PittsburghV1, PubMed, Checkpoint, bibRecord, 001493

Single-cell genetic analysis reveals insights into clonal development of prostate cancers and indicates loss of PTEN as a marker of poor prognosis.

Identifieur interne : 001493 ( PubMed/Checkpoint ); précédent : 001492; suivant : 001494

Single-cell genetic analysis reveals insights into clonal development of prostate cancers and indicates loss of PTEN as a marker of poor prognosis.

Auteurs : Kerstin M. Heselmeyer-Haddad [États-Unis] ; Lissa Y. Berroa Garcia [États-Unis] ; Amanda Bradley [États-Unis] ; Leanora Hernandez [États-Unis] ; Yue Hu [États-Unis] ; Jens K. Habermann [Allemagne] ; Christoph Dumke [Allemagne] ; Christoph Thorns [Allemagne] ; Sven Perner [Allemagne] ; Ekaterina Pestova [États-Unis] ; Catherine Burke [États-Unis] ; Salim A. Chowdhury [États-Unis] ; Russell Schwartz [États-Unis] ; Alejandro A. Sch Ffer [États-Unis] ; Pamela L. Paris [États-Unis] ; Thomas Ried [États-Unis]

Source :

The American journal of pathology [ 1525-2191 ] ; 2014.

RBID : pubmed:25131421

Descripteurs français

English descriptors

KwdEn :
- Adenocarcinoma (genetics), Adenocarcinoma (pathology), Aged, Biomarkers, Tumor (genetics), Biomarkers, Tumor (metabolism), Chromosomal Instability, Comparative Genomic Hybridization, Disease Progression, Humans, In Situ Hybridization, Fluorescence, Male, Middle Aged, Oncogene Proteins, Fusion (genetics), PTEN Phosphohydrolase (genetics), PTEN Phosphohydrolase (metabolism), Ploidies, Prognosis, Prostate (pathology), Prostatectomy, Prostatic Neoplasms (genetics), Prostatic Neoplasms (pathology), Single-Cell Analysis.
MESH :
- chemical , genetics : Biomarkers, Tumor, Oncogene Proteins, Fusion, PTEN Phosphohydrolase.
- genetics : Adenocarcinoma, Prostatic Neoplasms.
- chemical , metabolism : Biomarkers, Tumor, PTEN Phosphohydrolase.
- pathology : Adenocarcinoma, Prostate, Prostatic Neoplasms.
- Aged, Chromosomal Instability, Comparative Genomic Hybridization, Disease Progression, Humans, In Situ Hybridization, Fluorescence, Male, Middle Aged, Ploidies, Prognosis, Prostatectomy, Single-Cell Analysis.

Abstract

Gauging the risk of developing progressive disease is a major challenge in prostate cancer patient management. We used genetic markers to understand genomic alteration dynamics during disease progression. By using a novel, advanced, multicolor fluorescence in situ hybridization approach, we enumerated copy numbers of six genes previously identified by array comparative genomic hybridization to be involved in aggressive prostate cancer [TBL1XR1, CTTNBP2, MYC (alias c-myc), PTEN, MEN1, and PDGFB] in six nonrecurrent and seven recurrent radical prostatectomy cases. An ERG break-apart probe to detect TMPRSS2-ERG fusions was included. Subsequent hybridization of probe panels and cell relocation resulted in signal counts for all probes in each individual cell analyzed. Differences in the degree of chromosomal and genomic instability (ie, tumor heterogeneity) or the percentage of cells with TMPRSS2-ERG fusion between samples with or without progression were not observed. Tumors from patients that progressed had more chromosomal gains and losses, and showed a higher degree of selection for a predominant clonal pattern. PTEN loss was the most frequent aberration in progressers (57%), followed by TBL1XR1 gain (29%). MYC gain was observed in one progresser, which was the only lesion with an ERG gain, but no TMPRSS2-ERG fusion. According to our results, a probe set consisting of PTEN, MYC, and TBL1XR1 would detect progressers with 86% sensitivity and 100% specificity. This will be evaluated further in larger studies.

