Loss of PTEN in high grade advanced stage triple negative breast ductal cancers in African American women.
Identifieur interne : 000558 ( Main/Exploration ); précédent : 000557; suivant : 000559Loss of PTEN in high grade advanced stage triple negative breast ductal cancers in African American women.
Auteurs : Farhan Khan [États-Unis] ; Ashwini Esnakula [États-Unis] ; Luisel J. Ricks-Santi [États-Unis] ; Rabia Zafar [États-Unis] ; Yasmine Kanaan [États-Unis] ; Tammey Naab [États-Unis]Source :
- Pathology, research and practice [ 1618-0631 ] ; 2018.
Descripteurs français
- KwdFr :
- Adulte (MeSH), Adulte d'âge moyen (MeSH), Afro-Américains (MeSH), Carcinome canalaire du sein (anatomopathologie), Carcinome canalaire du sein (génétique), Femelle (MeSH), Humains (MeSH), Marqueurs biologiques tumoraux (analyse), Phosphatidylinositol 3-kinases (métabolisme), Phosphohydrolase PTEN (génétique), Pronostic (MeSH), Protéines proto-oncogènes c-akt (métabolisme), Sujet âgé (MeSH), Sujet âgé de 80 ans ou plus (MeSH), Sérine-thréonine kinases TOR (métabolisme), Tumeurs du sein (anatomopathologie), Tumeurs du sein triple-négatives (anatomopathologie), Tumeurs du sein triple-négatives (diagnostic).
- MESH :
- analyse : Marqueurs biologiques tumoraux.
- anatomopathologie : Carcinome canalaire du sein, Tumeurs du sein, Tumeurs du sein triple-négatives.
- diagnostic : Tumeurs du sein triple-négatives.
- génétique : Carcinome canalaire du sein, Phosphohydrolase PTEN.
- métabolisme : Phosphatidylinositol 3-kinases, Protéines proto-oncogènes c-akt, Sérine-thréonine kinases TOR.
- Adulte, Adulte d'âge moyen, Afro-Américains, Femelle, Humains, Pronostic, Sujet âgé, Sujet âgé de 80 ans ou plus.
English descriptors
- KwdEn :
- Adult (MeSH), African Americans (MeSH), Aged (MeSH), Aged, 80 and over (MeSH), Biomarkers, Tumor (analysis), Breast Neoplasms (pathology), Carcinoma, Ductal, Breast (genetics), Carcinoma, Ductal, Breast (pathology), Female (MeSH), Humans (MeSH), Middle Aged (MeSH), PTEN Phosphohydrolase (genetics), Phosphatidylinositol 3-Kinases (metabolism), Prognosis (MeSH), Proto-Oncogene Proteins c-akt (metabolism), TOR Serine-Threonine Kinases (metabolism), Triple Negative Breast Neoplasms (diagnosis), Triple Negative Breast Neoplasms (pathology).
- MESH :
- chemical , analysis : Biomarkers, Tumor.
- diagnosis : Triple Negative Breast Neoplasms.
- genetics : Carcinoma, Ductal, Breast, PTEN Phosphohydrolase.
- chemical , metabolism : Phosphatidylinositol 3-Kinases, Proto-Oncogene Proteins c-akt, TOR Serine-Threonine Kinases.
- pathology : Breast Neoplasms, Carcinoma, Ductal, Breast, Triple Negative Breast Neoplasms.
- Adult, African Americans, Aged, Aged, 80 and over, Female, Humans, Middle Aged, Prognosis.
Abstract
INTRODUCTION
PTEN is a tumor suppressor gene that inhibits cell proliferation by inhibiting the phosphoinositide 3-kinase (PI3 K) signaling pathway. The significance of PTEN mutations resulting in variable PTEN expression and their impact on prognosis of breast cancer is not well established. The objective of our study was to correlate the immunohistochemical expression of PTEN in the four major subtypes of breast carcinoma (Luminal A, Luminal B, HER2 positive, and Triple Negative) in a population of 202 African-American (AA) females with other clinicopathological factors.
MATERIALS AND METHODS
Tissue microarrays (TMAs) were constructed from FFPE tumor blocks from primary ductal breast carcinomas in 202 African-American females. Five micrometer sections were stained with a mouse monoclonal antibody against PTEN. The sections were evaluated for the intensity of cytoplasmic and nuclear reactivity. Bivariate analysis was done via χ2 analysis and survivability data was calculated via the generation of Kaplan-Meier curves (SPSS v19).
RESULTS
Loss of PTEN expression was associated with ER negative (p = 0.021), PR negative (p = 0.024) and triple negative (p = 0.0024) breast ductal cancers. It was marginally associated with distant metastasis (p = 0.074). There was no association between PTEN loss and recurrence-free survival or overall survival.
