Pre-Clinical Rationale for Amcenestrant Combinations in HER2+/ER+ Breast Cancer
HER2-positive/oestrogen receptor-positive (HER2+/ER+) represents a unique breast cancer subtype. The use of individual HER2- or ER-targeting agents can lead to the acquisition of therapeutic resistance due to compensatory receptor crosstalk. New drug combinations targeting HER2 and ER could improve...
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| Veröffentlicht in: | International journal of molecular sciences 2025-01, Vol.26 (2), p.460 |
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| creator | Mahdi, Amira F Ashfield, Niall Crown, John Collins, Denis M |
| description | HER2-positive/oestrogen receptor-positive (HER2+/ER+) represents a unique breast cancer subtype. The use of individual HER2- or ER-targeting agents can lead to the acquisition of therapeutic resistance due to compensatory receptor crosstalk. New drug combinations targeting HER2 and ER could improve outcomes for patients with HER2+/ER+ breast cancer. In this study, the pre-clinical rationale is explored for combining amcenestrant (Amc), a selective oestrogen receptor degrader (SERD), with HER2-targeted therapies including trastuzumab, trastuzumab-emtansine (T-DM1) and tyrosine kinase inhibitors (TKIs). The combination of Amc and anti-HER2 therapies was investigated in a panel of four HER2+/ER+ cell lines: BT-474, MDA-MB-361, EFM-192a and a trastuzumab-resistant variant BT-474-T. Proliferation (IC
and matrix combination assays) was determined using acid phosphatase assays. HER2/ER and intracellular signalling pathway protein levels/activity were investigated by western blot. Apoptosis was assessed using caspase 3/7 assays. Additivity and synergy were observed between Amc and the TKIs neratinib, lapatinib and tucatinib in all cell lines. Amc increased the anti-proliferative effect of trastuzumab in MDA-MB-361 and BT-474-T. Addition of Amc also increased anti-proliferative efficacy of T-DM1 in BT-474-T. TKI/Amc combinations reduced p-HER2 and ER levels and resulted in increased apoptosis. Higher ER expression in MDA-MB-361 and BT-474-T was associated with greater potential for synergy. In conclusion, the combination of Amc- and HER2-targeted treatments has potential as a therapeutic strategy for the treatment of HER2+/ER+ breast cancer and warrants further clinical investigation to validate safety and efficacy in patients. |
| doi_str_mv | 10.3390/ijms26020460 |
| format | Article |
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and matrix combination assays) was determined using acid phosphatase assays. HER2/ER and intracellular signalling pathway protein levels/activity were investigated by western blot. Apoptosis was assessed using caspase 3/7 assays. Additivity and synergy were observed between Amc and the TKIs neratinib, lapatinib and tucatinib in all cell lines. Amc increased the anti-proliferative effect of trastuzumab in MDA-MB-361 and BT-474-T. Addition of Amc also increased anti-proliferative efficacy of T-DM1 in BT-474-T. TKI/Amc combinations reduced p-HER2 and ER levels and resulted in increased apoptosis. Higher ER expression in MDA-MB-361 and BT-474-T was associated with greater potential for synergy. In conclusion, the combination of Amc- and HER2-targeted treatments has potential as a therapeutic strategy for the treatment of HER2+/ER+ breast cancer and warrants further clinical investigation to validate safety and efficacy in patients.</description><identifier>ISSN: 1422-0067</identifier><identifier>ISSN: 1661-6596</identifier><identifier>EISSN: 1422-0067</identifier><identifier>DOI: 10.3390/ijms26020460</identifier><identifier>PMID: 39859174</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>Ado-Trastuzumab Emtansine - pharmacology ; Ado-Trastuzumab Emtansine - therapeutic use ; Antineoplastic Combined Chemotherapy Protocols - pharmacology ; Antineoplastic Combined Chemotherapy Protocols - therapeutic use ; Apoptosis - drug effects ; Breast cancer ; Breast Neoplasms - drug therapy ; Breast Neoplasms - metabolism ; Breast Neoplasms - pathology ; Cell growth ; Cell Line, Tumor ; Cell Proliferation - drug effects ; Drug Resistance, Neoplasm - drug effects ; Drug Synergism ; Endocrine therapy ; Female ; Humans ; Kinases ; Lapatinib - pharmacology ; Lapatinib - therapeutic use ; Ligands ; Lymphocytes ; Oxazoles ; Protein Kinase Inhibitors - pharmacology ; Proteins ; Pyridines ; Quinazolines - pharmacology ; Quinazolines - therapeutic use ; Quinolines - pharmacology ; Receptor, ErbB-2 - metabolism ; Receptors, Estrogen - metabolism ; Trastuzumab - pharmacology ; Trastuzumab - therapeutic use</subject><ispartof>International journal of molecular sciences, 2025-01, Vol.26 (2), p.460</ispartof><rights>2025 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2025 by the authors. 