Prognostic significance of L1CAM expression and its association with mutant p53 expression in high-risk endometrial cancer.
Identifieur interne : 002253 ( PubMed/Corpus ); précédent : 002252; suivant : 002254Prognostic significance of L1CAM expression and its association with mutant p53 expression in high-risk endometrial cancer.
Auteurs : Inge C. Van Gool ; Ellen Stelloo ; Remi A. Nout ; Hans W. Nijman ; Richard J. Edmondson ; David N. Church ; Helen J. Mackay ; Alexandra Leary ; Melanie E. Powell ; Linda Mileshkin ; Carien L. Creutzberg ; Vincent T H B M. Smit ; Tjalling BosseSource :
- Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc [ 1530-0285 ] ; 2016.
English descriptors
- KwdEn :
- Adult, Aged, Aged, 80 and over, Biomarkers, Tumor (analysis), Biomarkers, Tumor (genetics), Carcinoma, Endometrioid (chemistry), Carcinoma, Endometrioid (genetics), Carcinoma, Endometrioid (mortality), Carcinoma, Endometrioid (secondary), Carcinoma, Endometrioid (therapy), DNA Mutational Analysis, Disease Progression, Disease-Free Survival, Endometrial Neoplasms (chemistry), Endometrial Neoplasms (genetics), Endometrial Neoplasms (mortality), Endometrial Neoplasms (pathology), Endometrial Neoplasms (therapy), Female, Genetic Predisposition to Disease, Humans, Immunohistochemistry, Kaplan-Meier Estimate, Middle Aged, Mutation, Neoplasm Grading, Neoplasm Invasiveness, Neoplasm Recurrence, Local, Neoplasm Staging, Neural Cell Adhesion Molecule L1 (analysis), Phenotype, Pilot Projects, Retrospective Studies, Risk Assessment, Risk Factors, Treatment Outcome, Tumor Suppressor Protein p53 (genetics), Young Adult.
- MESH :
- chemical , analysis : Biomarkers, Tumor, Neural Cell Adhesion Molecule L1.
- chemical , genetics : Biomarkers, Tumor, Tumor Suppressor Protein p53.
- chemistry : Carcinoma, Endometrioid, Endometrial Neoplasms.
- genetics : Carcinoma, Endometrioid, Endometrial Neoplasms.
- mortality : Carcinoma, Endometrioid, Endometrial Neoplasms.
- pathology : Endometrial Neoplasms.
- secondary : Carcinoma, Endometrioid.
- therapy : Carcinoma, Endometrioid, Endometrial Neoplasms.
- Adult, Aged, Aged, 80 and over, DNA Mutational Analysis, Disease Progression, Disease-Free Survival, Female, Genetic Predisposition to Disease, Humans, Immunohistochemistry, Kaplan-Meier Estimate, Middle Aged, Mutation, Neoplasm Grading, Neoplasm Invasiveness, Neoplasm Recurrence, Local, Neoplasm Staging, Phenotype, Pilot Projects, Retrospective Studies, Risk Assessment, Risk Factors, Treatment Outcome, Young Adult.
Abstract
Studies in early-stage, predominantly low- and intermediate-risk endometrial cancer have demonstrated that L1 cell adhesion molecule (L1CAM) overexpression identifies patients at increased risk of recurrence, yet its prognostic significance in high-risk endometrial cancer is unclear. To evaluate this, its frequency, and the relationship of L1CAM with the established endometrial cancer biomarker p53, we analyzed the expression of both markers by immunohistochemistry in a pilot series of 116 endometrial cancers (86 endometrioid, 30 non-endometrioid subtype) with high-risk features (such as high tumor grade and deep myometrial invasion) and correlated results with clinical outcome. We used The Cancer Genome Atlas (TCGA) endometrial cancer series to validate our findings. Using the previously reported cutoff of 10% positive staining, 51/116 (44%) tumors were classified as L1CAM-positive, with no significant association between L1CAM positivity and the rate of distant metastasis (P=0.195). However, increasing the threshold for L1CAM positivity to 50% resulted in a reduction of the frequency of L1CAM-positive tumors to 24% (28/116), and a significant association with the rate of distant metastasis (P=0.018). L1CAM expression was strongly associated with mutant p53 in the high-risk and TCGA series (P<0.001), although a substantial fraction (36% of endometrioid, 10% of non-endometrioid morphology) of p53-mutant endometrial cancers displayed <10% L1CAM positivity. Moreover, 30% of p53-wild-type non-endometrioid endometrial cancers demonstrated diffuse L1CAM staining, suggesting p53-independent mechanisms of L1CAM overexpression. In conclusion, the previously proposed threshold for L1CAM positivity of >10% does not predict prognosis in high-risk endometrial cancer, whereas an alternative threshold (>50%) does. L1CAM expression is strongly, but not universally, associated with mutant p53, and may be strong enough for clinical implementation as prognostic marker in combination with p53. The high frequency of L1CAM expression in high-risk endometrial cancers suggests that it may also be a promising therapeutic target in this tumor subset.
