Centrosome amplification is a frequent event in circulating tumor cells from subjects with metastatic breast cancer

Centrosome amplification (CA) is a common phenomenon in cancer, promotes genomic stability and cancer evolution, and has been reported to promote metastasis. CA promotes a stochastic gain/loss of chromosomes during cell division, known as chromosomal instability (CIN). However, it is unclear whether...

Ausführliche Beschreibung

Gespeichert in:

Bibliographische Detailangaben
Veröffentlicht in:	Molecular oncology Jg. 14; H. 8; S. 1898 - 1909
Hauptverfasser:	Singh, Ashok, Denu, Ryan A., Wolfe, Serena K., Sperger, Jamie M., Schehr, Jennifer, Witkowsky, Tessa, Esbona, Karla, Chappell, Richard J., Weaver, Beth A., Burkard, Mark E., Lang, Joshua M.
Format:	Journal Article
Sprache:	Englisch
Veröffentlicht:	United States John Wiley & Sons, Inc 01.08.2020 John Wiley and Sons Inc Wiley
Schlagworte:	Antibodies Automation Biomarkers Breast cancer CD45 antigen Cell culture Cell division centrin centrosome amplification Chemotherapy Chromosomes Clinical trials CTC Cytokeratin EpCAM Epithelial cells Genomic instability Laboratories Metastases Metastasis pericentrin Tumor cell lines Tumor cells Tumors United States > US Wisconsin centrosome amplification pericentrin breast cancer centrin CTC EpCAM
ISSN:	1574-7891, 1878-0261, 1878-0261
Online-Zugang:	Volltext
Tags:	Tag hinzufügen Keine Tags, Fügen Sie den ersten Tag hinzu!

Abstract	Centrosome amplification (CA) is a common phenomenon in cancer, promotes genomic stability and cancer evolution, and has been reported to promote metastasis. CA promotes a stochastic gain/loss of chromosomes during cell division, known as chromosomal instability (CIN). However, it is unclear whether CA is present in circulating tumor cells (CTCs), the seeds for metastasis. Here, we surveyed CA in CTCs from human subjects with metastatic breast cancer. CTCs were captured by CD45 exclusion and selection of EpCAM‐positive cells using an exclusion‐based sample preparation technology platform known as VERSA (versatile exclusion‐based rare sample analysis). Centriole amplification (centrin foci> 4) is the definitive assay for CA. However, determination of centrin foci is technically challenging and incompatible with automated analysis. To test if the more technically accessible centrosome marker pericentrin could serve as a surrogate for centriole amplification in CTCs, cells were stained with pericentrin and centrin antibodies to evaluate CA. This assay was first validated using breast cancer cell lines and a nontransformed epithelial cell line model of inducible CA, then translated to CTCs. Pericentrin area and pericentrin area x intensity correlate well with centrin foci, validating pericentrin as a surrogate marker of CA. CA is found in CTCs from 75% of subjects, with variability in the percentage and extent of CA in individual circulating cells in a given subject, similar to the variability previously seen in primary tumors and cell lines. In summary, we created, validated, and implemented a novel method to assess CA in CTCs from subjects with metastatic breast cancer. Such an assay will be useful for longitudinal monitoring of CA in cancer patients and in prospective clinical trials for assessing the impact of CA on response to therapy. Circulating tumor cells (CTCs) are a rare population of cancer cells released into peripheral circulation from primary and metastatic cancer sites. Centrosome amplification (CA) has been reported in virtually all human cancers and has been shown to make cells more invasive. In this study, we develop an assay to detect CA in CTCs. We find that CA is prevalent in CTCs from subjects with metastatic breast cancer.
AbstractList	Centrosome amplification (CA) is a common phenomenon in cancer, promotes genomic stability and cancer evolution, and has been reported to promote metastasis. CA promotes a stochastic gain/loss of chromosomes during cell division, known as chromosomal instability (CIN). However, it is unclear whether CA is present in circulating tumor cells (CTCs), the seeds for metastasis. Here, we surveyed CA in CTCs from human subjects with metastatic breast cancer. CTCs were captured by CD45 exclusion and selection of EpCAM‐positive cells using an exclusion‐based sample preparation technology platform known as VERSA (versatile exclusion‐based rare sample analysis). Centriole amplification (centrin foci> 4) is the definitive assay for CA. However, determination of centrin foci is technically challenging and incompatible with automated analysis. To test if the more technically accessible centrosome marker pericentrin could serve as a surrogate for centriole amplification in CTCs, cells were stained with pericentrin and centrin antibodies to evaluate CA. This assay was first validated using breast cancer cell lines and a nontransformed epithelial cell line model of inducible CA, then translated to CTCs. Pericentrin area and pericentrin area x intensity correlate well with centrin foci, validating pericentrin as a surrogate marker of CA. CA is found in CTCs from 75% of subjects, with variability in the percentage and extent of CA in individual circulating cells in a given subject, similar to the variability previously seen in primary tumors and cell lines. In summary, we created, validated, and implemented a novel method to assess CA in CTCs from subjects with metastatic breast cancer. Such an assay will be useful for longitudinal monitoring of CA in cancer patients and in prospective clinical trials for assessing the impact of CA on response to therapy. Centrosome amplification (CA) is a common phenomenon in cancer, promotes genomic stability and cancer evolution, and has been reported to promote metastasis. CA promotes a stochastic gain/loss of chromosomes during cell division, known as chromosomal instability (CIN). However, it is unclear whether CA is present in circulating tumor cells (CTCs), the seeds for metastasis. Here, we surveyed CA in CTCs from human subjects with metastatic breast cancer. CTCs were captured by CD45 exclusion and selection of EpCAM‐positive cells using an exclusion‐based sample preparation technology platform known as VERSA (versatile exclusion‐based rare sample analysis). Centriole amplification (centrin foci> 4) is the definitive assay for CA. However, determination of centrin foci is technically challenging and incompatible with automated analysis. To test if the more technically accessible centrosome marker pericentrin could serve as a surrogate for centriole amplification in CTCs, cells were stained with pericentrin and centrin antibodies to evaluate CA. This assay was first validated using breast cancer cell lines and a nontransformed epithelial cell line model of inducible CA, then translated to CTCs. Pericentrin area and pericentrin area x intensity correlate well with centrin foci, validating pericentrin as a surrogate marker of CA. CA is found in CTCs from 75% of subjects, with variability in the percentage and extent of CA in individual circulating cells in a given subject, similar to the variability previously seen in primary tumors and cell lines. In summary, we created, validated, and implemented a novel method to assess CA in CTCs from subjects with metastatic breast cancer. Such an assay will be useful for longitudinal monitoring of CA in cancer patients and in prospective clinical trials for assessing the impact of CA on response to therapy. Circulating tumor cells (CTCs) are a rare population of cancer cells released into peripheral circulation from primary and metastatic cancer sites. Centrosome amplification (CA) has been reported in virtually all human cancers and has been shown to make cells more invasive. In this study, we develop an assay to detect CA in CTCs. We find that CA is prevalent in CTCs from subjects with metastatic breast cancer. Centrosome amplification (CA) is a common phenomenon in cancer, promotes genomic