BP) is an 80-gene molecular subtyping test that classifies early-stage breast cancer (EBC) into Basal, Luminal, and HER2 subtypes. In most cases, breast tumors have one dominant subtype, representative of a single activated pathway. However, some tumors show a statistically equal representation of more than one subtype, referred to as dual subtype. This study aims to identify and examine dual subtype tumors by BP to understand their biology and possible implications for treatment guidance.
Methods
The BP scores of over 15,000 tumor samples from EBC patients were analyzed, and the differences between the highest and the lowest scoring subtypes were calculated. Based upon the distribution of the differences between BP scores, a threshold was determined for each subtype to identify dual versus single subtypes.
Results
Approximately 97% of samples had one single activated BluePrint molecular subtype, whereas ~ 3% of samples were classified as BP dual subtype. The most frequently occurring dual subtypes were the Luminal-Basal-type and Luminal-HER2-type. Luminal-Basal-type displays a distinct biology from the Luminal single type and Basal single type. Burstein’s classification of the single and dual Basal samples showed that the Luminal-Basal-type is mostly classified as ‘luminal androgen receptor’ and ‘mesenchymal’ subtypes, supporting molecular evidence of AR activation in the Luminal-Basal-type tumors. Tumors classified as Luminal-HER2-type resemble features of both Luminal-single-type and HER2-single-type. However, patients with dual Luminal-HER2-type have a lower pathological complete response after receiving HER2-targeted therapies in addition to chemotherapy in comparison with patients with a HER2-single-type.
Conclusion
This study demonstrates that BP identifies tumors with two active functional pathways (dual subtype) with specific transcriptional characteristics and highlights the added value of distinguishing BP dual from single subtypes as evidenced by distinct treatment response rates.</description><subject>Analysis</subject><subject>Androgen receptors</subject><subject>Biomarkers, Tumor - genetics</subject><subject>Biomarkers, Tumor - metabolism</subject><subject>Breast cancer</subject><subject>Breast Neoplasms - drug therapy</subject><subject>Breast Neoplasms - therapy</subject><subject>Cancer</subject><subject>Cancer research</subject><subject>Care and treatment</subject><subject>Chemotherapy</subject><subject>ErbB-2 protein</subject><subject>Female</subject><subject>Humans</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Mesenchyme</subject><subject>Oncology</subject><subject>Patients</subject><subject>Preclinical Study</subject><subject>Receptor, ErbB-2 - genetics</subject><subject>Receptor, ErbB-2 - metabolism</subject><subject>Receptors, Progesterone - metabolism</subject><subject>Tumors</subject><issn>0167-6806</issn><issn>1573-7217</issn><issn>1573-7217</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><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>eNp9kk1v1DAQhiMEomXhD3BAlpAQlxQ7TmznglQqvqRKcICz5TiTrCvHXvwBLSd-Ot7u0nYRQj74Y555RzN-q-opwScEY_4qEty1fY2bpsaM9aK-vFcdk47TmjeE36-OMWG8ZgKzo-pRjBcY457j_mF1RLtetJ3Ax9WvNzbD52BcQkMAFRPSymkIaPEWdLYqoJiHdLUxbkYBtJ-d-QkRxXK3gJQb0ZiV3UOAUl58iOiHSWtklo01WiXjXUSTDyitIagN5GQ0mrMZt5UeVw8mZSM82e-r6uu7t1_OPtTnn95_PDs9r3XHm1S3eGKNILRlLRNUDHSYKKYtLgc2tbrrhKI9HwU0bCTdMPQj5nxoldCDopMGuqpe73Q3eVhg1OBSUFZugllUuJJeGXkYcWYtZ_9d9qUkL0NdVS_3AsF_yxCTXEzUYK1y4HOUDcetKONtSUGf_4Ve-Bxcaa9QpGFdy0VzS83KgjRu8qWu3orKU06KkqAMF-rkH1RZIyxGeweTKe8HCS_uJKxB2bSO3ubrbzgEmx2og48xwHQzDILl1mByZzBZDCavDSYvS9Kzu2O8SfnjqALQHRBLyM0Qbnv_j-xv4iDd5g</recordid><startdate>20221001</startdate><enddate>20221001</enddate><creator>Kuilman, Midas M.</creator><creator>Ellappalayam, Architha</creator><creator>Barcaru, Andrei</creator><creator>Haan, Josien C.</creator><creator>Bhaskaran, Rajith</creator><creator>Wehkamp, Diederik</creator><creator>Menicucci, Andrea R.</creator><creator>Audeh, William M.</creator><creator>Mittempergher, Lorenza</creator><creator>Glas, Annuska M.</creator><general>Springer US</general><general>Springer</general><general>Springer Nature B.V</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>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>Q9U</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-0775-138X</orcidid><orcidid>https://orcid.org/0000-0003-3425-3965</orcidid></search><sort><creationdate>20221001</creationdate><title>BluePrint breast cancer molecular subtyping recognizes single and dual subtype tumors with implications for therapeutic guidance</title><author>Kuilman, Midas M. ; Ellappalayam, Architha ; Barcaru, Andrei ; Haan, Josien C. ; Bhaskaran, Rajith ; Wehkamp, Diederik ; Menicucci, Andrea R. ; Audeh, William M. ; Mittempergher, Lorenza ; Glas, Annuska M.