CONCLUSION
In our study, a statistically significant association between PTEN loss and the triple negative breast cancers (TNBC) was found in AA women. PTEN inhibits PI3 K resulting in decreased activation of downstream effector, mammalian target of rapamycin (mTOR). Loss of PTEN results in cell proliferation through activation of mTOR. Targeted therapy with mTOR inhibitors might be useful in the treatment of TNBC.
DOI: 10.1016/j.prp.2018.03.020
PubMed: 29653745
PubMed Central: PMC5963715
Affiliations:
Links toward previous steps (curation, corpus...)
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Electronic address: farhan.khan@wustl.edu.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Pathology, Howard University College of Medicine, Washington, DC</wicri:regionArea><placeName><region type="state">District de Columbia</region></placeName></affiliation></author><author><name sortKey="Esnakula, Ashwini" sort="Esnakula, Ashwini" uniqKey="Esnakula A" first="Ashwini" last="Esnakula">Ashwini Esnakula</name><affiliation wicri:level="2"><nlm:affiliation>Department of Pathology, Howard University College of Medicine, Washington, DC, United States.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Pathology, Howard University College of Medicine, Washington, DC</wicri:regionArea><placeName><region type="state">District de Columbia</region></placeName></affiliation></author><author><name sortKey="Ricks Santi, Luisel J" sort="Ricks Santi, Luisel J" uniqKey="Ricks Santi L" first="Luisel J" last="Ricks-Santi">Luisel J. Ricks-Santi</name><affiliation wicri:level="2"><nlm:affiliation>Cancer Research Center, Hampton University, Hampton, VA, United States.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Cancer Research Center, Hampton University, Hampton, VA</wicri:regionArea><placeName><region type="state">Virginie</region></placeName></affiliation></author><author><name sortKey="Zafar, Rabia" sort="Zafar, Rabia" uniqKey="Zafar R" first="Rabia" last="Zafar">Rabia Zafar</name><affiliation wicri:level="2"><nlm:affiliation>Department of Pathology, Howard University College of Medicine, Washington, DC, United States.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Pathology, Howard University College of Medicine, Washington, DC</wicri:regionArea><placeName><region type="state">District de Columbia</region></placeName></affiliation></author><author><name sortKey="Kanaan, Yasmine" sort="Kanaan, Yasmine" uniqKey="Kanaan Y" first="Yasmine" last="Kanaan">Yasmine Kanaan</name><affiliation wicri:level="2"><nlm:affiliation>Department of Microbiology, Howard University College of Medicine, Washington, DC, United States.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Microbiology, Howard University College of Medicine, Washington, DC</wicri:regionArea><placeName><region type="state">District de Columbia</region></placeName></affiliation></author><author><name sortKey="Naab, Tammey" sort="Naab, Tammey" uniqKey="Naab T" first="Tammey" last="Naab">Tammey Naab</name><affiliation wicri:level="2"><nlm:affiliation>Department of Pathology, Howard University College of Medicine, Washington, DC, United States.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Pathology, Howard University College of Medicine, Washington, DC</wicri:regionArea><placeName><region type="state">District de Columbia</region></placeName></affiliation></author></analytic><series><title level="j">Pathology, research and practice</title><idno type="eISSN">1618-0631</idno><imprint><date when="2018" type="published">2018</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adult (MeSH)</term><term>African Americans (MeSH)</term><term>Aged (MeSH)</term><term>Aged, 80 and over (MeSH)</term><term>Biomarkers, Tumor (analysis)</term><term>Breast Neoplasms (pathology)</term><term>Carcinoma, Ductal, Breast (genetics)</term><term>Carcinoma, Ductal, Breast (pathology)</term><term>Female (MeSH)</term><term>Humans (MeSH)</term><term>Middle Aged (MeSH)</term><term>PTEN Phosphohydrolase (genetics)</term><term>Phosphatidylinositol 3-Kinases (metabolism)</term><term>Prognosis (MeSH)</term><term>Proto-Oncogene Proteins c-akt (metabolism)</term><term>TOR Serine-Threonine Kinases (metabolism)</term><term>Triple Negative Breast Neoplasms (diagnosis)</term><term>Triple Negative Breast Neoplasms (pathology)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Adulte (MeSH)</term><term>Adulte d'âge moyen (MeSH)</term><term>Afro-Américains (MeSH)</term><term>Carcinome canalaire du sein (anatomopathologie)</term><term>Carcinome canalaire du sein (génétique)</term><term>Femelle (MeSH)</term><term>Humains (MeSH)</term><term>Marqueurs biologiques tumoraux (analyse)</term><term>Phosphatidylinositol 3-kinases (métabolisme)</term><term>Phosphohydrolase PTEN (génétique)</term><term>Pronostic (MeSH)</term><term>Protéines proto-oncogènes c-akt (métabolisme)</term><term>Sujet âgé (MeSH)</term><term>Sujet âgé de 80 ans ou plus (MeSH)</term><term>Sérine-thréonine kinases TOR (métabolisme)</term><term>Tumeurs du sein (anatomopathologie)</term><term>Tumeurs du sein triple-négatives (anatomopathologie)</term><term>Tumeurs du sein triple-négatives (diagnostic)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analysis" xml:lang="en"><term>Biomarkers, Tumor</term></keywords><keywords