PI3KCA mutations and/or PTEN loss in Her2-positive breast carcinomas treated with trastuzumab are not related to resistance to anti-Her2 therapy
The purpose of this study is to evaluate whether activating mutations of the p110α catalytic subunit of class A phosphoinositide 3-kinases ( PI3KCA ) or complete loss of phosphatase and tensin homolog (PTEN) is associated with response to anti-human epidermal growth factor receptor 2 (Her2) treatmen...
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| Veröffentlicht in: | Virchows Archiv : an international journal of pathology 2012-08, Vol.461 (2), p.129-139 |
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| container_title | Virchows Archiv : an international journal of pathology |
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| creator | Barbareschi, Mattia Cuorvo, Lucia Veronica Girlando, Salvatore Bragantini, Emma Eccher, Claudio Leonardi, Elena Ferro, Antonella Caldara, Alessia Triolo, Renza Cantaloni, Chiara Decarli, Nicola Galligioni, Enzo Palma, Paolo Dalla |
| description | The purpose of this study is to evaluate whether activating mutations of the p110α catalytic subunit of class A phosphoinositide 3-kinases (
PI3KCA
) or complete loss of phosphatase and tensin homolog (PTEN) is associated with response to anti-human epidermal growth factor receptor 2 (Her2) treatment in breast cancer (BC). We analysed
PI3KCA
hot-spot mutations and PTEN immunohistochemical expression in 129 Her2-positive infiltrating BC treated with trastuzumab, including 26 cases treated with neoadjuvant therapy, 48 metastatic infiltrating breast cancer (IBC; MBC) and 55 early-stage IBC, with complete clinical information (mean follow-up 37, 66 and 32 months, respectively).
PI3KCA
hot-spot mutations were observed in 25 cases (19 %): 12 (9 %) in exon 9 and 13 (10 %) in exon 20. No correlations were observed between mutations and pathological and biological parameters. In patients treated with neoadjuvant therapy and in MBC, we did not observe any relationship with response to trastuzumab-based therapy. PTEN loss was observed in 24 out of 86 informative cases (28 %), 3 (13 %) of which were also mutated for
PI3KCA
. PI3K pathway activation, defined as
PI3KCA
mutation and/or PTEN loss, was not associated with response to treatment or clinical outcome in MBC.
PI3KCA
mutation and/or PTEN loss should not exclude patients from potentially beneficial anti-Her2 therapy. |
| doi_str_mv | 10.1007/s00428-012-1267-2 |
| format | Article |
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PI3KCA
) or complete loss of phosphatase and tensin homolog (PTEN) is associated with response to anti-human epidermal growth factor receptor 2 (Her2) treatment in breast cancer (BC). We analysed
PI3KCA
hot-spot mutations and PTEN immunohistochemical expression in 129 Her2-positive infiltrating BC treated with trastuzumab, including 26 cases treated with neoadjuvant therapy, 48 metastatic infiltrating breast cancer (IBC; MBC) and 55 early-stage IBC, with complete clinical information (mean follow-up 37, 66 and 32 months, respectively).
PI3KCA
hot-spot mutations were observed in 25 cases (19 %): 12 (9 %) in exon 9 and 13 (10 %) in exon 20. No correlations were observed between mutations and pathological and biological parameters. In patients treated with neoadjuvant therapy and in MBC, we did not observe any relationship with response to trastuzumab-based therapy. PTEN loss was observed in 24 out of 86 informative cases (28 %), 3 (13 %) of which were also mutated for
PI3KCA
. PI3K pathway activation, defined as
PI3KCA
mutation and/or PTEN loss, was not associated with response to treatment or clinical outcome in MBC.