stability and cancer evolution, and has been reported to promote metastasis. CA promotes a stochastic gain/loss of chromosomes during cell division, known as chromosomal instability (CIN). However, it is unclear whether CA is present in circulating tumor cells (CTCs), the seeds for metastasis. Here, we surveyed CA in CTCs from human subjects with metastatic breast cancer. CTCs were captured by CD45 exclusion and selection of EpCAM‐positive cells using an exclusion‐based sample preparation technology platform known as VERSA (versatile exclusion‐based rare sample analysis). Centriole amplification (centrin foci> 4) is the definitive assay for CA. However, determination of centrin foci is technically challenging and incompatible with automated analysis. To test if the more technically accessible centrosome marker pericentrin could serve as a surrogate for centriole amplification in CTCs, cells were stained with pericentrin and centrin antibodies to evaluate CA. This assay was first validated using breast cancer cell lines and a nontransformed epithelial cell line model of inducible CA, then translated to CTCs. Pericentrin area and pericentrin area x intensity correlate well with centrin foci, validating pericentrin as a surrogate marker of CA. CA is found in CTCs from 75% of subjects, with variability in the percentage and extent of CA in individual circulating cells in a given subject, similar to the variability previously seen in primary tumors and cell lines. In summary, we created, validated, and implemented a novel method to assess CA in CTCs from subjects with metastatic breast cancer. Such an assay will be useful for longitudinal monitoring of CA in cancer patients and in prospective clinical trials for assessing the impact of CA on response to therapy. Centrosome amplification (CA) is a common phenomenon in cancer, promotes genomic stability and cancer evolution, and has been reported to promote metastasis. CA promotes a stochastic gain/loss of chromosomes during cell division, known as chromosomal instability (CIN). However, it is unclear whether CA is present in circulating tumor cells (CTCs), the seeds for metastasis. Here, we surveyed CA in CTCs from human subjects with metastatic breast cancer. CTCs were captured by CD45 exclusion and selection of EpCAM-positive cells using an exclusion-based sample preparation technology platform known as VERSA (versatile exclusion-based rare sample analysis). Centriole amplification (centrin foci> 4) is the definitive assay for CA. However, determination of centrin foci is technically challenging and incompatible with automated analysis. To test if the more technically accessible centrosome marker pericentrin could serve as a surrogate for centriole amplification in CTCs, cells were stained with pericentrin and centrin antibodies to evaluate CA. This assay was first validated using breast cancer cell lines and a nontransformed epithelial cell line model of inducible CA, then translated to CTCs. Pericentrin area and pericentrin area x intensity correlate well with centrin foci, validating pericentrin as a surrogate marker of CA. CA is found in CTCs from 75% of subjects, with variability in the percentage and extent of CA in individual circulating cells in a given subject, similar to the variability previously seen in primary tumors and cell lines. In summary, we created, validated, and implemented a novel method to assess CA in CTCs from subjects with metastatic breast cancer. Such an assay will be useful for longitudinal monitoring of CA in cancer patients and in prospective clinical trials for assessing the impact of CA on response to therapy.Centrosome amplification (CA) is a common phenomenon in cancer, promotes genomic stability and cancer evolution, and has been reported to promote metastasis. CA promotes a stochastic gain/loss of chromosomes during cell division, known as chromosomal instability (CIN). However, it is unclear whether CA is present in circulating tumor cells (CTCs), the seeds for metastasis. Here, we surveyed CA in CTCs from human subjects with metastatic breast cancer. CTCs were captured by CD45 exclusion and selection of EpCAM-positive cells using an exclusion-based sample preparation technology platform known as VERSA (versatile exclusion-based rare sample analysis). Centriole amplification (centrin foci> 4) is the definitive assay for CA. However, determination of centrin foci is technically challenging and incompatible with automated analysis. To test if the more technically accessible centrosome marker pericentrin could serve as a surrogate for centriole amplification in CTCs, cells were stained with pericentrin and centrin antibodies to evaluate CA. This assay was first validated using breast cancer cell lines and a nontransformed epithelial cell line model of inducible CA, then translated to CTCs. Pericentrin area and pericentrin area x intensity correlate well with centrin foci, validating pericentrin as a surrogate marker of CA. CA is found in CTCs from 75% of subjects, with variability in the percentage and extent of CA in individual circulating cells in a given subject, similar to the variability previously seen in primary tumors and cell lines. In summary, we created, validated, and implemented a novel method to assess CA in CTCs from subjects with metastatic breast cancer. Such an assay will be useful for longitudinal monitoring of CA in cancer patients and in prospective clinical trials for assessing the impact of CA on response to therapy. Centrosome amplification (CA) is a common phenomenon in cancer, promotes genomic stability and cancer evolution, and has been reported to promote metastasis. CA promotes a stochastic gain/loss of chromosomes during cell division, known as chromosomal instability (CIN). However, it is unclear whether CA is present in circulating tumor cells (CTCs), the seeds for metastasis. Here, we surveyed CA in CTCs from human subjects with metastatic breast cancer. CTCs were captured by CD45 exclusion and selection of EpCAM‐positive cells using an exclusion‐based sample preparation technology platform known as VERSA (versatile exclusion‐based rare sample analysis). Centriole amplification (centrin foci> 4) is the definitive assay for CA. However, determination of centrin foci is technically challenging and incompatible with automated analysis. To test if the more technically accessible centrosome marker pericentrin could serve as a surrogate for centriole amplification in CTCs, cells were stained with pericentrin and centrin antibodies to evaluate CA. This assay was first validated using breast cancer cell lines and a nontransformed epithelial cell line model of inducible CA, then translated to CTCs. Pericentrin area and pericentrin area x intensity correlate well with centrin foci, validating pericentrin as a surrogate marker of CA. CA is found in CTCs from 75% of subjects, with variability in the percentage and extent of CA in individual circulating cells in a given subject, similar to the variability previously seen in primary tumors and cell lines. In summary, we created, validated, and implemented a novel method to assess CA in CTCs from subjects with metastatic breast cancer. Such an assay will be useful for longitudinal monitoring of CA in cancer patients and in prospective clinical trials for assessing the impact of CA on response to therapy. Circulating tumor cells (CTCs) are a rare population of cancer cells released into peripheral circulation from primary and metastatic cancer sites. Centrosome amplification (CA) has been reported in virtually all human cancers and has been shown to make cells more invasive. In this study, we develop an assay to detect CA in CTCs. We find that CA is prevalent in CTCs from subjects with metastatic breast cancer.
Author	Witkowsky, Tessa Schehr, Jennifer Lang, Joshua M. Burkard, Mark E. Esbona, Karla Sperger, Jamie M. Denu, Ryan A. Weaver, Beth A. Singh, Ashok Wolfe, Serena K. Chappell, Richard J.
