PIK3CA mutations are associated with decreased benefit to neoadjuvant human epidermal growth factor receptor 2-targeted therapies in breast cancer
We investigated whether mutations in the gene encoding the phosphatidylinositol 3-kinase (PI3K) catalytic subunit (PIK3CA) correlates with response to neoadjuvant human epidermal growth factor receptor 2 (HER2) -targeted therapies in patients with breast cancer. Baseline tissue biopsies were availab...
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| Veröffentlicht in: | Journal of clinical oncology 2015-04, Vol.33 (12), p.1334-1339 |
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| creator | Majewski, Ian J Nuciforo, Paolo Mittempergher, Lorenza Bosma, Astrid J Eidtmann, Holger Holmes, Eileen Sotiriou, Christos Fumagalli, Debora Jimenez, Jose Aura, Claudia Prudkin, Ludmila Díaz-Delgado, Maria Carmen de la Peña, Lorena Loi, Sherene Ellis, Catherine Schultz, Nikolaus de Azambuja, Evandro Harbeck, Nadia Piccart-Gebhart, Martine Bernards, René Baselga, José |
| description | We investigated whether mutations in the gene encoding the phosphatidylinositol 3-kinase (PI3K) catalytic subunit (PIK3CA) correlates with response to neoadjuvant human epidermal growth factor receptor 2 (HER2) -targeted therapies in patients with breast cancer.
Baseline tissue biopsies were available from patients with HER2-positive early breast cancer who were enrolled onto the Neoadjuvant Lapatinib and/or Trastuzumab Treatment Optimization trial (NeoALTTO). Activating mutations in PIK3CA were identified using mass spectrometry-based genotyping.
PIK3CA mutations were identified in 23% of HER2-positive breast tumors, and these mutations were associated with poorer outcome in all of the treatment arms. Patients treated with a combination of trastuzumab and lapatinib who had wild-type PIK3CA obtained a total pathologic complete response (pCR) rate of 53.1%, which decreased to 28.6% in patients with tumors that carried PIK3CA activating mutations (P = .012).
Activating mutations in PIK3CA predicted poor pCR in patients with HER2-positive breast cancer treated with neoadjuvant therapies that target HER2. Consequently, the combination of anti-HER2 agents and PI3K inhibitors is being investigated. |
| doi_str_mv | 10.1200/JCO.2014.55.2158 |
| format | Article |
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Baseline tissue biopsies were available from patients with HER2-positive early breast cancer who were enrolled onto the Neoadjuvant Lapatinib and/or Trastuzumab Treatment Optimization trial (NeoALTTO). Activating mutations in PIK3CA were identified using mass spectrometry-based genotyping.
PIK3CA mutations were identified in 23% of HER2-positive breast tumors, and these mutations were associated with poorer outcome in all of the treatment arms. Patients treated with a combination of trastuzumab and lapatinib who had wild-type PIK3CA obtained a total pathologic complete response (pCR) rate of 53.1%, which decreased to 28.6% in patients with tumors that carried PIK3CA activating mutations (P = .012).
Activating mutations in PIK3CA predicted poor pCR in patients with HER2-positive breast cancer treated with neoadjuvant therapies that target HER2. Consequently, the combination of anti-HER2 agents and PI3K inhibitors is being investigated.</description><identifier>ISSN: 0732-183X</identifier><identifier>EISSN: 1527-7755</identifier><identifier>DOI: 10.1200/JCO.2014.55.2158</identifier><identifier>PMID: 25559818</identifier><language>eng</language><publisher>United States: American Society of Clinical Oncology</publisher><subject>Aged ; Antibodies, Monoclonal, Humanized - administration & dosage ; Antineoplastic Combined Chemotherapy Protocols - therapeutic use ; Breast Neoplasms - drug therapy ; Breast Neoplasms - enzymology ; Breast Neoplasms - genetics ; Breast Neoplasms - pathology ; Chemotherapy, Adjuvant ; Class I Phosphatidylinositol 3-Kinases ; Female ; Humans ; Lapatinib ; Middle Aged ; Molecular Targeted Therapy ; Mutation ; Neoadjuvant Therapy ; Neoplasm Staging ; ORIGINAL REPORTS ; Phosphatidylinositol 3-Kinases - genetics ; Quinazolines - administration & dosage ; Receptor, ErbB-2 - antagonists & inhibitors ; Receptor, ErbB-2 - metabolism ; Trastuzumab</subject><ispartof>Journal of clinical oncology, 2015-04, Vol.33 (12), p.1334-1339</ispartof><rights>2015 by American Society of Clinical Oncology.