PI3KCA
mutation and/or PTEN loss should not exclude patients from potentially beneficial anti-Her2 therapy.</description><identifier>ISSN: 0945-6317</identifier><identifier>EISSN: 1432-2307</identifier><identifier>DOI: 10.1007/s00428-012-1267-2</identifier><identifier>PMID: 22744290</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer-Verlag</publisher><subject>Antibodies, Monoclonal, Humanized - therapeutic use ; Antineoplastic Agents, Hormonal - therapeutic use ; Base Sequence ; Biological and medical sciences ; Breast Neoplasms - drug therapy ; Breast Neoplasms - genetics ; DNA Mutational Analysis ; Drug Resistance, Neoplasm - genetics ; Female ; Gynecology. Andrology. Obstetrics ; Humans ; Investigative techniques, diagnostic techniques (general aspects) ; Mammary gland diseases ; Medical sciences ; Medicine ; Medicine & Public Health ; Molecular Sequence Data ; Mutation ; Nuclear Proteins - genetics ; Original Article ; Pathology ; Pathology. Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques ; PTEN Phosphohydrolase - genetics ; Real-Time Polymerase Chain Reaction ; Receptor, ErbB-2 - biosynthesis ; Receptor, ErbB-2 - genetics ; Retrospective Studies ; Transcription Factors - genetics ; Trastuzumab ; Tumors</subject><ispartof>Virchows Archiv : an international journal of pathology, 2012-08, Vol.461 (2), p.129-139</ispartof><rights>Springer-Verlag 2012</rights><rights>2015 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c402t-2f20e75037abccb3927c028be97a129496f7d4fdf19f46d28ad8e635b34cb3353</citedby><cites>FETCH-LOGICAL-c402t-2f20e75037abccb3927c028be97a129496f7d4fdf19f46d28ad8e635b34cb3353</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00428-012-1267-2$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00428-012-1267-2$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=26290823$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22744290$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Barbareschi, Mattia</creatorcontrib><creatorcontrib>Cuorvo, Lucia Veronica</creatorcontrib><creatorcontrib>Girlando, Salvatore</creatorcontrib><creatorcontrib>Bragantini, Emma</creatorcontrib><creatorcontrib>Eccher, Claudio</creatorcontrib><creatorcontrib>Leonardi, Elena</creatorcontrib><creatorcontrib>Ferro, Antonella</creatorcontrib><creatorcontrib>Caldara, Alessia</creatorcontrib><creatorcontrib>Triolo, Renza</creatorcontrib><creatorcontrib>Cantaloni, Chiara</creatorcontrib><creatorcontrib>Decarli, Nicola</creatorcontrib><creatorcontrib>Galligioni, Enzo</creatorcontrib><creatorcontrib>Palma, Paolo Dalla</creatorcontrib><title>PI3KCA mutations and/or PTEN loss in Her2-positive breast carcinomas treated with trastuzumab are not related to resistance to anti-Her2 therapy</title><title>Virchows Archiv : an international journal of pathology</title><addtitle>Virchows Arch</addtitle><addtitle>Virchows Arch</addtitle><description>The purpose of this study is to evaluate whether activating mutations of the p110α catalytic subunit of class A phosphoinositide 3-kinases (
PI3KCA
) or complete loss of phosphatase and tensin homolog (PTEN) is associated with response to anti-human epidermal growth factor receptor 2 (Her2) treatment in breast cancer (BC). We analysed
PI3KCA
hot-spot mutations and PTEN immunohistochemical expression in 129 Her2-positive infiltrating BC treated with trastuzumab, including 26 cases treated with neoadjuvant therapy, 48 metastatic infiltrating breast cancer (IBC; MBC) and 55 early-stage IBC, with complete clinical information (mean follow-up 37, 66 and 32 months, respectively).
PI3KCA
hot-spot mutations were observed in 25 cases (19 %): 12 (9 %) in exon 9 and 13 (10 %) in exon 20. No correlations were observed between mutations and pathological and biological parameters. In patients treated with neoadjuvant therapy and in MBC, we did not observe any relationship with response to trastuzumab-based therapy. PTEN loss was observed in 24 out of 86 informative cases (28 %), 3 (13 %) of which were also mutated for
PI3KCA
. PI3K pathway activation, defined as
PI3KCA
mutation and/or PTEN loss, was not associated with response to treatment or clinical outcome in MBC.