AuthorAffiliation	2 Department of Medicine Division of Hematology/Oncology University of Wisconsin‐Madison WI USA 1 Carbone Cancer Center University of Wisconsin‐Madison WI USA 3 Departments of Statistics and of Biostatistics & Medical Informatics University of Wisconsin‐Madison WI USA 4 Department of Cell and Regenerative Biology and Department of Oncology McArdle Laboratory for Cancer Research University of Wisconsin‐Madison WI USA
AuthorAffiliation_xml	– name: 2 Department of Medicine Division of Hematology/Oncology University of Wisconsin‐Madison WI USA – name: 4 Department of Cell and Regenerative Biology and Department of Oncology McArdle Laboratory for Cancer Research University of Wisconsin‐Madison WI USA – name: 1 Carbone Cancer Center University of Wisconsin‐Madison WI USA – name: 3 Departments of Statistics and of Biostatistics & Medical Informatics University of Wisconsin‐Madison WI USA
Author_xml	– sequence: 1 givenname: Ashok surname: Singh fullname: Singh, Ashok organization: University of Wisconsin‐Madison – sequence: 2 givenname: Ryan A. orcidid: 0000-0001-9698-9201 surname: Denu fullname: Denu, Ryan A. organization: University of Wisconsin‐Madison – sequence: 3 givenname: Serena K. surname: Wolfe fullname: Wolfe, Serena K. organization: University of Wisconsin‐Madison – sequence: 4 givenname: Jamie M. surname: Sperger fullname: Sperger, Jamie M. organization: University of Wisconsin‐Madison – sequence: 5 givenname: Jennifer surname: Schehr fullname: Schehr, Jennifer organization: University of Wisconsin‐Madison – sequence: 6 givenname: Tessa surname: Witkowsky fullname: Witkowsky, Tessa organization: University of Wisconsin‐Madison – sequence: 7 givenname: Karla surname: Esbona fullname: Esbona, Karla organization: University of Wisconsin‐Madison – sequence: 8 givenname: Richard J. surname: Chappell fullname: Chappell, Richard J. organization: University of Wisconsin‐Madison – sequence: 9 givenname: Beth A. surname: Weaver fullname: Weaver, Beth A. organization: University of Wisconsin‐Madison – sequence: 10 givenname: Mark E. surname: Burkard fullname: Burkard, Mark E. organization: University of Wisconsin‐Madison – sequence: 11 givenname: Joshua M. surname: Lang fullname: Lang, Joshua M. email: jmlang@medicine.wisc.edu organization: University of Wisconsin‐Madison
BackLink	https://www.ncbi.nlm.nih.gov/pubmed/32255253$$D View this record in MEDLINE/PubMed
BookMark	eNqFkktr3DAUhUVJaR7tursi6KabSfS05E2hDH0EpmTTroUkyxMNtjWV7IT8-1yPk9AESje2kL5zOJx7T9HRkIaA0HtKzikh7IJqpVeEVfScskqrV-jk6eYIzlKJldI1PUanpewIkVVd1W_QMWdMSib5CSrrMIw5ldQHbPt9F9vo7RjTgGPBFrc5_JmAwOFm_sYB-5j91AEybPE49SljH7quAJl6XCa3C34s-DaO17gPoy0joB67HOCIvR18yG_R69Z2Jbx7-J-h39--_lr_WG2uvl-uv2xWXnKhVpRZUSvNuWtrrRpPnA2N94q3qmW84lIF7TzVlVO1UzawVvKqpkJoCyiR_AxdLr5Nsjuzz7G3-c4kG83hIuWtsRnSdcFYR7mSrhLaSeGaxqpaNXUtBNeUUS3A6_PitZ9cDzHm1mz3zPT5yxCvzTbdGCUIgRGAwacHg5yg0jKaPpa5OjuENBXDuFZMQngO6McX6C5NeYCqDBOcEAF1KKA-_J3oKcrjbAGQC-BhviWH1vg4HmYLAWNnKDHzDpl5Y8y8MeawQ6C7eKF7tP63oloUt7ELd__Dzc-rDVuE92xC2FM
CitedBy_id	crossref_primary_10_1016_j_tcb_2025_02_009 crossref_primary_10_1007_s10555_020_09937_z crossref_primary_10_1038_s41417_024_00824_1 crossref_primary_10_1016_j_toxlet_2023_03_008 crossref_primary_10_1038_s41419_023_05618_1 crossref_primary_10_3390_jpm15040134 crossref_primary_10_1016_j_bbcan_2021_188566 crossref_primary_10_3389_fonc_2023_1138049 crossref_primary_10_1038_s41576_024_00761_7 crossref_primary_10_1038_s41598_023_29712_8 crossref_primary_10_1126_scitranslmed_abd4811 crossref_primary_10_3389_fonc_2024_1370565
Cites_doi	10.1038/nrg3123 10.1038/nature03099 10.1158/1541-7786.MCR-17-0197 10.1371/journal.pone.0006564 10.1016/j.bbcan.2016.06.002 10.1158/1078-0432.CCR-08-0872 10.1186/1471-2407-13-252 10.15252/embj.201798576 10.1038/nature13277 10.4103/1477-3163.135578 10.1038/s41467-018-05429-5 10.1073/pnas.0904343106 10.7150/ijbs.7.1122 10.1091/mbc.E15-10-0747 10.1016/j.devcel.2016.10.023 10.1016/j.cellbi.2005.03.004 10.1093/annonc/mdv293 10.1016/j.celrep.2016.05.048 10.1007/s10555-008-9163-6 10.1158/1078-0432.CCR-15-1603 10.1016/S1470-2045(14)70069-5 10.1091/mbc.e14-04-0916 10.1038/labinvest.3780306 10.1083/jcb.138.5.953 10.4161/cc.9.14.12184 10.1038/nature08136 10.1016/S0002-9440(10)65513-7 10.1038/sj.leu.2403779 10.1073/pnas.1317042110 10.1158/1078-0432.CCR-16-1021 10.1186/s12885-016-2083-x 10.1073/pnas.95.6.2950 10.1016/j.ccr.2006.12.003 10.1126/scitranslmed.3007965 10.1038/nrc867
ContentType	Journal Article
Copyright	2020 The Authors. Published by FEBS Press and John Wiley & Sons Ltd. 2020. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.
Copyright_xml	– notice: 2020 The Authors. Published by FEBS Press and John Wiley & Sons Ltd. – notice: 2020. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.