DOI: 10.1016/j.ajpath.2014.06.030
PubMed: 25131421

Affiliations:

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<author><name sortKey="Ried, Thomas" sort="Ried, Thomas" uniqKey="Ried T" first="Thomas" last="Ried">Thomas Ried</name>
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<placeName><region type="state">Californie</region>
</placeName>
<wicri:cityArea>Department of Urology, Helen Diller Family Comprehensive Cancer Center, University of California at San Francisco, San Francisco</wicri:cityArea>
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<author><name sortKey="Chowdhury, Salim A" sort="Chowdhury, Salim A" uniqKey="Chowdhury S" first="Salim A" last="Chowdhury">Salim A. Chowdhury</name>
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<author><name sortKey="Sch Ffer, Alejandro A" sort="Sch Ffer, Alejandro A" uniqKey="Sch Ffer A" first="Alejandro A" last="Sch Ffer">Alejandro A. Sch Ffer</name>
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<country xml:lang="fr">États-Unis</country>
<placeName><region type="state">Maryland</region>
</placeName>
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<country>États-Unis</country>
<placeName><region type="state">Californie</region>
</placeName>
<wicri:cityArea>Department of Urology, Helen Diller Family Comprehensive Cancer Center, University of California at San Francisco, San Francisco</wicri:cityArea>
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<author><name sortKey="Ried, Thomas" sort="Ried, Thomas" uniqKey="Ried T" first="Thomas" last="Ried">Thomas Ried</name>
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<country xml:lang="fr">États-Unis</country>
<placeName><region type="state">Maryland</region>
</placeName>
<wicri:cityArea>Genetics Branch, Center for Cancer Research, National Cancer Institute, Bethesda</wicri:cityArea>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adenocarcinoma (genetics)</term>
<term>Adenocarcinoma (pathology)</term>
<term>Aged</term>
<term>Biomarkers, Tumor (genetics)</term>
<term>Biomarkers, Tumor (metabolism)</term>
<term>Chromosomal Instability</term>
<term>Comparative Genomic Hybridization</term>
<term>Disease Progression</term>
<term>Humans</term>
<term>In Situ Hybridization, Fluorescence</term>
<term>Male</term>
<term>Middle Aged</term>
<term>Oncogene Proteins, Fusion (genetics)</term>
<term>PTEN Phosphohydrolase (genetics)</term>
<term>PTEN Phosphohydrolase (metabolism)</term>
<term>Ploidies</term>
<term>Prognosis</term>
<term>Prostate (pathology)</term>
<term>Prostatectomy</term>
<term>Prostatic Neoplasms (genetics)</term>
<term>Prostatic Neoplasms (pathology)</term>
<term>Single-Cell Analysis</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Adulte d'âge moyen</term>
<term>Adénocarcinome (anatomopathologie)</term>
<term>Adénocarcinome (génétique)</term>
<term>Analyse sur cellule unique</term>
<term>Humains</term>
<term>Hybridation génomique comparative</term>
<term>Instabilité des chromosomes</term>
<term>Marqueurs biologiques tumoraux (génétique)</term>
<term>Marqueurs biologiques tumoraux (métabolisme)</term>
<term>Mâle</term>
<term>Phosphohydrolase PTEN (génétique)</term>
<term>Phosphohydrolase PTEN (métabolisme)</term>
<term>Ploïdies</term>
<term>Pronostic</term>
<term>Prostate (anatomopathologie)</term>
<term>Prostatectomie</term>
<term>Protéines de fusion oncogènes (génétique)</term>
<term>Sujet âgé</term>
<term>Technique FISH</term>
<term>Tumeurs de la prostate (anatomopathologie)</term>
<term>Tumeurs de la prostate (génétique)</term>
<term>Évolution de la maladie</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Biomarkers, Tumor</term>
<term>Oncogene Proteins, Fusion</term>
<term>PTEN Phosphohydrolase</term>
</keywords>
<keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Adénocarcinome</term>
<term>Prostate</term>
<term>Tumeurs de la prostate</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Adenocarcinoma</term>
<term>Prostatic Neoplasms</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Adénocarcinome</term>