scheme="MESH" qualifier="analyse" xml:lang="fr"><term>Marqueurs biologiques tumoraux</term></keywords><keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Carcinome canalaire du sein</term><term>Tumeurs du sein</term><term>Tumeurs du sein triple-négatives</term></keywords><keywords scheme="MESH" qualifier="diagnosis" xml:lang="en"><term>Triple Negative Breast Neoplasms</term></keywords><keywords scheme="MESH" qualifier="diagnostic" xml:lang="fr"><term>Tumeurs du sein triple-négatives</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Carcinoma, Ductal, Breast</term><term>PTEN Phosphohydrolase</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Carcinome canalaire du sein</term><term>Phosphohydrolase PTEN</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Phosphatidylinositol 3-Kinases</term><term>Proto-Oncogene Proteins c-akt</term><term>TOR Serine-Threonine Kinases</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Phosphatidylinositol 3-kinases</term><term>Protéines proto-oncogènes c-akt</term><term>Sérine-thréonine kinases TOR</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Breast Neoplasms</term><term>Carcinoma, Ductal, Breast</term><term>Triple Negative Breast Neoplasms</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adult</term><term>African Americans</term><term>Aged</term><term>Aged, 80 and over</term><term>Female</term><term>Humans</term><term>Middle Aged</term><term>Prognosis</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Adulte</term><term>Adulte d'âge moyen</term><term>Afro-Américains</term><term>Femelle</term><term>Humains</term><term>Pronostic</term><term>Sujet âgé</term><term>Sujet âgé de 80 ans ou plus</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p><b>INTRODUCTION</b></p><p>PTEN is a tumor suppressor gene that inhibits cell proliferation by inhibiting the phosphoinositide 3-kinase (PI3 K) signaling pathway. The significance of PTEN mutations resulting in variable PTEN expression and their impact on prognosis of breast cancer is not well established. The objective of our study was to correlate the immunohistochemical expression of PTEN in the four major subtypes of breast carcinoma (Luminal A, Luminal B, HER2 positive, and Triple Negative) in a population of 202 African-American (AA) females with other clinicopathological factors.</p></div><div type="abstract" xml:lang="en"><p><b>MATERIALS AND METHODS</b></p><p>Tissue microarrays (TMAs) were constructed from FFPE tumor blocks from primary ductal breast carcinomas in 202 African-American females. Five micrometer sections were stained with a mouse monoclonal antibody against PTEN. The sections were evaluated for the intensity of cytoplasmic and nuclear reactivity. Bivariate analysis was done via χ2 analysis and survivability data was calculated via the generation of Kaplan-Meier curves (SPSS v19).</p></div><div type="abstract" xml:lang="en"><p><b>RESULTS</b></p><p>Loss of PTEN expression was associated with ER negative (p = 0.021), PR negative (p = 0.024) and triple negative (p = 0.0024) breast ductal cancers. It was marginally associated with distant metastasis (p = 0.074). There was no association between PTEN loss and recurrence-free survival or overall survival.</p></div><div type="abstract" xml:lang="en"><p><b>CONCLUSION</b></p><p>In our study, a statistically significant association between PTEN loss and the triple negative breast cancers (TNBC) was found in AA women. PTEN inhibits PI3 K resulting in decreased activation of downstream effector, mammalian target of rapamycin (mTOR). Loss of PTEN results in cell proliferation through activation of mTOR. Targeted therapy with mTOR inhibitors might be useful in the treatment of TNBC.</p></div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">29653745</PMID><DateCompleted><Year>2018</Year><Month>09</Month><Day>28</Day></DateCompleted><DateRevised><Year>2019</Year><Month>05</Month><Day>01</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1618-0631</ISSN><JournalIssue CitedMedium="Internet"><Volume>214</Volume><Issue>5</Issue><PubDate><Year>2018</Year><Month>May</Month></PubDate></JournalIssue><Title>Pathology, research and practice</Title><ISOAbbreviation>Pathol Res Pract</ISOAbbreviation></Journal><ArticleTitle>Loss of PTEN in high grade advanced stage triple negative breast ductal cancers in African American women.</ArticleTitle><Pagination><MedlinePgn>673-678</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">S0344-0338(17)31307-9</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.prp.2018.03.020</ELocationID><Abstract><AbstractText Label="INTRODUCTION" NlmCategory="BACKGROUND">PTEN is a tumor suppressor gene that inhibits cell proliferation by inhibiting the phosphoinositide 3-kinase (PI3 K) signaling pathway. The significance of PTEN mutations resulting in variable PTEN expression and their impact on prognosis of breast cancer is not well established. The objective of our study was to correlate the immunohistochemical expression of PTEN in the four major subtypes of breast carcinoma (Luminal A, Luminal B, HER2 positive, and Triple Negative) in a population of 202 African-American (AA) females with other clinicopathological factors.