PI3KCA
mutation and/or PTEN loss should not exclude patients from potentially beneficial anti-Her2 therapy.</description><subject>Antibodies, Monoclonal, Humanized - therapeutic use</subject><subject>Antineoplastic Agents, Hormonal - therapeutic use</subject><subject>Base Sequence</subject><subject>Biological and medical sciences</subject><subject>Breast Neoplasms - drug therapy</subject><subject>Breast Neoplasms - genetics</subject><subject>DNA Mutational Analysis</subject><subject>Drug Resistance, Neoplasm - genetics</subject><subject>Female</subject><subject>Gynecology. Andrology. Obstetrics</subject><subject>Humans</subject><subject>Investigative techniques, diagnostic techniques (general aspects)</subject><subject>Mammary gland diseases</subject><subject>Medical sciences</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Molecular Sequence Data</subject><subject>Mutation</subject><subject>Nuclear Proteins - genetics</subject><subject>Original Article</subject><subject>Pathology</subject><subject>Pathology. Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques</subject><subject>PTEN Phosphohydrolase - genetics</subject><subject>Real-Time Polymerase Chain Reaction</subject><subject>Receptor, ErbB-2 - biosynthesis</subject><subject>Receptor, ErbB-2 - genetics</subject><subject>Retrospective Studies</subject><subject>Transcription Factors - genetics</subject><subject>Trastuzumab</subject><subject>Tumors</subject><issn>0945-6317</issn><issn>1432-2307</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp1kdFOHCEUhknTpm7XPkBvGpLGxBsqHNhhuDQbq0bTeqHXE4ZhKmYGtsBo7FP4yDLdrW2a9AoO5zs_J_-P0AdGPzNK5VGiVEBNKAPCoJIEXqEFExwIcCpfowVVYkUqzuQeepfSHaXAala9RXsAUghQdIGers75xfoYj1PW2QWfsPbdUYj46vrkKx5CSth5fGYjkE1ILrt7i9todcrY6GicD6NOOJeXbDv84PJtKUp3-jmNusU6WuxDxtEOv4AcyjW5lLU3dq60z47M8jjf2qg3j_voTa-HZN_vziW6-XJyvT4jl99Oz9fHl8QICplAD9TKFeVSt8a0XIE0FOrWKqkZKKGqXnai73qmelF1UOuuthVftVwUmq_4Eh1udTcx_Jhsys3okrHDoL0NU2oY5YIpxYufS_TpH_QuTNGX7WZKguSVqgvFtpSJxbVo-2YT3ajjY4GaOa5mG1dT4mrmuBooMx93ylM72u5l4nc-BTjYAToZPfSx-ObSH64qUA28cLDlUmn57zb-veL_fn8Gs1is2A</recordid><startdate>20120801</startdate><enddate>20120801</enddate><creator>Barbareschi, Mattia</creator><creator>Cuorvo, Lucia Veronica</creator><creator>Girlando, Salvatore</creator><creator>Bragantini, Emma</creator><creator>Eccher, Claudio</creator><creator>Leonardi, Elena</creator><creator>Ferro, Antonella</creator><creator>Caldara, Alessia</creator><creator>Triolo, Renza</creator><creator>Cantaloni, Chiara</creator><creator>Decarli, Nicola</creator><creator>Galligioni, Enzo</creator><creator>Palma, Paolo Dalla</creator><general>Springer-Verlag</general><general>Springer</general><general>Springer Nature B.V</general><scope>IQODW</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>7T5</scope><scope>7T7</scope><scope>7TM</scope><scope>7TO</scope><scope>7U7</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</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>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>7X8</scope></search><sort><creationdate>20120801</creationdate><title>PI3KCA mutations and/or PTEN loss in Her2-positive breast carcinomas treated with trastuzumab are not related to resistance to anti-Her2 therapy</title><author>Barbareschi, Mattia ; Cuorvo, Lucia Veronica ; Girlando, Salvatore ; Bragantini, Emma ; Eccher, Claudio ; Leonardi, Elena ; Ferro, Antonella ; Caldara, Alessia ; Triolo, Renza ; Cantaloni, Chiara ; Decarli, Nicola ; Galligioni, Enzo ; Palma, Paolo Dalla</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c402t-2f20e75037abccb3927c028be97a129496f7d4fdf19f46d28ad8e635b34cb3353</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Antibodies, Monoclonal, Humanized - therapeutic use</topic><topic>Antineoplastic Agents, Hormonal - therapeutic use</topic><topic>Base Sequence</topic><topic>Biological and medical sciences</topic><topic>Breast Neoplasms - drug therapy</topic><topic>Breast Neoplasms - genetics</topic><topic>DNA Mutational Analysis</topic><topic>Drug Resistance, Neoplasm - genetics</topic><topic>Female</topic><topic>Gynecology. Andrology. Obstetrics</topic><topic>Humans</topic><topic>Investigative techniques, diagnostic techniques (general aspects)</topic><topic>Mammary gland diseases</topic><topic>Medical sciences</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Molecular Sequence Data</topic><topic>Mutation</topic><topic>Nuclear Proteins - genetics</topic><topic>Original Article</topic><topic>Pathology</topic><topic>Pathology. Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques</topic><topic>PTEN Phosphohydrolase - genetics</topic><topic>Real-Time Polymerase Chain Reaction</topic><topic>Receptor, ErbB-2 - biosynthesis</topic><topic>Receptor, ErbB-2 - genetics</topic><topic>Retrospective Studies</topic><topic>Transcription Factors - genetics</topic><topic>Trastuzumab</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Barbareschi, Mattia</creatorcontrib><creatorcontrib>Cuorvo, Lucia Veronica</creatorcontrib><creatorcontrib>Girlando, Salvatore</creatorcontrib><creatorcontrib>Bragantini, Emma</creatorcontrib><creatorcontrib>Eccher, Claudio</creatorcontrib><creatorcontrib>Leonardi, Elena</creatorcontrib><creatorcontrib>Ferro, Antonella</creatorcontrib><creatorcontrib>Caldara, Alessia</creatorcontrib><creatorcontrib>Triolo, Renza</creatorcontrib><creatorcontrib>Cantaloni, Chiara</creatorcontrib><creatorcontrib>Decarli, Nicola</creatorcontrib><creatorcontrib>Galligioni, Enzo</creatorcontrib><creatorcontrib>Palma, Paolo Dalla</creatorcontrib><collection>Pascal-Francis</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>Nursing & Allied Health Database</collection><collection>Immunology Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</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 Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>Nursing & Allied Health Premium</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>MEDLINE - Academic</collection><jtitle>Virchows Archiv : an international journal of pathology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Barbareschi, Mattia</au><au>Cuorvo, Lucia Veronica</au><au>Girlando, Salvatore</au><au>Bragantini, Emma</au><au>Eccher, Claudio</au><au>Leonardi, Elena</au><au>Ferro, Antonella</au><au>Caldara, Alessia</au><au>Triolo, Renza</au><au>Cantaloni, Chiara</au><au>Decarli, Nicola</au><au>Galligioni, Enzo</au><au>Palma, Paolo Dalla</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>PI3KCA mutations and/or PTEN loss in Her2-positive breast carcinomas treated with trastuzumab are not related to resistance to anti-Her2 therapy</atitle><jtitle>Virchows Archiv : an international journal of pathology</jtitle><stitle>Virchows Arch</stitle><addtitle>Virchows Arch</addtitle><date>2012-08-01</date><risdate>2012</risdate><volume>461</volume><issue>2</issue><spage>129</spage><epage>139</epage><pages>129-139</pages><issn>0945-6317</issn><eissn>1432-2307</eissn><abstract>The purpose of this study is to evaluate whether activating mutations of the p110α catalytic subunit of class A phosphoinositide 3-kinases (
PI3KCA
) or complete loss of phosphatase and tensin homolog (PTEN) is associated with response to anti-human epidermal growth factor receptor 2 (Her2) treatment in breast cancer (BC). We analysed
PI3KCA
hot-spot mutations and PTEN immunohistochemical expression in 129 Her2-positive infiltrating BC treated with trastuzumab, including 26 cases treated with neoadjuvant therapy, 48 metastatic infiltrating breast cancer (IBC; MBC) and 55 early-stage IBC, with complete clinical information (mean follow-up 37, 66 and 32 months, respectively).
PI3KCA
hot-spot mutations were observed in 25 cases (19 %): 12 (9 %) in exon 9 and 13 (10 %) in exon 20. No correlations were observed between mutations and pathological and biological parameters. In patients treated with neoadjuvant therapy and in MBC, we did not observe any relationship with response to trastuzumab-based therapy. PTEN loss was observed in 24 out of 86 informative cases (28 %), 3 (13 %) of which were also mutated for
PI3KCA
. PI3K pathway activation, defined as
PI3KCA
mutation and/or PTEN loss, was not associated with response to treatment or clinical outcome in MBC.
PI3KCA
mutation and/or PTEN loss should not exclude patients from potentially beneficial anti-Her2 therapy.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer-Verlag</pub><pmid>22744290</pmid><doi>10.1007/s00428-012-1267-2</doi><tpages>11</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0945-6317 |
| ispartof | Virchows Archiv : an international journal of pathology, 2012-08, Vol.461 (2), p.129-139 |
| issn | 0945-6317 1432-2307 |
| language | eng |
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| source | MEDLINE; SpringerNature Journals |
| subjects | Antibodies, Monoclonal, Humanized - therapeutic use Antineoplastic Agents, Hormonal - therapeutic use Base Sequence Biological and medical sciences Breast Neoplasms - drug therapy Breast Neoplasms - genetics DNA Mutational Analysis Drug Resistance, Neoplasm - genetics Female Gynecology. Andrology. Obstetrics Humans Investigative techniques, diagnostic techniques (general aspects) Mammary gland diseases Medical sciences Medicine Medicine & Public Health Molecular Sequence Data Mutation Nuclear Proteins - genetics Original Article Pathology Pathology. Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques PTEN Phosphohydrolase - genetics Real-Time Polymerase Chain Reaction Receptor, ErbB-2 - biosynthesis Receptor, ErbB-2 - genetics Retrospective Studies Transcription Factors - genetics Trastuzumab Tumors |
| title | PI3KCA mutations and/or PTEN loss in Her2-positive breast carcinomas treated with trastuzumab are not related to resistance to anti-Her2 therapy |
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