<term>Marqueurs biologiques tumoraux</term>
<term>Phosphohydrolase PTEN</term>
<term>Protéines de fusion oncogènes</term>
<term>Tumeurs de la prostate</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Biomarkers, Tumor</term>
<term>PTEN Phosphohydrolase</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Marqueurs biologiques tumoraux</term>
<term>Phosphohydrolase PTEN</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Adenocarcinoma</term>
<term>Prostate</term>
<term>Prostatic Neoplasms</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Aged</term>
<term>Chromosomal Instability</term>
<term>Comparative Genomic Hybridization</term>
<term>Disease Progression</term>
<term>Humans</term>
<term>In Situ Hybridization, Fluorescence</term>
<term>Male</term>
<term>Middle Aged</term>
<term>Ploidies</term>
<term>Prognosis</term>
<term>Prostatectomy</term>
<term>Single-Cell Analysis</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Adulte d'âge moyen</term>
<term>Analyse sur cellule unique</term>
<term>Humains</term>
<term>Hybridation génomique comparative</term>
<term>Instabilité des chromosomes</term>
<term>Mâle</term>
<term>Ploïdies</term>
<term>Pronostic</term>
<term>Prostatectomie</term>
<term>Sujet âgé</term>
<term>Technique FISH</term>
<term>Évolution de la maladie</term>
</keywords>
</textClass>
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<front><div type="abstract" xml:lang="en">Gauging the risk of developing progressive disease is a major challenge in prostate cancer patient management. We used genetic markers to understand genomic alteration dynamics during disease progression. By using a novel, advanced, multicolor fluorescence in situ hybridization approach, we enumerated copy numbers of six genes previously identified by array comparative genomic hybridization to be involved in aggressive prostate cancer [TBL1XR1, CTTNBP2, MYC (alias c-myc), PTEN, MEN1, and PDGFB] in six nonrecurrent and seven recurrent radical prostatectomy cases. An ERG break-apart probe to detect TMPRSS2-ERG fusions was included. Subsequent hybridization of probe panels and cell relocation resulted in signal counts for all probes in each individual cell analyzed. Differences in the degree of chromosomal and genomic instability (ie, tumor heterogeneity) or the percentage of cells with TMPRSS2-ERG fusion between samples with or without progression were not observed. Tumors from patients that progressed had more chromosomal gains and losses, and showed a higher degree of selection for a predominant clonal pattern. PTEN loss was the most frequent aberration in progressers (57%), followed by TBL1XR1 gain (29%). MYC gain was observed in one progresser, which was the only lesion with an ERG gain, but no TMPRSS2-ERG fusion. According to our results, a probe set consisting of PTEN, MYC, and TBL1XR1 would detect progressers with 86% sensitivity and 100% specificity. This will be evaluated further in larger studies.</div>
</front>
</TEI>
<pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">25131421</PMID>
<DateCreated><Year>2014</Year>
<Month>09</Month>
<Day>20</Day>
</DateCreated>
<DateCompleted><Year>2016</Year>
<Month>05</Month>
<Day>02</Day>
</DateCompleted>
<DateRevised><Year>2017</Year>
<Month>02</Month>
<Day>20</Day>
</DateRevised>
<Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1525-2191</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>184</Volume>
<Issue>10</Issue>
<PubDate><Year>2014</Year>
<Month>Oct</Month>
</PubDate>
</JournalIssue>
<Title>The American journal of pathology</Title>
<ISOAbbreviation>Am. J. Pathol.</ISOAbbreviation>
</Journal>
<ArticleTitle>Single-cell genetic analysis reveals insights into clonal development of prostate cancers and indicates loss of PTEN as a marker of poor prognosis.</ArticleTitle>
<Pagination><MedlinePgn>2671-86</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.1016/j.ajpath.2014.06.030</ELocationID>
<ELocationID EIdType="pii" ValidYN="Y">S0002-9440(14)00418-0</ELocationID>