</rights><rights>2015 by American Society of Clinical Oncology 2015 American Society of Clinical Oncology</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c443t-cdc42721f2a40b78c981f477ee39beb515915cf66404140cfe0c9ff85550619d3</citedby><cites>FETCH-LOGICAL-c443t-cdc42721f2a40b78c981f477ee39beb515915cf66404140cfe0c9ff85550619d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,3729,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25559818$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Majewski, Ian J</creatorcontrib><creatorcontrib>Nuciforo, Paolo</creatorcontrib><creatorcontrib>Mittempergher, Lorenza</creatorcontrib><creatorcontrib>Bosma, Astrid J</creatorcontrib><creatorcontrib>Eidtmann, Holger</creatorcontrib><creatorcontrib>Holmes, Eileen</creatorcontrib><creatorcontrib>Sotiriou, Christos</creatorcontrib><creatorcontrib>Fumagalli, Debora</creatorcontrib><creatorcontrib>Jimenez, Jose</creatorcontrib><creatorcontrib>Aura, Claudia</creatorcontrib><creatorcontrib>Prudkin, Ludmila</creatorcontrib><creatorcontrib>Díaz-Delgado, Maria Carmen</creatorcontrib><creatorcontrib>de la Peña, Lorena</creatorcontrib><creatorcontrib>Loi, Sherene</creatorcontrib><creatorcontrib>Ellis, Catherine</creatorcontrib><creatorcontrib>Schultz, Nikolaus</creatorcontrib><creatorcontrib>de Azambuja, Evandro</creatorcontrib><creatorcontrib>Harbeck, Nadia</creatorcontrib><creatorcontrib>Piccart-Gebhart, Martine</creatorcontrib><creatorcontrib>Bernards, René</creatorcontrib><creatorcontrib>Baselga, José</creatorcontrib><title>PIK3CA mutations are associated with decreased benefit to neoadjuvant human epidermal growth factor receptor 2-targeted therapies in breast cancer</title><title>Journal of clinical oncology</title><addtitle>J Clin Oncol</addtitle><description>We investigated whether mutations in the gene encoding the phosphatidylinositol 3-kinase (PI3K) catalytic subunit (PIK3CA) correlates with response to neoadjuvant human epidermal growth factor receptor 2 (HER2) -targeted therapies in patients with breast cancer.
Baseline tissue biopsies were available from patients with HER2-positive early breast cancer who were enrolled onto the Neoadjuvant Lapatinib and/or Trastuzumab Treatment Optimization trial (NeoALTTO). Activating mutations in PIK3CA were identified using mass spectrometry-based genotyping.
PIK3CA mutations were identified in 23% of HER2-positive breast tumors, and these mutations were associated with poorer outcome in all of the treatment arms. Patients treated with a combination of trastuzumab and lapatinib who had wild-type PIK3CA obtained a total pathologic complete response (pCR) rate of 53.1%, which decreased to 28.6% in patients with tumors that carried PIK3CA activating mutations (P = .012).
Activating mutations in PIK3CA predicted poor pCR in patients with HER2-positive breast cancer treated with neoadjuvant therapies that target HER2. Consequently, the combination of anti-HER2 agents and PI3K inhibitors is being investigated.</description><subject>Aged</subject><subject>Antibodies, Monoclonal, Humanized - administration & dosage</subject><subject>Antineoplastic Combined Chemotherapy Protocols - therapeutic use</subject><subject>Breast Neoplasms - drug therapy</subject><subject>Breast Neoplasms - enzymology</subject><subject>Breast Neoplasms - genetics</subject><subject>Breast Neoplasms - pathology</subject><subject>Chemotherapy, Adjuvant</subject><subject>Class I Phosphatidylinositol 3-Kinases</subject><subject>Female</subject><subject>Humans</subject><subject>Lapatinib</subject><subject>Middle Aged</subject><subject>Molecular Targeted Therapy</subject><subject>Mutation</subject><subject>Neoadjuvant Therapy</subject><subject>Neoplasm