Molecular analysis of a male breast cancer patient with prolonged stable disease under mTOR/PI3K inhibitors BEZ235/everolimus.
Identifieur interne : 000005 ( PubMed/Corpus ); précédent : 000004; suivant : 000006Molecular analysis of a male breast cancer patient with prolonged stable disease under mTOR/PI3K inhibitors BEZ235/everolimus.
Auteurs : A Rose Brannon ; Melissa Frizziero ; David Chen ; Jennifer Hummel ; Jorge Gallo ; Markus Riester ; Parul Patel ; Wing Cheung ; Michael Morrissey ; Carmine Carbone ; Silvia Cottini ; Giampaolo Tortora ; Davide MelisiSource :
- Cold Spring Harbor molecular case studies [ 2373-2865 ] ; 2016.
Abstract
The mTORC1 inhibitor everolimus (Afinitor/RAD001) has been approved for multiple cancer indications, including ER(+)/HER2(-) metastatic breast cancer. However, the combination of everolimus with the dual PI3K/mTOR inhibitor BEZ235 was shown to be more efficacious than either everolimus or BEZ235 alone in preclinical models. Herein, we describe a male breast cancer (MBC) patient who was diagnosed with hormone receptor-positive (HR(+))/HER2(-) stage IIIA invasive ductal carcinoma and sequentially treated with chemoradiotherapy and hormonal therapy. Upon the development of metastases, the patient began a 200 mg twice-daily BEZ235 and 2.5 mg weekly everolimus combination regimen. The patient sustained a prolonged stable disease of 18 mo while undergoing the therapy, before his tumor progressed again. Therefore, we sought to both better understand MBC and investigate the underlying molecular mechanisms of the patient's sensitivity and subsequent resistance to the BEZ235/everolimus combination therapy. Genomic and immunohistochemical analyses were performed on samples collected from the initial invasive ductal carcinoma pretreatment and a metastasis postprogression on the BEZ235/everolimus combination treatment. Both tumors were relatively quiet genomically with no overlap to recurrent MBC alterations in the literature. Markers of PI3K/mTOR pathway hyperactivation were not identified in the pretreatment sample, which complements previous reports of HR(+) female breast cancers being responsive to mTOR inhibition without this activation. The postprogression sample, however, demonstrated greater than fivefold increased estrogen receptor and pathogenesis-related protein expression, which could have constrained the PI3K/mTOR pathway inhibition by BEZ235/everolimus. Overall, these analyses have augmented the limited episteme on MBC genetics and treatment.
DOI: 10.1101/mcs.a000620
PubMed: 27148582
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Comprehensive Cancer Center, Azienda Ospedaliera Universitaria Integrata, 37126 Verona, Italy;; Digestive Molecular Clinical Oncology Research Unit, Department of Medicine, Università degli studi di Verona, 37134 Verona, Italy.</nlm:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2016">2016</date><idno type="doi">10.1101/mcs.a000620</idno><idno type="RBID">pubmed:27148582</idno><idno type="pmid">27148582</idno><idno type="wicri:Area/PubMed/Corpus">000005</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000005</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Molecular analysis of a male breast cancer patient with prolonged stable disease under mTOR/PI3K inhibitors BEZ235/everolimus.</title><author><name sortKey="Brannon, A Rose" sort="Brannon, A Rose" uniqKey="Brannon A" first="A Rose" last="Brannon">A Rose Brannon</name><affiliation><nlm:affiliation>Novartis Institutes for BioMedical Research, Cambridge, Massachusetts 02139, USA;</nlm:affiliation></affiliation></author><author><name sortKey="Frizziero, Melissa" sort="Frizziero, Melissa" uniqKey="Frizziero M" first="Melissa" last="Frizziero">Melissa Frizziero</name><affiliation><nlm:affiliation>Medical Oncology Unit, Azienda Ospedaliera Universitaria Integrata, 37126 Verona, Italy;; Comprehensive Cancer Center, Azienda Ospedaliera Universitaria Integrata, 37126 Verona, Italy;</nlm:affiliation></affiliation></author><author><name sortKey="Chen, David" sort="Chen, David" uniqKey="Chen D" first="David" last="Chen">David Chen</name><affiliation><nlm:affiliation>Oncology Global Development, Novartis Pharmaceuticals Corporation, East Hanover, New Jersey 07936, USA;</nlm:affiliation></affiliation></author><author><name