2025</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c2131-651a06acbb1163611a996436ba61f91baf08beaeb5a3246dc1ddd53fb25a7fa13</cites><orcidid>0000-0002-7698-657X ; 0000-0003-1043-6169</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC11765389/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC11765389/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/39859174$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Mahdi, Amira F</creatorcontrib><creatorcontrib>Ashfield, Niall</creatorcontrib><creatorcontrib>Crown, John</creatorcontrib><creatorcontrib>Collins, Denis M</creatorcontrib><title>Pre-Clinical Rationale for Amcenestrant Combinations in HER2+/ER+ Breast Cancer</title><title>International journal of molecular sciences</title><addtitle>Int J Mol Sci</addtitle><description>HER2-positive/oestrogen receptor-positive (HER2+/ER+) represents a unique breast cancer subtype. The use of individual HER2- or ER-targeting agents can lead to the acquisition of therapeutic resistance due to compensatory receptor crosstalk. New drug combinations targeting HER2 and ER could improve outcomes for patients with HER2+/ER+ breast cancer. In this study, the pre-clinical rationale is explored for combining amcenestrant (Amc), a selective oestrogen receptor degrader (SERD), with HER2-targeted therapies including trastuzumab, trastuzumab-emtansine (T-DM1) and tyrosine kinase inhibitors (TKIs). The combination of Amc and anti-HER2 therapies was investigated in a panel of four HER2+/ER+ cell lines: BT-474, MDA-MB-361, EFM-192a and a trastuzumab-resistant variant BT-474-T. Proliferation (IC
and matrix combination assays) was determined using acid phosphatase assays. HER2/ER and intracellular signalling pathway protein levels/activity were investigated by western blot. Apoptosis was assessed using caspase 3/7 assays. Additivity and synergy were observed between Amc and the TKIs neratinib, lapatinib and tucatinib in all cell lines. Amc increased the anti-proliferative effect of trastuzumab in MDA-MB-361 and BT-474-T. Addition of Amc also increased anti-proliferative efficacy of T-DM1 in BT-474-T. TKI/Amc combinations reduced p-HER2 and ER levels and resulted in increased apoptosis. Higher ER expression in MDA-MB-361 and BT-474-T was associated with greater potential for synergy. In conclusion, the combination of Amc- and HER2-targeted treatments has potential as a therapeutic strategy for the treatment of HER2+/ER+ breast cancer and warrants further clinical investigation to validate safety and efficacy in patients.</description><subject>Ado-Trastuzumab Emtansine - pharmacology</subject><subject>Ado-Trastuzumab Emtansine - therapeutic use</subject><subject>Antineoplastic Combined Chemotherapy Protocols - pharmacology</subject><subject>Antineoplastic Combined Chemotherapy Protocols - therapeutic use</subject><subject>Apoptosis - drug effects</subject><subject>Breast cancer</subject><subject>Breast Neoplasms - drug therapy</subject><subject>Breast Neoplasms - metabolism</subject><subject>Breast Neoplasms - pathology</subject><subject>Cell growth</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation - drug effects</subject><subject>Drug Resistance, Neoplasm - drug effects</subject><subject>Drug Synergism</subject><subject>Endocrine therapy</subject><subject>Female</subject><subject>Humans</subject><subject>Kinases</subject><subject>Lapatinib - pharmacology</subject><subject>Lapatinib - therapeutic use</subject><subject>Ligands</subject><subject>Lymphocytes</subject><subject>Oxazoles</subject><subject>Protein Kinase Inhibitors - pharmacology</subject><subject>Proteins</subject><subject>Pyridines</subject><subject>Quinazolines - pharmacology</subject><subject>Quinazolines - therapeutic use</subject><subject>Quinolines - pharmacology</subject><subject>Receptor, ErbB-2 - metabolism</subject><subject>Receptors, Estrogen - metabolism</subject><subject>Trastuzumab - pharmacology</subject><subject>Trastuzumab - therapeutic