DOI: 10.1038/modpathol.2015.147
PubMed: 26743472
Links to Exploration step
pubmed:26743472Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Prognostic significance of L1CAM expression and its association with mutant p53 expression in high-risk endometrial cancer.</title><author><name sortKey="Van Gool, Inge C" sort="Van Gool, Inge C" uniqKey="Van Gool I" first="Inge C" last="Van Gool">Inge C. Van Gool</name><affiliation><nlm:affiliation>Department of Pathology, Leiden University Medical Center, Leiden, The Netherlands.</nlm:affiliation></affiliation></author><author><name sortKey="Stelloo, Ellen" sort="Stelloo, Ellen" uniqKey="Stelloo E" first="Ellen" last="Stelloo">Ellen Stelloo</name><affiliation><nlm:affiliation>Department of Pathology, Leiden University Medical Center, Leiden, The Netherlands.</nlm:affiliation></affiliation></author><author><name sortKey="Nout, Remi A" sort="Nout, Remi A" uniqKey="Nout R" first="Remi A" last="Nout">Remi A. Nout</name><affiliation><nlm:affiliation>Department of Radiation Oncology, Leiden University Medical Center, Leiden, The Netherlands.</nlm:affiliation></affiliation></author><author><name sortKey="Nijman, Hans W" sort="Nijman, Hans W" uniqKey="Nijman H" first="Hans W" last="Nijman">Hans W. Nijman</name><affiliation><nlm:affiliation>Department of Gynecology, University Medical Center Groningen, Groningen, The Netherlands.</nlm:affiliation></affiliation></author><author><name sortKey="Edmondson, Richard J" sort="Edmondson, Richard J" uniqKey="Edmondson R" first="Richard J" last="Edmondson">Richard J. Edmondson</name><affiliation><nlm:affiliation>Institute of Cancer Sciences, University of Manchester, St Marys Hospital, Manchester, UK.</nlm:affiliation></affiliation></author><author><name sortKey="Church, David N" sort="Church, David N" uniqKey="Church D" first="David N" last="Church">David N. Church</name><affiliation><nlm:affiliation>Molecular and Population Genetics Laboratory, The Wellcome Trust Centre for Human Genetics, University of Oxford, Oxford, UK.</nlm:affiliation></affiliation></author><author><name sortKey="Mackay, Helen J" sort="Mackay, Helen J" uniqKey="Mackay H" first="Helen J" last="Mackay">Helen J. Mackay</name><affiliation><nlm:affiliation>Division of Gynecologic Oncology, Department of Obstetrics and Gynecology, Princess Margaret Hospital/University Health Network, University of Toronto, Toronto, Ontario, Canada.</nlm:affiliation></affiliation></author><author><name sortKey="Leary, Alexandra" sort="Leary, Alexandra" uniqKey="Leary A" first="Alexandra" last="Leary">Alexandra Leary</name><affiliation><nlm:affiliation>Department of Medicine, Gynecology Unit, Gustave Roussy, Villejuif, France.</nlm:affiliation></affiliation></author><author><name sortKey="Powell, Melanie E" sort="Powell, Melanie E" uniqKey="Powell M" first="Melanie E" last="Powell">Melanie E. Powell</name><affiliation><nlm:affiliation>Department of Clinical Oncology, Barts Health NHS Trust, London, UK.</nlm:affiliation></affiliation></author><author><name sortKey="Mileshkin, Linda" sort="Mileshkin, Linda" uniqKey="Mileshkin L" first="Linda" last="Mileshkin">Linda Mileshkin</name><affiliation><nlm:affiliation>Division of Cancer Medicine, Peter MacCallum Cancer Centre, East Melbourne, VIC, Australia.</nlm:affiliation></affiliation></author><author><name sortKey="Creutzberg, Carien L" sort="Creutzberg, Carien L" uniqKey="Creutzberg C" first="Carien L" last="Creutzberg">Carien L. Creutzberg</name><affiliation><nlm:affiliation>Department of Radiation Oncology, Leiden University Medical Center, Leiden, The Netherlands.</nlm:affiliation></affiliation></author><author><name sortKey="Smit, Vincent T H B M" sort="Smit, Vincent T H B M" uniqKey="Smit V" first="Vincent T H B M" last="Smit">Vincent T H B M. Smit</name><affiliation><nlm:affiliation>Department of Pathology, Leiden University Medical Center, Leiden, The Netherlands.</nlm:affiliation></affiliation></author><author><name sortKey="Bosse, Tjalling" sort="Bosse, Tjalling" uniqKey="Bosse T" first="Tjalling" last="Bosse">Tjalling Bosse</name><affiliation><nlm:affiliation>Department of Pathology, Leiden University Medical Center, Leiden, The Netherlands.