DBID	24P AAYXX CITATION NPM 3V. 7X7 7XB 88E 8FE 8FH 8FI 8FJ 8FK ABUWG AFKRA AZQEC BBNVY BENPR BHPHI CCPQU DWQXO FYUFA GHDGH GNUQQ HCIFZ K9. LK8 M0S M1P M7P PHGZM PHGZT PIMPY PJZUB PKEHL PPXIY PQEST PQGLB PQQKQ PQUKI PRINS 7X8 5PM DOA
DOI	10.1002/1878-0261.12687
DatabaseName	Wiley Online Library Open Access CrossRef PubMed ProQuest Central (Corporate) Health & Medical Collection ProQuest Central (purchase pre-March 2016) Medical Database (Alumni Edition) ProQuest SciTech Collection ProQuest Natural Science Collection Hospital Premium Collection Hospital Premium Collection (Alumni Edition) ProQuest Central (Alumni) (purchase pre-March 2016) ProQuest Central (Alumni) ProQuest Central UK/Ireland ProQuest Central Essentials Biological Science Collection ProQuest Central Natural Science Collection ProQuest One Community College ProQuest Central Proquest Health Research Premium Collection Health Research Premium Collection (Alumni) ProQuest Central Student SciTech Premium Collection (via ProQuest) ProQuest Health & Medical Complete (Alumni) Biological Sciences Health & Medical Collection (Alumni) Medical Database Biological Science Database Proquest Central Premium ProQuest One Academic (New) Publicly Available Content Database ProQuest Health & Medical Research Collection ProQuest One Academic Middle East (New) ProQuest One Health & Nursing ProQuest One Academic Eastern Edition (DO NOT USE) ProQuest One Applied & Life Sciences ProQuest One Academic (retired) ProQuest One Academic UKI Edition ProQuest Central China MEDLINE - Academic PubMed Central (Full Participant titles) DOAJ Directory of Open Access Journals
DatabaseTitle	CrossRef PubMed Publicly Available Content Database ProQuest Central Student ProQuest One Academic Middle East (New) ProQuest Central Essentials ProQuest Health & Medical Complete (Alumni) ProQuest Central (Alumni Edition) SciTech Premium Collection ProQuest One Community College ProQuest One Health & Nursing ProQuest Natural Science Collection ProQuest Central China ProQuest Central ProQuest One Applied & Life Sciences ProQuest Health & Medical Research Collection Health Research Premium Collection Health and Medicine Complete (Alumni Edition) Natural Science Collection ProQuest Central Korea Health & Medical Research Collection Biological Science Collection ProQuest Central (New) ProQuest Medical Library (Alumni) ProQuest Biological Science Collection ProQuest One Academic Eastern Edition ProQuest Hospital Collection Health Research Premium Collection (Alumni) Biological Science Database ProQuest SciTech Collection ProQuest Hospital Collection (Alumni) ProQuest Health & Medical Complete ProQuest Medical Library ProQuest One Academic UKI Edition ProQuest One Academic ProQuest One Academic (New) ProQuest Central (Alumni) MEDLINE - Academic
DatabaseTitleList	Publicly Available Content Database CrossRef PubMed MEDLINE - Academic
Database_xml	– sequence: 1 dbid: 24P name: Wiley Online Library Open Access url: https://authorservices.wiley.com/open-science/open-access/browse-journals.html sourceTypes: Publisher – sequence: 2 dbid: DOA name: DOAJ Directory of Open Access Journals url: https://www.doaj.org/ sourceTypes: Open Website – sequence: 3 dbid: NPM name: PubMed url: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed sourceTypes: Index Database – sequence: 4 dbid: PIMPY name: Publicly Available Content Database url: http://search.proquest.com/publiccontent sourceTypes: Aggregation Database
DeliveryMethod	fulltext_linktorsrc
Discipline	Medicine
DocumentTitleAlternate	Centrosome amplification in CTCs from metastatic breast cancer subjects
EISSN	1878-0261
EndPage	1909
ExternalDocumentID	oai_doaj_org_article_ab1375b648b54bdda797d99443812184 PMC7400789 32255253 10_1002_1878_0261_12687 MOL212687
Genre	article Research Support, U.S. Gov't, Non-P.H.S Research Support, Non-U.S. Gov't Journal Article Research Support, N.I.H., Extramural
GeographicLocations	United States--US Wisconsin
GeographicLocations_xml	– name: Wisconsin – name: United States--US
GrantInformation_xml	– fundername: Prostate Cancer Foundation funderid: Movember Challenge Award; Young Investigator Award – fundername: National Institutes of Health funderid: TL1TR000429; UL1TR000427 – fundername: National Cancer Institute funderid: 1R01CA181648; F30CA203271; P30CA014520; R01CA234904 – fundername: U.S. Department of Defense funderid: W81XWH‐16‐1‐0049; W81XWH‐16‐1‐0050; W81XWH‐16‐1‐0052 – fundername: National Institute of General Medical Sciences funderid: T32GM008692 – fundername: NCATS NIH HHS grantid: TL1 TR000429 – fundername: NCI NIH HHS grantid: R01 CA181648 – fundername: NCI NIH HHS grantid: F30 CA203271 – fundername: NCI NIH HHS grantid: P30 CA014520 – fundername: NCATS NIH HHS grantid: UL1 TR000427 – fundername: NIGMS NIH HHS grantid: T32 GM008692 – fundername: NCI NIH HHS grantid: R01 CA234904 – fundername: NCATS NIH HHS grantid: UL1 TR002373 – fundername: ; grantid: TL1TR000429; UL1TR000427 – fundername: ; grantid: 1R01CA181648; F30CA203271; P30CA014520; R01CA234904 – fundername: ; grantid: W81XWH‐16‐1‐0049; W81XWH‐16‐1‐0050; W81XWH‐16‐1‐0052 – fundername: ; grantid: Movember Challenge Award; Young Investigator Award – fundername: ; grantid: T32GM008692
GroupedDBID	--- --K .~1 0R~ 0SF 123 1B1 1OC 1~. 24P 4.4 457 4G. 53G 5VS 6I. 7-5 71M 8FE 8FH 8P~ AACTN AAEDW AAFTH AAFWJ AAHHS AAIKJ AALRI AAQFI AAXUO ABBQC ABFRF ABGSF ABMAC ABVKL ABWVN ACCFJ ACCMX ACGFO ACGFS ACRPL ACXQS ADBBV ADEZE ADMUD ADNMO ADPDF ADUVX ADVLN AEEZP AEFWE AEKER AENEX AEQDE AEXQZ AFKRA AFPKN AGHFR AGYEJ AITUG AIWBW AJBDE AJOXV AJRQY AKRWK ALMA_UNASSIGNED_HOLDINGS ALUQN AMRAJ AOIJS AVUZU BAWUL BBNVY BCNDV BENPR BHPHI BLXMC CCPQU CS3 DIK DU5 E3Z EBS EJD EMOBN EO9 EP2 EP3 F5P FDB FEDTE FIRID FNPLU GBLVA GROUPED_DOAJ HCIFZ HVGLF HYE HZ~ IAO IHE IHR ITC IXB J1W LK8 M41 M7P MO0 N9A NCXOZ O-L OAUVE OK1 OVD OVEED OZT P-8 P-9 P2P PC. PIMPY PROAC Q38 RIG ROL RPM RPZ SDF SDG SEL SES SSZ TEORI TR2 UNMZH WIN 7X7 88E 8FI 8FJ 9DU AAMMB AAYWO AAYXX ABUWG ACVFH ADCNI AEFGJ AEUPX AFFHD AFPUW AGXDD AIDQK AIDYY AIGII AKBMS AKYEP CITATION EFLBG FYUFA HMCUK M1P PHGZM PHGZT PJZUB PPXIY PQGLB PSQYO UKHRP ~HD NPM 3V. 7XB 8FK AZQEC DWQXO GNUQQ K9. PKEHL PQEST PQQKQ PQUKI PRINS 7X8 PUEGO 5PM
ID	FETCH-LOGICAL-c5347-12a497833bf987dc0baedcc73f7f236357e8bc186b79b7ae2f53691448a0ba053
IEDL.DBID	24P
ISICitedReferencesCount	15
ISICitedReferencesURI	http://www.webofscience.com/api/gateway?GWVersion=2&SrcApp=Summon&SrcAuth=ProQuest&DestLinkType=CitingArticles&DestApp=WOS_CPL&KeyUT=000534533600001&url=https%3A%2F%2Fcvtisr.summon.serialssolutions.com%2F%23%21%2Fsearch%3Fho%3Df%26include.ft.matches%3Dt%26l%3Dnull%26q%3D
ISSN	1574-7891 1878-0261
IngestDate	Fri Oct 03 12:50:40 EDT 2025 Tue Nov 04 01:46:48 EST 2025 Sun Sep 28 08:46:54 EDT 2025 Tue Oct 07 07:23:25 EDT 2025 Thu Apr 03 06:59:12 EDT 2025 Tue Nov 18 21:45:03 EST 2025 Sat Nov 29 02:40:17 EST 2025 Wed Jan 22 16:32:41 EST 2025
IsDoiOpenAccess	true
IsOpenAccess	true
IsPeerReviewed	true
IsScholarly	true
Issue	8
Keywords	centrosome amplification pericentrin breast cancer centrin CTC EpCAM
Language	English
License	Attribution 2020 The Authors. Published by FEBS Press and John Wiley & Sons Ltd. This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
LinkModel	DirectLink
MergedId	FETCHMERGED-LOGICAL-c5347-12a497833bf987dc0baedcc73f7f236357e8bc186b79b7ae2f53691448a0ba053
Notes	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 Ashok Singh and Ryan A. Denu contributed equally.