<Abstract><AbstractText>Gauging the risk of developing progressive disease is a major challenge in prostate cancer patient management. We used genetic markers to understand genomic alteration dynamics during disease progression. By using a novel, advanced, multicolor fluorescence in situ hybridization approach, we enumerated copy numbers of six genes previously identified by array comparative genomic hybridization to be involved in aggressive prostate cancer [TBL1XR1, CTTNBP2, MYC (alias c-myc), PTEN, MEN1, and PDGFB] in six nonrecurrent and seven recurrent radical prostatectomy cases. An ERG break-apart probe to detect TMPRSS2-ERG fusions was included. Subsequent hybridization of probe panels and cell relocation resulted in signal counts for all probes in each individual cell analyzed. Differences in the degree of chromosomal and genomic instability (ie, tumor heterogeneity) or the percentage of cells with TMPRSS2-ERG fusion between samples with or without progression were not observed. Tumors from patients that progressed had more chromosomal gains and losses, and showed a higher degree of selection for a predominant clonal pattern. PTEN loss was the most frequent aberration in progressers (57%), followed by TBL1XR1 gain (29%). MYC gain was observed in one progresser, which was the only lesion with an ERG gain, but no TMPRSS2-ERG fusion. According to our results, a probe set consisting of PTEN, MYC, and TBL1XR1 would detect progressers with 86% sensitivity and 100% specificity. This will be evaluated further in larger studies.</AbstractText>
<CopyrightInformation>Copyright © 2014 American Society for Investigative Pathology. Published by Elsevier Inc. All rights reserved.</CopyrightInformation>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Heselmeyer-Haddad</LastName>
<ForeName>Kerstin M</ForeName>
<Initials>KM</Initials>
<AffiliationInfo><Affiliation>Genetics Branch, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland. Electronic address: heselmek@mail.nih.gov.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Berroa Garcia</LastName>
<ForeName>Lissa Y</ForeName>
<Initials>LY</Initials>
<AffiliationInfo><Affiliation>Genetics Branch, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Bradley</LastName>
<ForeName>Amanda</ForeName>
<Initials>A</Initials>
<AffiliationInfo><Affiliation>Genetics Branch, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Hernandez</LastName>
<ForeName>Leanora</ForeName>
<Initials>L</Initials>
<AffiliationInfo><Affiliation>Genetics Branch, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Hu</LastName>
<ForeName>Yue</ForeName>
<Initials>Y</Initials>
<AffiliationInfo><Affiliation>Genetics Branch, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Habermann</LastName>
<ForeName>Jens K</ForeName>
<Initials>JK</Initials>
<AffiliationInfo><Affiliation>Section for Translational Surgical Oncology and Biobanking, Department of Surgery, University of Lübeck and University Medical Center Schleswig-Holstein, Campus University of Lübeck, Lübeck, Germany.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Dumke</LastName>
<ForeName>Christoph</ForeName>
<Initials>C</Initials>
<AffiliationInfo><Affiliation>Section for Translational Surgical Oncology and Biobanking, Department of Surgery, University of Lübeck and University Medical Center Schleswig-Holstein, Campus University of Lübeck, Lübeck, Germany.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Thorns</LastName>
<ForeName>Christoph</ForeName>
<Initials>C</Initials>
<AffiliationInfo><Affiliation>Institute of Pathology, University of Lübeck and University Medical Center Schleswig-Holstein, Campus University of Lübeck, Lübeck, Germany.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Perner</LastName>
<ForeName>Sven</ForeName>
<Initials>S</Initials>
<AffiliationInfo><Affiliation>Department of Prostate Cancer Research, Institute of Pathology, University Hospital of Bonn, Bonn, Germany.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Pestova</LastName>