</nlm:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2016">2016</date><idno type="RBID">pubmed:26743472</idno><idno type="pmid">26743472</idno><idno type="doi">10.1038/modpathol.2015.147</idno><idno type="wicri:Area/PubMed/Corpus">002253</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">002253</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Prognostic significance of L1CAM expression and its association with mutant p53 expression in high-risk endometrial cancer.</title><author><name sortKey="Van Gool, Inge C" sort="Van Gool, Inge C" uniqKey="Van Gool I" first="Inge C" last="Van Gool">Inge C. Van Gool</name><affiliation><nlm:affiliation>Department of Pathology, Leiden University Medical Center, Leiden, The Netherlands.</nlm:affiliation></affiliation></author><author><name sortKey="Stelloo, Ellen" sort="Stelloo, Ellen" uniqKey="Stelloo E" first="Ellen" last="Stelloo">Ellen Stelloo</name><affiliation><nlm:affiliation>Department of Pathology, Leiden University Medical Center, Leiden, The Netherlands.</nlm:affiliation></affiliation></author><author><name sortKey="Nout, Remi A" sort="Nout, Remi A" uniqKey="Nout R" first="Remi A" last="Nout">Remi A. Nout</name><affiliation><nlm:affiliation>Department of Radiation Oncology, Leiden University Medical Center, Leiden, The Netherlands.</nlm:affiliation></affiliation></author><author><name sortKey="Nijman, Hans W" sort="Nijman, Hans W" uniqKey="Nijman H" first="Hans W" last="Nijman">Hans W. Nijman</name><affiliation><nlm:affiliation>Department of Gynecology, University Medical Center Groningen, Groningen, The Netherlands.</nlm:affiliation></affiliation></author><author><name sortKey="Edmondson, Richard J" sort="Edmondson, Richard J" uniqKey="Edmondson R" first="Richard J" last="Edmondson">Richard J. Edmondson</name><affiliation><nlm:affiliation>Institute of Cancer Sciences, University of Manchester, St Marys Hospital, Manchester, UK.</nlm:affiliation></affiliation></author><author><name sortKey="Church, David N" sort="Church, David N" uniqKey="Church D" first="David N" last="Church">David N. Church</name><affiliation><nlm:affiliation>Molecular and Population Genetics Laboratory, The Wellcome Trust Centre for Human Genetics, University of Oxford, Oxford, UK.</nlm:affiliation></affiliation></author><author><name sortKey="Mackay, Helen J" sort="Mackay, Helen J" uniqKey="Mackay H" first="Helen J" last="Mackay">Helen J. Mackay</name><affiliation><nlm:affiliation>Division of Gynecologic Oncology, Department of Obstetrics and Gynecology, Princess Margaret Hospital/University Health Network, University of Toronto, Toronto, Ontario, Canada.</nlm:affiliation></affiliation></author><author><name sortKey="Leary, Alexandra" sort="Leary, Alexandra" uniqKey="Leary A" first="Alexandra" last="Leary">Alexandra Leary</name><affiliation><nlm:affiliation>Department of Medicine, Gynecology Unit, Gustave Roussy, Villejuif, France.</nlm:affiliation></affiliation></author><author><name sortKey="Powell, Melanie E" sort="Powell, Melanie E" uniqKey="Powell M" first="Melanie E" last="Powell">Melanie E. Powell</name><affiliation><nlm:affiliation>Department of Clinical Oncology, Barts Health NHS Trust, London, UK.</nlm:affiliation></affiliation></author><author><name sortKey="Mileshkin, Linda" sort="Mileshkin, Linda" uniqKey="Mileshkin L" first="Linda" last="Mileshkin">Linda Mileshkin</name><affiliation><nlm:affiliation>Division of Cancer Medicine, Peter MacCallum Cancer Centre, East Melbourne, VIC, Australia.</nlm:affiliation></affiliation></author><author><name sortKey="Creutzberg, Carien L" sort="Creutzberg, Carien L" uniqKey="Creutzberg C" first="Carien L" last="Creutzberg">Carien L. Creutzberg</name><affiliation><nlm:affiliation>Department of Radiation Oncology, Leiden University Medical Center, Leiden, The Netherlands.</nlm:affiliation></affiliation></author><author><name sortKey="Smit, Vincent T H B M" sort="Smit, Vincent T H B M" uniqKey="Smit V" first="Vincent T H B M" last="Smit">Vincent T H B M. Smit</name><affiliation><nlm:affiliation>Department of Pathology, Leiden University Medical Center, Leiden, The Netherlands.