ORCID	0000-0001-9698-9201
OpenAccessLink	https://onlinelibrary.wiley.com/doi/abs/10.1002%2F1878-0261.12687
PMID	32255253
PQID	2430049877
PQPubID	4370298
PageCount	12
ParticipantIDs	doaj_primary_oai_doaj_org_article_ab1375b648b54bdda797d99443812184 pubmedcentral_primary_oai_pubmedcentral_nih_gov_7400789 proquest_miscellaneous_2387254483 proquest_journals_2430049877 pubmed_primary_32255253 crossref_citationtrail_10_1002_1878_0261_12687 crossref_primary_10_1002_1878_0261_12687 wiley_primary_10_1002_1878_0261_12687_MOL212687
PublicationCentury	2000
PublicationDate	August 2020
PublicationDateYYYYMMDD	2020-08-01
PublicationDate_xml	– month: 08 year: 2020 text: August 2020
PublicationDecade	2020
PublicationPlace	United States
PublicationPlace_xml	– name: United States – name: Hoboken
PublicationTitle	Molecular oncology
PublicationTitleAlternate	Mol Oncol
PublicationYear	2020
Publisher	John Wiley & Sons, Inc John Wiley and Sons Inc Wiley
Publisher_xml	– name: John Wiley & Sons, Inc – name: John Wiley and Sons Inc – name: Wiley
References	1997; 138 2008; 14 2002; 2 2016; 1866 2014; 25 2016; 39 2012; 13 2016; 16 2007; 11 2005; 29 2016; 15 2014; 510 2011; 7 2009; 28 2001; 81 2018; 9 2015; 26 2005; 19 2004; 432 2013; 13 2014; 15 2014; 13 2009; 460 1999; 155 2013; 110 2009; 4 1998; 95 2016; 27 2014; 6 2018; 16 2018; 37 2010; 9 1998; 58 2016; 23 2016; 22 2009; 106 e_1_2_10_23_1 e_1_2_10_24_1 e_1_2_10_21_1 e_1_2_10_22_1 e_1_2_10_20_1 e_1_2_10_2_1 e_1_2_10_4_1 e_1_2_10_18_1 e_1_2_10_3_1 e_1_2_10_19_1 Pihan GA (e_1_2_10_25_1) 1998; 58 e_1_2_10_6_1 e_1_2_10_16_1 e_1_2_10_5_1 e_1_2_10_17_1 e_1_2_10_8_1 e_1_2_10_14_1 e_1_2_10_37_1 e_1_2_10_7_1 e_1_2_10_15_1 e_1_2_10_36_1 e_1_2_10_12_1 e_1_2_10_35_1 e_1_2_10_9_1 e_1_2_10_13_1 e_1_2_10_34_1 e_1_2_10_10_1 e_1_2_10_33_1 e_1_2_10_11_1 e_1_2_10_32_1 e_1_2_10_31_1 e_1_2_10_30_1 e_1_2_10_29_1 e_1_2_10_27_1 e_1_2_10_28_1 e_1_2_10_26_1
References_xml	– volume: 81 start-page: 945 year: 2001 end-page: 952 article-title: Stepwise progression of centrosome defects associated with local tumor growth and metastatic process of human pancreatic carcinoma cells transplanted orthotopically into nude mice publication-title: Lab Invest – volume: 13 start-page: 8 year: 2014 article-title: Circulating tumor cells in breast cancer publication-title: J Carcinog – volume: 106 start-page: 19108 year: 2009 end-page: 19113 article-title: Elevating the frequency of chromosome mis‐segregation as a strategy to kill tumor cells publication-title: Proc Natl Acad Sci U S A – volume: 138 start-page: 953 year: 1997 end-page: 956 article-title: Pathways of spindle pole formation: different mechanisms; conserved components publication-title: J Cell Biol – volume: 6 start-page: 229ra243 year: 2014 article-title: Cytotoxicity of paclitaxel in breast cancer is due to chromosome missegregation on multipolar spindles publication-title: Sci Transl Med – volume: 14 start-page: 6302 year: 2008 end-page: 6309 article-title: Circulating tumor cells predict survival benefit from treatment in metastatic castration‐resistant prostate cancer publication-title: Clin Cancer Res – volume: 16 start-page: 517 year: 2018 end-page: 527 article-title: Centriole overduplication is the predominant mechanism leading to centrosome amplification in melanoma publication-title: Mol Cancer Res – volume: 155 start-page: 1941 year: 1999 end-page: 1951 article-title: Altered centrosome structure is associated with abnormal mitoses in human breast tumors publication-title: Am J Pathol – volume: 26 start-page: 2180 year: 2015 end-page: 2192 article-title: Inhibition of the spindle assembly checkpoint kinase TTK enhances the efficacy of docetaxel in a triple‐negative breast cancer model publication-title: Ann Oncol – volume: 7 start-page: 1122 year: 2011 end-page: 1144 article-title: A clinical overview of centrosome amplification in human cancers publication-title: Int J Biol Sci – volume: 29 start-page: 375 year: 2005 end-page: 383 article-title: Centrosome aberrations in hematological malignancies publication-title: Cell Biol Int – volume: 95 start-page: 2950 year: 1998 end-page: 2955 article-title: Centrosome hypertrophy in human breast tumors: implications for genomic stability and cell polarity publication-title: Proc Natl Acad Sci U S A – volume: 432 start-page: 338 year: 2004 end-page: 341 article-title: Aneuploidy and cancer publication-title: Nature – volume: 510 start-page: 167 year: 2014 end-page: 171 article-title: Oncogene‐like induction of cellular invasion from centrosome amplification publication-title: Nature – volume: 1866 start-page: 64 year: 2016 end-page: 75 article-title: Chromosomal instability: a common feature and a therapeutic target of cancer publication-title: Biochim Biophys Acta – volume: 27 start-page: 1981 year: 2016 end-page: 1989 article-title: High rates of chromosome missegregation suppress tumor progression but do not inhibit tumor initiation publication-title: Mol Biol Cell – volume: 11 start-page: 25 year: 2007 end-page: 36 article-title: Aneuploidy acts both oncogenically and as a tumor suppressor publication-title: Cancer Cell – volume: 28 start-page: 85 year: 2009 end-page: 98 article-title: Centrosomes and cancer: how cancer cells divide with too many centrosomes publication-title: Cancer Metastasis Rev – volume: 9 start-page: 3012 year: 2018 article-title: Plk1 overexpression induces chromosomal instability and suppresses tumor development