sortKey="Hummel, Jennifer" sort="Hummel, Jennifer" uniqKey="Hummel J" first="Jennifer" last="Hummel">Jennifer Hummel</name><affiliation><nlm:affiliation>Genoptix, Inc., Carlsbad, California 92008, USA;</nlm:affiliation></affiliation></author><author><name sortKey="Gallo, Jorge" sort="Gallo, Jorge" uniqKey="Gallo J" first="Jorge" last="Gallo">Jorge Gallo</name><affiliation><nlm:affiliation>Oncology Global Development, Novartis Pharmaceuticals Corporation, East Hanover, New Jersey 07936, USA;</nlm:affiliation></affiliation></author><author><name sortKey="Riester, Markus" sort="Riester, Markus" uniqKey="Riester M" first="Markus" last="Riester">Markus Riester</name><affiliation><nlm:affiliation>Novartis Institutes for BioMedical Research, Cambridge, Massachusetts 02139, USA;</nlm:affiliation></affiliation></author><author><name sortKey="Patel, Parul" sort="Patel, Parul" uniqKey="Patel P" first="Parul" last="Patel">Parul Patel</name><affiliation><nlm:affiliation>Oncology Global Development, Novartis Pharmaceuticals Corporation, East Hanover, New Jersey 07936, USA;</nlm:affiliation></affiliation></author><author><name sortKey="Cheung, Wing" sort="Cheung, Wing" uniqKey="Cheung W" first="Wing" last="Cheung">Wing Cheung</name><affiliation><nlm:affiliation>Oncology Global Development, Novartis Pharmaceuticals Corporation, East Hanover, New Jersey 07936, USA;</nlm:affiliation></affiliation></author><author><name sortKey="Morrissey, Michael" sort="Morrissey, Michael" uniqKey="Morrissey M" first="Michael" last="Morrissey">Michael Morrissey</name><affiliation><nlm:affiliation>Novartis Institutes for BioMedical Research, Cambridge, Massachusetts 02139, USA;</nlm:affiliation></affiliation></author><author><name sortKey="Carbone, Carmine" sort="Carbone, Carmine" uniqKey="Carbone C" first="Carmine" last="Carbone">Carmine Carbone</name><affiliation><nlm:affiliation>Comprehensive Cancer Center, Azienda Ospedaliera Universitaria Integrata, 37126 Verona, Italy;; Digestive Molecular Clinical Oncology Research Unit, Department of Medicine, Università degli studi di Verona, 37134 Verona, Italy.</nlm:affiliation></affiliation></author><author><name sortKey="Cottini, Silvia" sort="Cottini, Silvia" uniqKey="Cottini S" first="Silvia" last="Cottini">Silvia Cottini</name><affiliation><nlm:affiliation>Medical Oncology Unit, Azienda Ospedaliera Universitaria Integrata, 37126 Verona, Italy;; Comprehensive Cancer Center, Azienda Ospedaliera Universitaria Integrata, 37126 Verona, Italy;</nlm:affiliation></affiliation></author><author><name sortKey="Tortora, Giampaolo" sort="Tortora, Giampaolo" uniqKey="Tortora G" first="Giampaolo" last="Tortora">Giampaolo Tortora</name><affiliation><nlm:affiliation>Medical Oncology Unit, Azienda Ospedaliera Universitaria Integrata, 37126 Verona, Italy;; Comprehensive Cancer Center, Azienda Ospedaliera Universitaria Integrata, 37126 Verona, Italy;</nlm:affiliation></affiliation></author><author><name sortKey="Melisi, Davide" sort="Melisi, Davide" uniqKey="Melisi D" first="Davide" last="Melisi">Davide Melisi</name><affiliation><nlm:affiliation>Medical Oncology Unit, Azienda Ospedaliera Universitaria Integrata, 37126 Verona, Italy;; Comprehensive Cancer Center, Azienda Ospedaliera Universitaria Integrata, 37126 Verona, Italy;; Digestive Molecular Clinical Oncology Research Unit, Department of Medicine, Università degli studi di Verona, 37134 Verona, Italy.</nlm:affiliation></affiliation></author></analytic><series><title level="j">Cold Spring Harbor molecular case studies</title><idno type="ISSN">2373-2865</idno><imprint><date when="2016" type="published">2016</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The mTORC1 inhibitor everolimus (Afinitor/RAD001) has been approved for multiple cancer indications, including ER(+)/HER2(-) metastatic breast cancer. However, the combination of everolimus with the dual PI3K/mTOR inhibitor BEZ235 was shown to be more efficacious than either everolimus or BEZ235 alone in preclinical models. Herein, we describe a male breast cancer (MBC) patient who was diagnosed with hormone receptor-positive (HR(+))/HER2(-) stage IIIA invasive ductal carcinoma and sequentially treated with chemoradiotherapy and hormonal therapy. Upon the development of metastases, the patient began a 200 mg twice-daily BEZ235 and 2.5 mg weekly