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c572t-40f628134646838b3bf30340b3b6f4c558a397d8e26d15bb9d077b4a8cba3fce3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Analysis</topic><topic>Androgen receptors</topic><topic>Biomarkers, Tumor - genetics</topic><topic>Biomarkers, Tumor - metabolism</topic><topic>Breast cancer</topic><topic>Breast Neoplasms - drug therapy</topic><topic>Breast Neoplasms - therapy</topic><topic>Cancer</topic><topic>Cancer research</topic><topic>Care and treatment</topic><topic>Chemotherapy</topic><topic>ErbB-2 protein</topic><topic>Female</topic><topic>Humans</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Mesenchyme</topic><topic>Oncology</topic><topic>Patients</topic><topic>Preclinical Study</topic><topic>Receptor, ErbB-2 - genetics</topic><topic>Receptor, ErbB-2 - metabolism</topic><topic>Receptors, Progesterone - metabolism</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kuilman, Midas M.</creatorcontrib><creatorcontrib>Ellappalayam, Architha</creatorcontrib><creatorcontrib>Barcaru, Andrei</creatorcontrib><creatorcontrib>Haan, Josien C.</creatorcontrib><creatorcontrib>Bhaskaran, Rajith</creatorcontrib><creatorcontrib>Wehkamp, Diederik</creatorcontrib><creatorcontrib>Menicucci, Andrea R.</creatorcontrib><creatorcontrib>Audeh, William M.</creatorcontrib><creatorcontrib>Mittempergher, Lorenza</creatorcontrib><creatorcontrib>Glas, Annuska M.</creatorcontrib><collection>Springer Nature OA Free Journals</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>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 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>Kuilman, Midas M.</au><au>Ellappalayam, Architha</au><au>Barcaru, Andrei</au><au>Haan, Josien C.</au><au>Bhaskaran, Rajith</au><au>Wehkamp, Diederik</au><au>Menicucci, Andrea R.</au><au>Audeh, William M.</au><au>Mittempergher, Lorenza</au><au>Glas, Annuska M.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>BluePrint breast cancer molecular subtyping recognizes single and dual subtype tumors with implications for therapeutic guidance</atitle><jtitle>Breast cancer research and treatment</jtitle><stitle>Breast Cancer Res Treat</stitle><addtitle>Breast Cancer Res Treat</addtitle><date>2022-10-01</date><risdate>2022</risdate><volume>195</volume><issue>3</issue><spage>263</spage><epage>274</epage><pages>263-274</pages><issn>0167-6806</issn><issn>1573-7217</issn><eissn>1573-7217</eissn><abstract>Purpose
BluePrint (BP) is an 80-gene molecular subtyping test that classifies early-stage breast cancer (EBC) into Basal, Luminal, and HER2 subtypes. In most cases, breast tumors have one dominant subtype, representative of a single activated pathway. However, some tumors show a statistically equal representation of more than one subtype, referred to as dual subtype. This study aims to identify and examine dual subtype tumors by BP to understand their biology and possible implications for treatment guidance.
Methods
The BP scores of over 15,000 tumor samples from EBC patients were analyzed, and the differences between the highest and the lowest scoring subtypes were calculated. Based upon the distribution of the differences between BP scores, a threshold was determined for each subtype to identify dual versus single subtypes.
Results
Approximately 97% of samples had one single activated BluePrint molecular subtype, whereas ~ 3% of samples were classified as BP dual subtype. The most frequently occurring dual subtypes were the Luminal-Basal-type and Luminal-HER2-type. Luminal-Basal-type displays a distinct biology from the Luminal single type and Basal single type. Burstein’s classification of the single and dual Basal samples showed that the Luminal-Basal-type is mostly classified as ‘luminal androgen receptor’ and ‘mesenchymal’ subtypes, supporting molecular evidence of AR activation in the Luminal-Basal-type tumors. Tumors classified as Luminal-HER2-type resemble features of both Luminal-single-type and HER2-single-type. However, patients with dual Luminal-HER2-type have a lower pathological complete response after receiving HER2-targeted therapies in addition to chemotherapy in comparison with patients with a HER2-single-type.
Conclusion
This study demonstrates that BP identifies tumors with two active functional pathways (dual subtype) with specific transcriptional characteristics and highlights the added value of distinguishing BP dual from single subtypes as evidenced by distinct treatment response rates.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>35984580</pmid><doi>10.1007/s10549-022-06698-x</doi><tpages>12</tpages><orcidid>https://orcid.org/0000-0002-0775-138X</orcidid><orcidid>https://orcid.org/0000-0003-3425-3965</orcidid><oa>free_for_read</oa></addata></record> |
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| ispartof | Breast cancer research and treatment, 2022-10, Vol.195 (3), p.263-274 |
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| subjects | Analysis Androgen receptors Biomarkers, Tumor - genetics Biomarkers, Tumor - metabolism Breast cancer Breast Neoplasms - drug therapy Breast Neoplasms - therapy Cancer Cancer research Care and treatment Chemotherapy ErbB-2 protein Female Humans Medicine Medicine & Public Health Mesenchyme Oncology Patients Preclinical Study Receptor, ErbB-2 - genetics Receptor, ErbB-2 - metabolism Receptors, Progesterone - metabolism Tumors |
| title | BluePrint breast cancer molecular subtyping recognizes single and dual subtype tumors with implications for therapeutic guidance |
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