</nlm:affiliation></affiliation></author><author><name sortKey="Bosse, Tjalling" sort="Bosse, Tjalling" uniqKey="Bosse T" first="Tjalling" last="Bosse">Tjalling Bosse</name><affiliation><nlm:affiliation>Department of Pathology, Leiden University Medical Center, Leiden, The Netherlands.</nlm:affiliation></affiliation></author></analytic><series><title level="j">Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc</title><idno type="eISSN">1530-0285</idno><imprint><date when="2016" type="published">2016</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adult</term><term>Aged</term><term>Aged, 80 and over</term><term>Biomarkers, Tumor (analysis)</term><term>Biomarkers, Tumor (genetics)</term><term>Carcinoma, Endometrioid (chemistry)</term><term>Carcinoma, Endometrioid (genetics)</term><term>Carcinoma, Endometrioid (mortality)</term><term>Carcinoma, Endometrioid (secondary)</term><term>Carcinoma, Endometrioid (therapy)</term><term>DNA Mutational Analysis</term><term>Disease Progression</term><term>Disease-Free Survival</term><term>Endometrial Neoplasms (chemistry)</term><term>Endometrial Neoplasms (genetics)</term><term>Endometrial Neoplasms (mortality)</term><term>Endometrial Neoplasms (pathology)</term><term>Endometrial Neoplasms (therapy)</term><term>Female</term><term>Genetic Predisposition to Disease</term><term>Humans</term><term>Immunohistochemistry</term><term>Kaplan-Meier Estimate</term><term>Middle Aged</term><term>Mutation</term><term>Neoplasm Grading</term><term>Neoplasm Invasiveness</term><term>Neoplasm Recurrence, Local</term><term>Neoplasm Staging</term><term>Neural Cell Adhesion Molecule L1 (analysis)</term><term>Phenotype</term><term>Pilot Projects</term><term>Retrospective Studies</term><term>Risk Assessment</term><term>Risk Factors</term><term>Treatment Outcome</term><term>Tumor Suppressor Protein p53 (genetics)</term><term>Young Adult</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analysis" xml:lang="en"><term>Biomarkers, Tumor</term><term>Neural Cell Adhesion Molecule L1</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Biomarkers, Tumor</term><term>Tumor Suppressor Protein p53</term></keywords><keywords scheme="MESH" qualifier="chemistry" xml:lang="en"><term>Carcinoma, Endometrioid</term><term>Endometrial Neoplasms</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Carcinoma, Endometrioid</term><term>Endometrial Neoplasms</term></keywords><keywords scheme="MESH" qualifier="mortality" xml:lang="en"><term>Carcinoma, Endometrioid</term><term>Endometrial Neoplasms</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Endometrial Neoplasms</term></keywords><keywords scheme="MESH" qualifier="secondary" xml:lang="en"><term>Carcinoma, Endometrioid</term></keywords><keywords scheme="MESH" qualifier="therapy" xml:lang="en"><term>Carcinoma, Endometrioid</term><term>Endometrial Neoplasms</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adult</term><term>Aged</term><term>Aged, 80 and over</term><term>DNA Mutational Analysis</term><term>Disease Progression</term><term>Disease-Free Survival</term><term>Female</term><term>Genetic Predisposition to Disease</term><term>Humans</term><term>Immunohistochemistry</term><term>Kaplan-Meier Estimate</term><term>Middle Aged</term><term>Mutation</term><term>Neoplasm Grading</term><term>Neoplasm Invasiveness</term><term>Neoplasm Recurrence, Local</term><term>Neoplasm Staging</term><term>Phenotype</term><term>Pilot Projects</term><term>Retrospective Studies</term><term>Risk Assessment</term><term>Risk Factors</term><term>Treatment Outcome</term><term>Young Adult</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Studies in early-stage, predominantly low- and intermediate-risk endometrial cancer have demonstrated that L1 cell adhesion molecule (L1CAM) overexpression identifies patients at increased risk of recurrence, yet its prognostic significance in high-risk endometrial cancer is unclear. To evaluate this, its frequency, and the relationship of L1CAM with the established endometrial cancer biomarker p53, we analyzed the expression of both markers by immunohistochemistry in a pilot series of 116 endometrial cancers (86 endometrioid, 30 non-endometrioid subtype) with high-risk features (such as high tumor grade and deep myometrial invasion) and correlated results with clinical outcome. We used The Cancer Genome