publication-title: Nat Commun – volume: 110 start-page: E4134 year: 2013 end-page: 4141 article-title: Chromosome missegregation rate predicts whether aneuploidy will promote or suppress tumors publication-title: Proc Natl Acad Sci U S A – volume: 22 start-page: 2583 year: 2016 end-page: 2593 article-title: Pooled analysis of the prognostic relevance of circulating tumor cells in primary breast cancer publication-title: Clin Cancer Res – volume: 16 start-page: 47 year: 2016 article-title: Centrosome amplification induces high grade features and is prognostic of worse outcomes in breast cancer publication-title: BMC Cancer – volume: 460 start-page: 278 year: 2009 end-page: 282 article-title: A mechanism linking extra centrosomes to chromosomal instability publication-title: Nature – volume: 13 start-page: 189 year: 2012 end-page: 203 article-title: Causes and consequences of aneuploidy in cancer publication-title: Nat Rev Genet – volume: 23 start-page: 746 year: 2016 end-page: 756 article-title: Integrated analysis of multiple biomarkers from circulating tumor cells enabled by exclusion‐based analyte isolation publication-title: Clin Cancer Res – volume: 9 start-page: 2731 year: 2010 end-page: 2736 article-title: Centriole duplication: a lesson in self‐control publication-title: Cell Cycle (Georgetown, Tex) – volume: 15 start-page: 406 year: 2014 end-page: 414 article-title: Clinical validity of circulating tumour cells in patients with metastatic breast cancer: a pooled analysis of individual patient data publication-title: Lancet Oncol – volume: 13 start-page: 252 year: 2013 article-title: A new assay for measuring chromosome instability (CIN) and identification of drugs that elevate CIN in cancer cells publication-title: BMC Cancer – volume: 39 start-page: 638 year: 2016 end-page: 652 article-title: Living in CIN: mitotic infidelity and its consequences for tumor promotion and suppression publication-title: Dev Cell – volume: 19 start-page: 1192 year: 2005 end-page: 1197 article-title: Centrosome aberrations in chronic myeloid leukemia correlate with stage of disease and chromosomal instability publication-title: Leukemia – volume: 37 year: 2018 article-title: Structural centrosome aberrations promote non‐cell‐autonomous invasiveness publication-title: EMBO J – volume: 4 year: 2009 article-title: Multipolar spindle pole coalescence is a major source of kinetochore mis‐attachment and chromosome mis‐segregation in cancer cells publication-title: PLoS ONE – volume: 25 start-page: 2677 year: 2014 end-page: 2681 article-title: How Taxol/paclitaxel kills cancer cells publication-title: Mol Biol Cell – volume: 58 start-page: 3974 year: 1998 end-page: 3985 article-title: Centrosome defects and genetic instability in malignant tumors publication-title: Cancer Res – volume: 2 start-page: 584 year: 2002 end-page: 593 article-title: Metastasis to bone: causes, consequences and therapeutic opportunities publication-title: Nat Rev Cancer – volume: 15 start-page: 2679 year: 2016 end-page: 2691 article-title: Negative selection and chromosome instability induced by Mad2 overexpression delay breast cancer but facilitate oncogene‐independent outgrowth publication-title: Cell Rep – ident: e_1_2_10_14_1 doi: 10.1038/nrg3123 – ident: e_1_2_10_27_1 doi: 10.1038/nature03099 – ident: e_1_2_10_6_1 doi: 10.1158/1541-7786.MCR-17-0197 – ident: e_1_2_10_31_1 doi: 10.1371/journal.pone.0006564 – volume: 58 start-page: 3974 year: 1998 ident: e_1_2_10_25_1 article-title: Centrosome defects and genetic instability in malignant tumors publication-title: Cancer Res – ident: e_1_2_10_33_1 doi: 10.1016/j.bbcan.2016.06.002 – ident: e_1_2_10_4_1 doi: 10.1158/1078-0432.CCR-08-0872 – ident: e_1_2_10_19_1 doi: 10.1186/1471-2407-13-252 – ident: e_1_2_10_10_1 doi: 10.15252/embj.201798576 – ident: e_1_2_10_13_1 doi: 10.1038/nature13277 – ident: e_1_2_10_26_1 doi: 10.4103/1477-3163.135578 – ident: e_1_2_10_5_1 doi: 10.1038/s41467-018-05429-5 – ident: e_1_2_10_17_1 doi: 10.1073/pnas.0904343106 – ident: e_1_2_10_3_1 doi: 10.7150/ijbs.7.1122 – ident: e_1_2_10_37_1 doi: 10.1091/mbc.E15-10-0747 – ident: e_1_2_10_8_1 doi: 10.1016/j.devcel.2016.10.023 – ident: e_1_2_10_18_1 doi: 10.1016/j.cellbi.2005.03.004 – ident: e_1_2_10_22_1 doi: 10.1093/annonc/mdv293 – ident: e_1_2_10_28_1 doi: 10.1016/j.celrep.2016.05.048 – ident: e_1_2_10_12_1 doi: 10.1007/s10555-008-9163-6 – ident: e_1_2_10_16_1 doi: 10.1158/1078-0432.CCR-15-1603 – ident: e_1_2_10_2_1 doi: 10.1016/S1470-2045(14)70069-5 – ident: e_1_2_10_34_1 doi: 10.1091/mbc.e14-04-0916 – ident: e_1_2_10_29_1 doi: 10.1038/labinvest.3780306 – ident: e_1_2_10_23_1 doi: 10.1083/jcb.138.5.953 – ident: e_1_2_10_15_1 doi: 10.4161/cc.9.14.12184 – ident: e_1_2_10_9_1 doi: 10.1038/nature08136 – ident: e_1_2_10_21_1 doi: 10.1016/S0002-9440(10)65513-7 – ident: e_1_2_10_11_1 doi: 10.1038/sj.leu.2403779 – ident: e_1_2_10_30_1 doi: 10.1073/pnas.1317042110 – ident: e_1_2_10_32_1 doi: 10.1158/1078-0432.CCR-16-1021 – ident: e_1_2_10_7_1 doi: 10.1186/s12885-016-2083-x – ident: e_1_2_10_20_1 doi: 10.1073/pnas.95.6.2950 – ident: e_1_2_10_35_1 doi: 10.1016/j.ccr.2006.12.003 – ident: e_1_2_10_36_1 doi: 10.1126/scitranslmed.3007965 – ident: e_1_2_10_24_1 doi: 10.1038/nrc867
SSID	ssj0056969
Score	2.3384774
Snippet	Centrosome amplification (CA) is a common phenomenon in cancer, promotes genomic stability and cancer evolution, and has been reported to promote metastasis....