Staging</subject><subject>ORIGINAL REPORTS</subject><subject>Phosphatidylinositol 3-Kinases - genetics</subject><subject>Quinazolines - administration & dosage</subject><subject>Receptor, ErbB-2 - antagonists & inhibitors</subject><subject>Receptor, ErbB-2 - metabolism</subject><subject>Trastuzumab</subject><issn>0732-183X</issn><issn>1527-7755</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVkU9v1DAQxS1ERZeFOyfkI5cs_hsnF6RqVaBQqT20EjfLcca7rpI42E4rvgafGEctFZw81rz37JkfQu8o2VFGyMdv-6sdI1TspNwxKpsXaEMlU5VSUr5EG6I4q2jDf5yi1yndkaJsuHyFTpmUsm1os0G_ry--8_0ZHpdssg9TwiYCNikF602GHj_4fMQ92AgmlWsHEzifcQ54gmD6u-XeTBkfl9FMGGbfQxzNgA8xPBSfMzaHiCNYmNeCVdnEA6y5-QjRzB4S9hPu1vSMrZksxDfoxJkhwdunc4tuP5_f7L9Wl1dfLvZnl5UVgufK9lYwxahjRpBONbYM5IRSALztoJNUtlRaV9eCCCqIdUBs61xTRic1bXu-RZ8ec-elG6G3MOVoBj1HP5r4Swfj9f-dyR_1IdxrSRrFy1q36MNTQAw_F0hZjz5ZGAZTVrMkTWslGKk5oUVKHqU2hpQiuOdnKNErSl1Q6hWlllKvKIvl_b_fezb8Zcf_AP1enY0</recordid><startdate>20150420</startdate><enddate>20150420</enddate><creator>Majewski, Ian J</creator><creator>Nuciforo, Paolo</creator><creator>Mittempergher, Lorenza</creator><creator>Bosma, Astrid J</creator><creator>Eidtmann, Holger</creator><creator>Holmes, Eileen</creator><creator>Sotiriou, Christos</creator><creator>Fumagalli, Debora</creator><creator>Jimenez, Jose</creator><creator>Aura, Claudia</creator><creator>Prudkin, Ludmila</creator><creator>Díaz-Delgado, Maria Carmen</creator><creator>de la Peña, Lorena</creator><creator>Loi, Sherene</creator><creator>Ellis, Catherine</creator><creator>Schultz, Nikolaus</creator><creator>de Azambuja, Evandro</creator><creator>Harbeck, Nadia</creator><creator>Piccart-Gebhart, Martine</creator><creator>Bernards, René</creator><creator>Baselga, José</creator><general>American Society of Clinical Oncology</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>7X8</scope><scope>5PM</scope></search><sort><creationdate>20150420</creationdate><title>PIK3CA mutations are associated with decreased benefit to neoadjuvant human epidermal growth factor receptor 2-targeted therapies in breast cancer</title><author>Majewski, Ian J ; Nuciforo, Paolo ; Mittempergher, Lorenza ; Bosma, Astrid J ; Eidtmann, Holger ; Holmes, Eileen ; Sotiriou, Christos ; Fumagalli, Debora ; Jimenez, Jose ; Aura, Claudia ; Prudkin, Ludmila ; Díaz-Delgado, Maria Carmen ; de la Peña, Lorena ; Loi, Sherene ; Ellis, Catherine ; Schultz, Nikolaus ; de Azambuja, Evandro ; Harbeck, Nadia ; Piccart-Gebhart, Martine ; Bernards, René ; Baselga, José</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c443t-cdc42721f2a40b78c981f477ee39beb515915cf66404140cfe0c9ff85550619d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Aged</topic><topic>Antibodies, Monoclonal, Humanized - administration & dosage</topic><topic>Antineoplastic Combined Chemotherapy Protocols - therapeutic use</topic><topic>Breast Neoplasms - drug therapy</topic><topic>Breast Neoplasms - enzymology</topic><topic>Breast Neoplasms - genetics</topic><topic>Breast Neoplasms - pathology</topic><topic>Chemotherapy, Adjuvant</topic><topic>Class I Phosphatidylinositol 3-Kinases</topic><topic>Female</topic><topic>Humans</topic><topic>Lapatinib</topic><topic>Middle Aged</topic><topic>Molecular Targeted Therapy</topic><topic>Mutation</topic><topic>Neoadjuvant Therapy</topic><topic>Neoplasm Staging</topic><topic>ORIGINAL REPORTS</topic><topic>Phosphatidylinositol 3-Kinases - genetics</topic><topic>Quinazolines - administration & dosage</topic><topic>Receptor, ErbB-2 - antagonists & inhibitors</topic><topic>Receptor, ErbB-2 - metabolism</topic><topic>Trastuzumab</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Majewski, Ian J</creatorcontrib><creatorcontrib>Nuciforo, Paolo</creatorcontrib><creatorcontrib>Mittempergher, Lorenza</creatorcontrib><creatorcontrib>Bosma, Astrid J</creatorcontrib><creatorcontrib>Eidtmann, Holger</creatorcontrib><creatorcontrib>Holmes, Eileen</creatorcontrib><creatorcontrib>Sotiriou, Christos</creatorcontrib><creatorcontrib>Fumagalli, Debora</creatorcontrib><creatorcontrib>Jimenez, Jose</creatorcontrib><creatorcontrib>Aura, Claudia</creatorcontrib><creatorcontrib>Prudkin, Ludmila</creatorcontrib><creatorcontrib>Díaz-Delgado, Maria