everolimus combination regimen. The patient sustained a prolonged stable disease of 18 mo while undergoing the therapy, before his tumor progressed again. Therefore, we sought to both better understand MBC and investigate the underlying molecular mechanisms of the patient's sensitivity and subsequent resistance to the BEZ235/everolimus combination therapy. Genomic and immunohistochemical analyses were performed on samples collected from the initial invasive ductal carcinoma pretreatment and a metastasis postprogression on the BEZ235/everolimus combination treatment. Both tumors were relatively quiet genomically with no overlap to recurrent MBC alterations in the literature. Markers of PI3K/mTOR pathway hyperactivation were not identified in the pretreatment sample, which complements previous reports of HR(+) female breast cancers being responsive to mTOR inhibition without this activation. The postprogression sample, however, demonstrated greater than fivefold increased estrogen receptor and pathogenesis-related protein expression, which could have constrained the PI3K/mTOR pathway inhibition by BEZ235/everolimus. Overall, these analyses have augmented the limited episteme on MBC genetics and treatment.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="PubMed-not-MEDLINE"><PMID Version="1">27148582</PMID><DateCreated><Year>2016</Year><Month>05</Month><Day>05</Day></DateCreated><DateCompleted><Year>2016</Year><Month>05</Month><Day>05</Day></DateCompleted><DateRevised><Year>2016</Year><Month>05</Month><Day>07</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">2373-2865</ISSN><JournalIssue CitedMedium="Print"><Volume>2</Volume><Issue>2</Issue><PubDate><Year>2016</Year><Month>Mar</Month></PubDate></JournalIssue><Title>Cold Spring Harbor molecular case studies</Title><ISOAbbreviation>Cold Spring Harb Mol Case Stud</ISOAbbreviation></Journal><ArticleTitle>Molecular analysis of a male breast cancer patient with prolonged stable disease under mTOR/PI3K inhibitors BEZ235/everolimus.</ArticleTitle><Pagination><MedlinePgn>a000620</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1101/mcs.a000620</ELocationID><Abstract><AbstractText>The mTORC1 inhibitor everolimus (Afinitor/RAD001) has been approved for multiple cancer indications, including ER(+)/HER2(-) metastatic breast cancer. However, the combination of everolimus with the dual PI3K/mTOR inhibitor BEZ235 was shown to be more efficacious than either everolimus or BEZ235 alone in preclinical models. Herein, we describe a male breast cancer (MBC) patient who was diagnosed with hormone receptor-positive (HR(+))/HER2(-) stage IIIA invasive ductal carcinoma and sequentially treated with chemoradiotherapy and hormonal therapy. Upon the development of metastases, the patient began a 200 mg twice-daily BEZ235 and 2.5 mg weekly everolimus combination regimen. The patient sustained a prolonged stable disease of 18 mo while undergoing the therapy, before his tumor progressed again. Therefore, we sought to both better understand MBC and investigate the underlying molecular mechanisms of the patient's sensitivity and subsequent resistance to the BEZ235/everolimus combination therapy. Genomic and immunohistochemical analyses were performed on samples collected from the initial invasive ductal carcinoma pretreatment and a metastasis postprogression on the BEZ235/everolimus combination treatment. Both tumors were relatively quiet genomically with no overlap to recurrent MBC alterations in the literature. Markers of PI3K/mTOR pathway hyperactivation were not identified in the pretreatment sample, which complements previous reports of HR(+) female breast cancers being responsive to mTOR inhibition without this activation. The postprogression sample, however, demonstrated greater than fivefold increased estrogen receptor and pathogenesis-related protein expression, which could have constrained the PI3K/mTOR pathway inhibition by BEZ235/everolimus. Overall, these analyses have augmented the limited episteme on MBC genetics and treatment.