SourceID	doaj pubmedcentral proquest pubmed crossref wiley
SourceType	Open Website Open Access Repository Aggregation Database Index Database Enrichment Source Publisher
StartPage	1898
SubjectTerms	Antibodies Automation Biomarkers Breast cancer CD45 antigen Cell culture Cell division centrin centrosome amplification Chemotherapy Chromosomes Clinical trials CTC Cytokeratin EpCAM Epithelial cells Genomic instability Laboratories Metastases Metastasis pericentrin Tumor cell lines Tumor cells Tumors
SummonAdditionalLinks	– databaseName: DOAJ Directory of Open Access Journals dbid: DOA link: http://cvtisr.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwrV1Lb9QwELZQVSEuqOWZUpCROHBJd2MnfhwBUXFoCwdAvVm2Y0MkNkFJtr-_M052tStAvXCL4onizMOZGY-_IeRNjbs_UaicC6fzMnBYBy04crwE37gMwvN0Ku37hby6UtfX-stOqy-sCZvggSfGLawruKycKJWrSlfXVmpZa10iNBWGJ7j6gtezCaamNbgSOjWzKyqsNlS62ID6LNmiUIgpC4HDWcEEVtLt_I8SbP_ffM0_SyZ3Xdn0Lzo_Ig9nJ5K-myZ_TO6F9hG5fzlvkz8mQ8rZdkO3CtRiyXicM3O0GailsU_10yNN6E20aalvep_6eLU_6LhedT3FhP5A8fAJHdYOkzUDxZwtXYXR4imkxlOHBe0j9ag4_RPy7fzj1w-f8rm7Qu5BCjIvmMXucpy7qJWs_dJZ-DwveZSRcYSpC8r5QgkntZM2sFhxoSH-UhZIwXafkoO2a8NzQstYMVUsPcgmlMJGy0OEMM-xwAIEMDYjZxseGz9Dj2MHjF9mAk1mBoViUCgmCSUjb7cP_J5QN_5N-h6FtiVDuOx0A5TIzEpk7lKijJxuRG5mGx4MKxGNDHgD73i9HQbrQwnYNnRroOFKIsib4hl5NmnIdia4VFasghG5pzt7U90faZufCeFbYrd6pTOySFp2Fw_M5ecLlq5O_gc3XpAHDLMKqczxlByM_Tq8JIf-ZmyG_lUytFuWOCa6 priority: 102 providerName: Directory of Open Access Journals – databaseName: Biological Science Database dbid: M7P link: http://cvtisr.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwpV1Lb9QwEB5BQYgLb2igICNx4JLuxk5i-4QAUXFoSw-AerNsx24jsUmbZPn9eLzepSteB25R7Ei2ZzyZGX_-BuBVg6c_vhY5q43MS8eCHdTBkWNl8I1LV1sWb6V9PeTHx-L0VJ6khNuYYJVrmxgNddNbzJHPaIncUCFC5m8uLnOsGoWnq6mExnW4gSwJLEL3TtaWuKplLGlXVIg5FLJYU_vM6awQyCwbwof9gtaIp7vyV4rk_b_zOH8FTl51aOMf6eDu_87lHtxJvih5u1Ke-3DNdQ_g1lE6bX8IY0z99mO_cEQj8tynBB9pR6KJHyIMeyKRBIq0HbHtYGM5sO6MTMtFPxA8FxgJ3mEh49JgzmckmPolCzdpvMzUWmIQFz8Ri_o3PIIvBx8-v_-YpyINuQ3C5HlBNRapY8z4MKHGzo0O62M589xThmx3ThhbiNpwabh21FesliGMEzp0DSbgMex0fed2gZS-oqKYW82lK2vtNXM-RIuGOupCHKQz2F8LSdnEYI6FNL6pFfcyVShVhVJVUaoZvN58cLEi7_hz13co9U03ZN2OL_rhTKVNrLQpGK9MXQpTlaZpwkB5I2WJNGkYKmewt5a3SqZgVD-FncHLTXPYxCgB3bl-GfowwZErTrAMnqxUbDMStLgVrUIL31K-raFut3TteSQK51j0XsgMZlFN_7UG6ujTIY1PT_8-kWdwm2LaIeIg92BnGpbuOdy036d2HF7EPfgDiXA1yw priority: 102 providerName: ProQuest
Title	Centrosome amplification is a frequent event in circulating tumor cells from subjects with metastatic breast cancer
URI	https://onlinelibrary.wiley.com/doi/abs/10.1002%2F1878-0261.12687 https://www.ncbi.nlm.nih.gov/pubmed/32255253 https://www.proquest.com/docview/2430049877 https://www.proquest.com/docview/2387254483 https://pubmed.ncbi.nlm.nih.gov/PMC7400789 https://doaj.org/article/ab1375b648b54bdda797d99443812184
Volume	14
WOSCitedRecordID	wos000534533600001&url=https%3A%2F%2Fcvtisr.summon.serialssolutions.com%2F%23%21%2Fsearch%3Fho%3Df%26include.ft.matches%3Dt%26l%3Dnull%26q%3D
hasFullText	1
inHoldings	1
isFullTextHit
isPrint
journalDatabaseRights	– providerCode: PRVAON databaseName: DOAJ Directory of Open Access Journals customDbUrl: eissn: 1878-0261 dateEnd: 99991231 omitProxy: false ssIdentifier: ssj0056969 issn: 1574-7891 databaseCode: DOA dateStart: 20170101 isFulltext: true titleUrlDefault: https://www.doaj.org/ providerName: Directory of Open Access Journals – providerCode: PRVPQU databaseName: Biological Science Database customDbUrl: eissn: 1878-0261 dateEnd: 99991231 omitProxy: false ssIdentifier: ssj0056969 issn: 1574-7891 databaseCode: M7P dateStart: 20070601 isFulltext: true titleUrlDefault: http://search.proquest.com/biologicalscijournals providerName: ProQuest – providerCode: PRVPQU databaseName: Health & Medical Collection customDbUrl: eissn: 1878-0261 dateEnd: 99991231 omitProxy: false ssIdentifier: ssj0056969 issn: 1574-7891 databaseCode: 7X7 dateStart: 20070601 isFulltext: true titleUrlDefault: https://search.proquest.com/healthcomplete providerName: ProQuest – providerCode: PRVPQU databaseName: ProQuest Central customDbUrl: eissn: 1878-0261 dateEnd: 99991231 omitProxy: false ssIdentifier: ssj0056969 issn: 1574-7891 databaseCode: BENPR dateStart: 20070601 isFulltext: true titleUrlDefault: https://www.proquest.com/central providerName: ProQuest – providerCode: PRVPQU databaseName: Publicly Available Content Database customDbUrl: eissn: 1878-0261 dateEnd: 