Carmen</creatorcontrib><creatorcontrib>de la Peña, Lorena</creatorcontrib><creatorcontrib>Loi, Sherene</creatorcontrib><creatorcontrib>Ellis, Catherine</creatorcontrib><creatorcontrib>Schultz, Nikolaus</creatorcontrib><creatorcontrib>de Azambuja, Evandro</creatorcontrib><creatorcontrib>Harbeck, Nadia</creatorcontrib><creatorcontrib>Piccart-Gebhart, Martine</creatorcontrib><creatorcontrib>Bernards, René</creatorcontrib><creatorcontrib>Baselga, José</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of clinical oncology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Majewski, Ian J</au><au>Nuciforo, Paolo</au><au>Mittempergher, Lorenza</au><au>Bosma, Astrid J</au><au>Eidtmann, Holger</au><au>Holmes, Eileen</au><au>Sotiriou, Christos</au><au>Fumagalli, Debora</au><au>Jimenez, Jose</au><au>Aura, Claudia</au><au>Prudkin, Ludmila</au><au>Díaz-Delgado, Maria Carmen</au><au>de la Peña, Lorena</au><au>Loi, Sherene</au><au>Ellis, Catherine</au><au>Schultz, Nikolaus</au><au>de Azambuja, Evandro</au><au>Harbeck, Nadia</au><au>Piccart-Gebhart, Martine</au><au>Bernards, René</au><au>Baselga, José</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>PIK3CA mutations are associated with decreased benefit to neoadjuvant human epidermal growth factor receptor 2-targeted therapies in breast cancer</atitle><jtitle>Journal of clinical oncology</jtitle><addtitle>J Clin Oncol</addtitle><date>2015-04-20</date><risdate>2015</risdate><volume>33</volume><issue>12</issue><spage>1334</spage><epage>1339</epage><pages>1334-1339</pages><issn>0732-183X</issn><eissn>1527-7755</eissn><abstract>We investigated whether mutations in the gene encoding the phosphatidylinositol 3-kinase (PI3K) catalytic subunit (PIK3CA) correlates with response to neoadjuvant human epidermal growth factor receptor 2 (HER2) -targeted therapies in patients with breast cancer.
Baseline tissue biopsies were available from patients with HER2-positive early breast cancer who were enrolled onto the Neoadjuvant Lapatinib and/or Trastuzumab Treatment Optimization trial (NeoALTTO). Activating mutations in PIK3CA were identified using mass spectrometry-based genotyping.
PIK3CA mutations were identified in 23% of HER2-positive breast tumors, and these mutations were associated with poorer outcome in all of the treatment arms. Patients treated with a combination of trastuzumab and lapatinib who had wild-type PIK3CA obtained a total pathologic complete response (pCR) rate of 53.1%, which decreased to 28.6% in patients with tumors that carried PIK3CA activating mutations (P = .012).
Activating mutations in PIK3CA predicted poor pCR in patients with HER2-positive breast cancer treated with neoadjuvant therapies that target HER2. Consequently, the combination of anti-HER2 agents and PI3K inhibitors is being investigated.</abstract><cop>United States</cop><pub>American Society of Clinical Oncology</pub><pmid>25559818</pmid><doi>10.1200/JCO.2014.55.2158</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; American Society of Clinical Oncology Journals; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | Aged Antibodies, Monoclonal, Humanized - administration & dosage Antineoplastic Combined Chemotherapy Protocols - therapeutic use Breast Neoplasms - drug therapy Breast Neoplasms - enzymology Breast Neoplasms - genetics Breast Neoplasms - pathology Chemotherapy, Adjuvant Class I Phosphatidylinositol 3-Kinases Female Humans Lapatinib Middle Aged Molecular Targeted Therapy Mutation Neoadjuvant Therapy Neoplasm Staging ORIGINAL REPORTS Phosphatidylinositol 3-Kinases - genetics Quinazolines - administration & dosage Receptor, ErbB-2 - antagonists & inhibitors Receptor, ErbB-2 - metabolism Trastuzumab |
| title | PIK3CA mutations are associated with decreased benefit to neoadjuvant human epidermal growth factor receptor 2-targeted therapies in breast cancer |
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