</AbstractText><AbstractText Label="MATERIALS AND METHODS" NlmCategory="METHODS">Tissue microarrays (TMAs) were constructed from FFPE tumor blocks from primary ductal breast carcinomas in 202 African-American females. Five micrometer sections were stained with a mouse monoclonal antibody against PTEN. The sections were evaluated for the intensity of cytoplasmic and nuclear reactivity. Bivariate analysis was done via χ2 analysis and survivability data was calculated via the generation of Kaplan-Meier curves (SPSS v19).</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">Loss of PTEN expression was associated with ER negative (p = 0.021), PR negative (p = 0.024) and triple negative (p = 0.0024) breast ductal cancers. It was marginally associated with distant metastasis (p = 0.074). There was no association between PTEN loss and recurrence-free survival or overall survival.</AbstractText><AbstractText Label="CONCLUSION" NlmCategory="CONCLUSIONS">In our study, a statistically significant association between PTEN loss and the triple negative breast cancers (TNBC) was found in AA women. PTEN inhibits PI3 K resulting in decreased activation of downstream effector, mammalian target of rapamycin (mTOR). Loss of PTEN results in cell proliferation through activation of mTOR. Targeted therapy with mTOR inhibitors might be useful in the treatment of TNBC.</AbstractText><CopyrightInformation>Copyright © 2018 Elsevier GmbH. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Khan</LastName><ForeName>Farhan</ForeName><Initials>F</Initials><AffiliationInfo><Affiliation>Department of Pathology, Howard University College of Medicine, Washington, DC, United States. Electronic address: farhan.khan@wustl.edu.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Esnakula</LastName><ForeName>Ashwini</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Department of Pathology, Howard University College of Medicine, Washington, DC, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ricks-Santi</LastName><ForeName>Luisel J</ForeName><Initials>LJ</Initials><AffiliationInfo><Affiliation>Cancer Research Center, Hampton University, Hampton, VA, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zafar</LastName><ForeName>Rabia</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Department of Pathology, Howard University College of Medicine, Washington, DC, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kanaan</LastName><ForeName>Yasmine</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Microbiology, Howard University College of Medicine, Washington, DC, United States.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Naab</LastName><ForeName>Tammey</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Department of Pathology, Howard University College of Medicine, Washington, DC, United States.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>G12 RR003048</GrantID><Acronym>RR</Acronym><Agency>NCRR NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>U54 CA091431</GrantID><Acronym>CA</Acronym><Agency>NCI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>UL1 RR031975</GrantID><Acronym>RR</Acronym><Agency>NCRR NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2018</Year><Month>03</Month><Day>27</Day></ArticleDate></Article><MedlineJournalInfo><Country>Germany</Country><MedlineTA>Pathol Res Pract</MedlineTA><NlmUniqueID>7806109</NlmUniqueID><ISSNLinking>0344-0338</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D014408">Biomarkers, Tumor</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.1.-</RegistryNumber><NameOfSubstance UI="D019869">Phosphatidylinositol 3-Kinases</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.1.1</RegistryNumber><NameOfSubstance UI="C546842">MTOR protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.1.1</RegistryNumber><NameOfSubstance UI="D058570">TOR Serine-Threonine Kinases</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.11.1</RegistryNumber><NameOfSubstance UI="D051057">Proto-Oncogene Proteins c-akt</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.1.3.67</RegistryNumber><NameOfSubstance UI="D051059">PTEN Phosphohydrolase</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.1.3.67</RegistryNumber><NameOfSubstance UI="C494929">PTEN protein, human</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001741" MajorTopicYN="N">African Americans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000369" MajorTopicYN="N">Aged, 80 and over</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D014408" MajorTopicYN="N">Biomarkers, Tumor</DescriptorName><QualifierName UI="Q000032" MajorTopicYN="N">analysis</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001943" MajorTopicYN="N">Breast Neoplasms</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018270" MajorTopicYN="N">Carcinoma, Ductal, Breast</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000473" MajorTopicYN="Y">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051059" MajorTopicYN="N">PTEN Phosphohydrolase</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D019869" MajorTopicYN="N">Phosphatidylinositol 3-Kinases</DescriptorName><QualifierName UI="Q000378" 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Naab</name><name sortKey="Ricks Santi, Luisel J" sort="Ricks Santi, Luisel J" uniqKey="Ricks Santi L" first="Luisel J" last="Ricks-Santi">Luisel J. 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