99991231 omitProxy: false ssIdentifier: ssj0056969 issn: 1574-7891 databaseCode: PIMPY dateStart: 20070601 isFulltext: true titleUrlDefault: http://search.proquest.com/publiccontent providerName: ProQuest – providerCode: PRVWIB databaseName: Wiley Online Library Free Content customDbUrl: eissn: 1878-0261 dateEnd: 99991231 omitProxy: false ssIdentifier: ssj0056969 issn: 1574-7891 databaseCode: WIN dateStart: 20070101 isFulltext: true titleUrlDefault: https://onlinelibrary.wiley.com providerName: Wiley-Blackwell – providerCode: PRVWIB databaseName: Wiley Online Library Open Access customDbUrl: eissn: 1878-0261 dateEnd: 99991231 omitProxy: false ssIdentifier: ssj0056969 issn: 1574-7891 databaseCode: 24P dateStart: 20070101 isFulltext: true titleUrlDefault: https://authorservices.wiley.com/open-science/open-access/browse-journals.html providerName: Wiley-Blackwell
link	http://cvtisr.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwrV1Lj9MwELZgixAX3guBpTISBy7Z1o_E9pFFu2KlbYkQj3KKbMdZItEEJSm_H4-TFspDCIlL1NZO4o5nxjPj8TcIPStg96dMZcxSo2LumNeD2htyjHvbmLvUsnAq7f2FWC7laqWyMZsQzsIM-BC7gBtIRtDXIODadLPvoKFEAjasdwCOCU2luIomhDAJ1Rsoz7bKOElVqGpHEkg7lIps0X3mdPbTA_YWpoDf_zuj89fcyR9t2rAond36D3_nNro5WqT4xcBCd9AVV99F1xfjnvs91IUAcNM1a4c15J-XY5gPVx3WuGxDMnaPAxQUrmpsq9aGomD1Je4366bFsDvQYTjJgruNgchPhyEAjNeu13CkqbLYQHZ8jy1wYXsfvTs7ffvyVTyWaoitn1IRE6qhVB1jplRSFHZutCeRFawUJWWAeeeksUSmRigjtKNlwlLlnTmpfVevCA7RQd3U7iHCvEyoJHOrhXI81aVmrvQ-o6GOOu8N6Qgdb-cptyOOOZTT-JwPCMw0B1LmQMo8kDJCz3c3fBkgPP7c9QQmftcNsLfDD017mY-inGtDmEhMyqVJuCkKP1BRKMUBLA0c5ggdbdkmHxVCl1MO0GaeNv4dT3fNXpRhBnTtmo3vw6QAxDjJIvRg4LLdSEDvJjTxLWKP__aGut9SV58CXLjgYAeqCM0C__2NBvni9QUNnx798x2P0Q0K8YiQIHmEDvp2456ga_ZrX3XtNEimv4qVCFc5RZOT02X2ZhoiIVPIu_Xtk-x8kX303z6cL78BTho9QA
linkProvider	Wiley-Blackwell
linkToHtml	http://cvtisr.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMw1V1Lb9QwEB5VBQEX3o9AASOBxCXdjZ3EzgEhXlWr7i49FNSbsR2nRGKTkmRB_Cl-Ix5vsnTF69QDt9Xa2XWSz-OZ8edvAB7nuPtTpCJkqc7C2DJnB5Vz5FjsfOPYpob5U2nvJ3w2E0dH2cEGfB_OwiCtcrCJ3lDntcEc-YjGqA3lImT-_ORziFWjcHd1KKGxhMW-_fbVhWzts73X7v0-oXTnzeGr3bCvKhAa9-88jKjCqmqM6cL9Wm7GWtncGM4KXlCG8mxWaBOJVPNMc2VpkbA0c3GHUK7rGKtEOJN_zrkRVHiq4MFg-ZM08yX0ogQ5jiKLBimhMR1FApVsXbiyHdEU-XunVkFfLOB3Hu6vRM3TDrRfAXeu_G_P7ipc7n1t8mI5Oa7Bhq2uw4Vpzya4Aa1PbddtPbdEIbO-6BOYpGyJIkXjaeYd8SJXpKyIKRvjy51Vx6RbzOuG4L5HS_CMDmkXGnNaLcHUNpnbTuFhrdIQjbz_jhicX81NeHcmt3wLNqu6sneAxEVCRTQ2imc2TlWhmC1cNKyppdbFeSqA7QEU0vQK7Vgo5JNcaktTiSiSiCLpURTA09UFJ0txkj93fYkoW3VDVXH_Rd0cy95ISaUjxhOdxkInsc5zN1CeZ1mMMnCYCghga8CX7E1dK3-CK4BHq2ZnpPANqMrWC9eHCY5aeIIFcHsJ6dVIcEVJaOJa-BrY14a63lKVH70QOo_Rw80CGPlp8a9nIKdvJ9R_uvv3G3kIF3cPpxM52Zvt34NLFFMsnvO5BZtds7D34bz50pVt88DPfwIfznrS_AB6uJHY
linkToPdf	http://cvtisr.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMw1V1Lb9QwELaqgiouvB-BAkYCiUu6GzuJnQNCQFlRdbvsAVBvru3YJVI3aZMsiL_Gr8PjJEtXvE49cFvFzspJZsYz42--QehpDqc_NuUhTVUWxoY6OyidI0dj5xvHJtXUV6V9mrLZjB8eZvMN9H2ohQFY5WATvaHOKw058hGJgRvKRchsZHtYxHx38vL0LIQOUnDSOrTT6ERk33z76sK35sXervvWzwiZvP3w5l3YdxgItVsJCyMiocMapcq6f871WEmTa82oZZZQoGozXOmIp4pliklDbELTzMUgXLqpY-gY4cz_JQak5R42OB92gSTNfDu9KAG8I8-igVZoTEYRB1ZbF7rsRCQFLN-5HdE3Dvidt_sraPO8M-13w8m1__k9XkdXex8cv-qU5gbaMOVNtHXQowxuocanvKumWhgsAXFv-8QmLhossa09_LzFnvwKFyXWRa19G7TyGLfLRVVjOA9pMNTu4GapINfVYEh544VpJRRxFRorqAdosQa9q2-jjxfyyHfQZlmV5h7CsU0Ij8ZasszEqbSSGuuiZEUMMS7-kwHaGQRE6J65HRqInIiOc5oIkCgBEiW8RAXo-eqG04605M9TX4PEraYB27i_UNXHojdeQqqIskSlMVdJrPLcLZTlWRYDPRykCAK0Pcia6E1gI34KWoCerIad8YIvIEtTLd0cyhlw5HEaoLudeK9WAjtNQhI3wtYEf22p6yNl8dkTpLMYPN8sQCOvIv96B-Lg_ZT4X_f__iCP0ZbTFTHdm-0_QFcIZF48FHQbbbb10jxEl_WXtmjqR94UYHR00TrzA0cHmpU
openUrl	ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=Centrosome+amplification+is+a+frequent+event+in+circulating+tumor+cells+from+subjects+with+metastatic+breast+cancer&rft.jtitle=Molecular+oncology&rft.au=Singh%2C+Ashok&rft.au=Denu%2C+Ryan+A.&rft.au=Wolfe%2C+Serena+K.&rft.au=Sperger%2C+Jamie+M.&rft.date=2020-08-01&rft.issn=1574-7891&rft.eissn=1878-0261&rft.volume=14&rft.issue=8&rft.spage=1898&rft.epage=1909&rft_id=info:doi/10.1002%2F1878-0261.12687&rft.externalDBID=10.1002%252F1878-0261.12687&rft.externalDocID=MOL212687
thumbnail_l	http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=1574-7891&client=summon
thumbnail_m	http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=1574-7891&client=summon
thumbnail_s	http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=1574-7891&client=summon