Atlas (TCGA) endometrial cancer series to validate our findings. Using the previously reported cutoff of 10% positive staining, 51/116 (44%) tumors were classified as L1CAM-positive, with no significant association between L1CAM positivity and the rate of distant metastasis (P=0.195). However, increasing the threshold for L1CAM positivity to 50% resulted in a reduction of the frequency of L1CAM-positive tumors to 24% (28/116), and a significant association with the rate of distant metastasis (P=0.018). L1CAM expression was strongly associated with mutant p53 in the high-risk and TCGA series (P<0.001), although a substantial fraction (36% of endometrioid, 10% of non-endometrioid morphology) of p53-mutant endometrial cancers displayed <10% L1CAM positivity. Moreover, 30% of p53-wild-type non-endometrioid endometrial cancers demonstrated diffuse L1CAM staining, suggesting p53-independent mechanisms of L1CAM overexpression. In conclusion, the previously proposed threshold for L1CAM positivity of >10% does not predict prognosis in high-risk endometrial cancer, whereas an alternative threshold (>50%) does. L1CAM expression is strongly, but not universally, associated with mutant p53, and may be strong enough for clinical implementation as prognostic marker in combination with p53. The high frequency of L1CAM expression in high-risk endometrial cancers suggests that it may also be a promising therapeutic target in this tumor subset.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">26743472</PMID><DateCreated><Year>2016</Year><Month>01</Month><Day>28</Day></DateCreated><DateCompleted><Year>2016</Year><Month>10</Month><Day>25</Day></DateCompleted><DateRevised><Year>2017</Year><Month>02</Month><Day>20</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1530-0285</ISSN><JournalIssue CitedMedium="Internet"><Volume>29</Volume><Issue>2</Issue><PubDate><Year>2016</Year><Month>Feb</Month></PubDate></JournalIssue><Title>Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc</Title><ISOAbbreviation>Mod. Pathol.</ISOAbbreviation></Journal><ArticleTitle>Prognostic significance of L1CAM expression and its association with mutant p53 expression in high-risk endometrial cancer.</ArticleTitle><Pagination><MedlinePgn>174-81</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1038/modpathol.2015.147</ELocationID><Abstract><AbstractText>Studies in early-stage, predominantly low- and intermediate-risk endometrial cancer have demonstrated that L1 cell adhesion molecule (L1CAM) overexpression identifies patients at increased risk of recurrence, yet its prognostic significance in high-risk endometrial cancer is unclear. To evaluate this, its frequency, and the relationship of L1CAM with the established endometrial cancer biomarker p53, we analyzed the expression of both markers by immunohistochemistry in a pilot series of 116 endometrial cancers (86 endometrioid, 30 non-endometrioid subtype) with high-risk features (such as high tumor grade and deep myometrial invasion) and correlated results with clinical outcome. We used The Cancer Genome Atlas (TCGA) endometrial cancer series to validate our findings. Using the previously reported cutoff of 10% positive staining, 51/116 (44%) tumors were classified as L1CAM-positive, with no significant association between L1CAM positivity and the rate of distant metastasis (P=0.195). However, increasing the threshold for L1CAM positivity to 50% resulted in a reduction of the frequency of L1CAM-positive tumors to 24% (28/116), and a significant association with the rate of distant metastasis (P=0.018). L1CAM expression was strongly associated with mutant p53 in the high-risk and TCGA series (P<0.001), although a substantial fraction (36% of endometrioid, 10% of non-endometrioid morphology) of p53-mutant endometrial cancers displayed <10% L1CAM positivity. Moreover, 30% of p53-wild-type non-endometrioid endometrial cancers demonstrated diffuse L1CAM staining, suggesting p53-independent mechanisms of L1CAM overexpression. In conclusion, the previously proposed threshold for L1CAM positivity of >10% does not predict prognosis in high-risk endometrial cancer, whereas an alternative threshold (>50%) does. L1CAM expression is strongly, but not universally, associated with mutant p53, and may be strong enough for clinical implementation as prognostic marker in combination with p53. The high frequency of L1CAM expression in high-risk endometrial cancers suggests that it may also be a promising therapeutic target in this tumor subset.