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Brannon</LastName><ForeName>A Rose</ForeName><Initials>AR</Initials><AffiliationInfo><Affiliation>Novartis Institutes for BioMedical Research, Cambridge, Massachusetts 02139, USA;</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Frizziero</LastName><ForeName>Melissa</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Medical Oncology Unit, Azienda Ospedaliera Universitaria Integrata, 37126 Verona, Italy;; Comprehensive Cancer Center, Azienda Ospedaliera Universitaria Integrata, 37126 Verona, Italy;</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chen</LastName><ForeName>David</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Oncology Global Development, Novartis Pharmaceuticals Corporation, East Hanover, New Jersey 07936, USA;</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hummel</LastName><ForeName>Jennifer</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Genoptix, Inc., Carlsbad, California 92008, USA;</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Gallo</LastName><ForeName>Jorge</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Oncology Global Development, Novartis Pharmaceuticals Corporation, East Hanover, New Jersey 07936, USA;</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Riester</LastName><ForeName>Markus</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Novartis Institutes for BioMedical Research, Cambridge, Massachusetts 02139, USA;</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Patel</LastName><ForeName>Parul</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Oncology Global Development, Novartis Pharmaceuticals Corporation, East Hanover, New Jersey 07936, USA;</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Cheung</LastName><ForeName>Wing</ForeName><Initials>W</Initials><AffiliationInfo><Affiliation>Oncology Global Development, Novartis Pharmaceuticals Corporation, East Hanover, New Jersey 07936, USA;</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Morrissey</LastName><ForeName>Michael</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Novartis Institutes for BioMedical Research, Cambridge, Massachusetts 02139, USA;</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Carbone</LastName><ForeName>Carmine</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Comprehensive Cancer Center, Azienda Ospedaliera Universitaria Integrata, 37126 Verona, Italy;; Digestive Molecular Clinical Oncology Research Unit, Department of Medicine, Università degli studi di Verona, 37134 Verona, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Cottini</LastName><ForeName>Silvia</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Medical Oncology Unit, Azienda Ospedaliera Universitaria Integrata, 37126 Verona, Italy;; Comprehensive Cancer Center, Azienda Ospedaliera Universitaria Integrata, 37126 Verona, Italy;</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tortora</LastName><ForeName>Giampaolo</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>Medical Oncology Unit, Azienda Ospedaliera Universitaria Integrata, 37126 Verona, Italy;; Comprehensive Cancer Center, Azienda Ospedaliera Universitaria Integrata, 37126 Verona, Italy;</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Melisi</LastName><ForeName>Davide</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Medical Oncology Unit, Azienda Ospedaliera Universitaria Integrata, 37126 Verona, Italy;; Comprehensive Cancer Center, Azienda Ospedaliera Universitaria Integrata, 37126 Verona, Italy;; Digestive Molecular Clinical Oncology Research Unit, Department of Medicine, Università degli studi di Verona, 37134 Verona, Italy.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Cold Spring Harb Mol Case Stud</MedlineTA><NlmUniqueID>101660017</NlmUniqueID><ISSNLinking>2373-2865</ISSNLinking></MedlineJournalInfo><OtherID Source="NLM">PMC4849849</OtherID><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">neoplasm of the breast</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2016</Year><Month>5</Month><Day>6</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2016</Year><Month>5</Month><Day>6</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2016</Year><Month>5</Month><Day>6</Day><Hour>6</Hour><Minute>1</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="doi">10.1101/mcs.a000620</ArticleId><ArticleId IdType="pii">BrannonMCS000620</ArticleId><ArticleId IdType="pubmed">27148582</ArticleId><ArticleId IdType="pmc">PMC4849849</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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