use</subject><issn>1422-0067</issn><issn>1661-6596</issn><issn>1422-0067</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2025</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNpdkc1LAzEQxYMoft88y4IXQVczySbbnERL_QChUvQcJrtZTdlNNGkF_3u3VqV6moH58XhvHiEHQM84V_TcTbvEJGW0kHSNbEPBWE6pLNdX9i2yk9KUUsaZUJtki6uBUFAW22T8EG0-bJ13FbbZBGcueGxt1oSYXXaV9TbNIvpZNgydcf7rnjLns9vRhJ2cjyYn2VW0mHoAfWXjHtlosE12_3vukqfr0ePwNr8f39wNL-_zigGHXApAKrEyBkByCYBKyYJLgxIaBQYbOjAWrRHIWSHrCuq6FrwxTGDZIPBdcrHUfZ2bzta90d5mq1-j6zB-6IBO_71496Kfw7sGKKXgA9UrHH8rxPA272PqzqXKti16G-ZJc5BUMT4oeY8e_UOnYR77Py0ooQQtaLEQPF1SVQwpRdv8ugGqF1Xp1ap6_HA1wS_80w3_BBE4jmw</recordid><startdate>20250108</startdate><enddate>20250108</enddate><creator>Mahdi, Amira F</creator><creator>Ashfield, Niall</creator><creator>Crown, John</creator><creator>Collins, Denis M</creator><general>MDPI AG</general><general>MDPI</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>7X7</scope><scope>7XB</scope><scope>88E</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>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-7698-657X</orcidid><orcidid>https://orcid.org/0000-0003-1043-6169</orcidid></search><sort><creationdate>20250108</creationdate><title>Pre-Clinical Rationale for Amcenestrant Combinations in HER2+/ER+ Breast Cancer</title><author>Mahdi, Amira F ; 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The use of individual HER2- or ER-targeting agents can lead to the acquisition of therapeutic resistance due to compensatory receptor crosstalk. New drug combinations targeting HER2 and ER could improve outcomes for patients with HER2+/ER+ breast cancer. In this study, the pre-clinical rationale is explored for combining amcenestrant (Amc), a selective oestrogen receptor degrader (SERD), with HER2-targeted therapies including trastuzumab, trastuzumab-emtansine (T-DM1) and tyrosine kinase inhibitors (TKIs). The combination of Amc and anti-HER2 therapies was investigated in a panel of four HER2+/ER+ cell lines: BT-474, MDA-MB-361, EFM-192a and a trastuzumab-resistant variant BT-474-T. Proliferation (IC
and matrix combination assays) was determined using acid phosphatase assays. HER2/ER and intracellular signalling pathway protein levels/activity were investigated by western blot. Apoptosis was assessed using caspase 3/7 assays. Additivity and synergy were observed between Amc and the TKIs neratinib, lapatinib and tucatinib in all cell lines. Amc increased the anti-proliferative effect of trastuzumab in MDA-MB-361 and BT-474-T. Addition of Amc also increased anti-proliferative efficacy of T-DM1 in BT-474-T. TKI/Amc combinations reduced p-HER2 and ER levels and resulted in increased apoptosis. Higher ER expression in MDA-MB-361 and BT-474-T was associated with greater potential for synergy. In conclusion, the combination of Amc- and HER2-targeted treatments has potential as a therapeutic strategy for the treatment of HER2+/ER+ breast cancer and warrants further clinical investigation to validate safety and efficacy in patients.</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>39859174</pmid><doi>10.3390/ijms26020460</doi><orcidid>https://orcid.org/0000-0002-7698-657X</orcidid><orcidid>https://orcid.org/0000-0003-1043-6169</orcidid><oa>free_for_read</oa></addata></record> |
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| ispartof | International journal of molecular sciences, 2025-01, Vol.26 (2), p.460 |
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| source | MDPI - Multidisciplinary Digital Publishing Institute; MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central |
| subjects | Ado-Trastuzumab Emtansine - pharmacology Ado-Trastuzumab Emtansine - therapeutic use Antineoplastic Combined Chemotherapy Protocols - pharmacology Antineoplastic Combined Chemotherapy Protocols - therapeutic use Apoptosis - drug effects Breast cancer Breast Neoplasms - drug therapy Breast Neoplasms - metabolism Breast Neoplasms - pathology Cell growth Cell Line, Tumor Cell Proliferation - drug effects Drug Resistance, Neoplasm - drug effects Drug Synergism Endocrine therapy Female Humans Kinases Lapatinib - pharmacology Lapatinib - therapeutic use Ligands Lymphocytes Oxazoles Protein Kinase Inhibitors - pharmacology Proteins Pyridines Quinazolines - pharmacology Quinazolines - therapeutic use Quinolines - pharmacology Receptor, ErbB-2 - metabolism Receptors, Estrogen - metabolism Trastuzumab - pharmacology Trastuzumab - therapeutic use |
| title | Pre-Clinical Rationale for Amcenestrant Combinations in HER2+/ER+ Breast Cancer |
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