<ForeName>Ekaterina</ForeName>
<Initials>E</Initials>
<AffiliationInfo><Affiliation>Abbott Molecular, Des Plaines, Illinois.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Burke</LastName>
<ForeName>Catherine</ForeName>
<Initials>C</Initials>
<AffiliationInfo><Affiliation>Department of Urology, Helen Diller Family Comprehensive Cancer Center, University of California at San Francisco, San Francisco, California.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Chowdhury</LastName>
<ForeName>Salim A</ForeName>
<Initials>SA</Initials>
<AffiliationInfo><Affiliation>Joint Carnegie Mellon/University of Pittsburgh Ph.D. Program in Computational Biology, Carnegie Mellon University, Pittsburgh, Pennsylvania; Lane Center for Computational Biology, Carnegie Mellon University, Pittsburgh, Pennsylvania.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Schwartz</LastName>
<ForeName>Russell</ForeName>
<Initials>R</Initials>
<AffiliationInfo><Affiliation>Lane Center for Computational Biology, Carnegie Mellon University, Pittsburgh, Pennsylvania; Department of Biological Sciences, Carnegie Mellon University, Pittsburgh, Pennsylvania.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Schäffer</LastName>
<ForeName>Alejandro A</ForeName>
<Initials>AA</Initials>
<AffiliationInfo><Affiliation>Computational Biology Branch, National Center for Biotechnology Information, the National Institutes of Health, Bethesda, Maryland.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Paris</LastName>
<ForeName>Pamela L</ForeName>
<Initials>PL</Initials>
<AffiliationInfo><Affiliation>Department of Urology, Helen Diller Family Comprehensive Cancer Center, University of California at San Francisco, San Francisco, California.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Ried</LastName>
<ForeName>Thomas</ForeName>
<Initials>T</Initials>
<AffiliationInfo><Affiliation>Genetics Branch, Center for Cancer Research, National Cancer Institute, Bethesda, Maryland.</Affiliation>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>eng</Language>
<GrantList CompleteYN="Y"><Grant><GrantID>R01 AI076318</GrantID>
<Acronym>AI</Acronym>
<Agency>NIAID NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>R01 CA115484</GrantID>
<Acronym>CA</Acronym>
<Agency>NCI NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><GrantID>R01 CA140214</GrantID>
<Acronym>CA</Acronym>
<Agency>NCI NIH HHS</Agency>
<Country>United States</Country>
</Grant>
<Grant><Agency>Intramural NIH HHS</Agency>
<Country>United States</Country>
</Grant>
</GrantList>
<PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType>
<PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType>
<PublicationType UI="D052060">Research Support, N.I.H., Intramural</PublicationType>
</PublicationTypeList>
<ArticleDate DateType="Electronic"><Year>2014</Year>
<Month>08</Month>
<Day>14</Day>
</ArticleDate>
</Article>
<MedlineJournalInfo><Country>United States</Country>
<MedlineTA>Am J Pathol</MedlineTA>
<NlmUniqueID>0370502</NlmUniqueID>
<ISSNLinking>0002-9440</ISSNLinking>
</MedlineJournalInfo>
<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D014408">Biomarkers, Tumor</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D015514">Oncogene Proteins, Fusion</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>AIM</CitationSubset>
<CitationSubset>IM</CitationSubset>
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   |texte=   Single-cell genetic analysis reveals insights into clonal development of prostate cancers and indicates loss of PTEN as a marker of poor prognosis.
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Single-cell genetic analysis reveals insights into clonal development of prostate cancers and indicates loss of PTEN as a marker of poor prognosis.

Single-cell genetic analysis reveals insights into clonal development of prostate cancers and indicates loss of PTEN as a marker of poor prognosis.

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