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Van Gool</LastName><ForeName>Inge C</ForeName><Initials>IC</Initials><AffiliationInfo><Affiliation>Department of Pathology, Leiden University Medical Center, Leiden, The Netherlands.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Stelloo</LastName><ForeName>Ellen</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>Department of Pathology, Leiden University Medical Center, Leiden, The Netherlands.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Nout</LastName><ForeName>Remi A</ForeName><Initials>RA</Initials><AffiliationInfo><Affiliation>Department of Radiation Oncology, Leiden University Medical Center, Leiden, The Netherlands.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Nijman</LastName><ForeName>Hans W</ForeName><Initials>HW</Initials><AffiliationInfo><Affiliation>Department of Gynecology, University Medical Center Groningen, Groningen, The Netherlands.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Edmondson</LastName><ForeName>Richard J</ForeName><Initials>RJ</Initials><AffiliationInfo><Affiliation>Institute of Cancer Sciences, University of Manchester, St Marys Hospital, Manchester, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Church</LastName><ForeName>David N</ForeName><Initials>DN</Initials><Identifier Source="ORCID">http://orcid.org/0000-0002-4617-962X</Identifier><AffiliationInfo><Affiliation>Molecular and Population Genetics Laboratory, The Wellcome Trust Centre for Human Genetics, University of Oxford, Oxford, UK.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Oxford Cancer Centre, Churchill Hospital, Oxford, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>MacKay</LastName><ForeName>Helen J</ForeName><Initials>HJ</Initials><AffiliationInfo><Affiliation>Division of Gynecologic Oncology, Department of Obstetrics and Gynecology, Princess Margaret Hospital/University Health Network, University of Toronto, Toronto, Ontario, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Leary</LastName><ForeName>Alexandra</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Department of Medicine, Gynecology Unit, Gustave Roussy, Villejuif, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Powell</LastName><ForeName>Melanie E</ForeName><Initials>ME</Initials><AffiliationInfo><Affiliation>Department of Clinical Oncology, Barts Health NHS Trust, London, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mileshkin</LastName><ForeName>Linda</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Division of Cancer Medicine, Peter MacCallum Cancer Centre, East Melbourne, VIC, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Creutzberg</LastName><ForeName>Carien L</ForeName><Initials>CL</Initials><AffiliationInfo><Affiliation>Department of Radiation Oncology, Leiden University Medical Center, Leiden, The Netherlands.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Smit</LastName><ForeName>Vincent T H B M</ForeName><Initials>VT</Initials><AffiliationInfo><Affiliation>Department of Pathology, Leiden University Medical Center, Leiden, The Netherlands.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bosse</LastName><ForeName>Tjalling</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Department of Pathology, Leiden University Medical Center, Leiden, The Netherlands.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016448">Multicenter Study</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2016</Year><Month>01</Month><Day>08</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Mod Pathol</MedlineTA><NlmUniqueID>8806605</NlmUniqueID><ISSNLinking>0893-3952</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D014408">Biomarkers, Tumor</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D039842">Neural Cell Adhesion Molecule L1</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C495901">TP53 protein, 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