Refining prognosis and identifying targetable pathways for high-risk endometrial cancer; a TransPORTEC initiative.
Identifieur interne : 002D32 ( PubMed/Corpus ); précédent : 002D31; suivant : 002D33Refining prognosis and identifying targetable pathways for high-risk endometrial cancer; a TransPORTEC initiative.
Auteurs : Ellen Stelloo ; Tjalling Bosse ; Remi A. Nout ; Helen J. Mackay ; David N. Church ; Hans W. Nijman ; Alexandra Leary ; Richard J. Edmondson ; Melanie E. Powell ; Emma J. Crosbie ; Henry C. Kitchener ; Linda Mileshkin ; Pamela M. Pollock ; Vincent T. Smit ; Carien L. CreutzbergSource :
- Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc [ 1530-0285 ] ; 2015.
English descriptors
- KwdEn :
- Adult, Aged, Biomarkers, Tumor (analysis), DNA Mutational Analysis, Endometrial Neoplasms (classification), Endometrial Neoplasms (genetics), Endometrial Neoplasms (pathology), Female, Humans, Immunohistochemistry, Kaplan-Meier Estimate, Middle Aged, Polymerase Chain Reaction, Prognosis, Risk Factors, Tissue Array Analysis.
- MESH :
- chemical , analysis : Biomarkers, Tumor.
- classification : Endometrial Neoplasms.
- genetics : Endometrial Neoplasms.
- pathology : Endometrial Neoplasms.
- Adult, Aged, DNA Mutational Analysis, Female, Humans, Immunohistochemistry, Kaplan-Meier Estimate, Middle Aged, Polymerase Chain Reaction, Prognosis, Risk Factors, Tissue Array Analysis.
Abstract
This study aimed to investigate whether molecular analysis can be used to refine risk assessment, direct adjuvant therapy, and identify actionable alterations in high-risk endometrial cancer. TransPORTEC, an international consortium related to the PORTEC3 trial, was established for translational research in high-risk endometrial cancer. In this explorative study, routine molecular analyses were used to detect prognostic subgroups: p53 immunohistochemistry, microsatellite instability and POLE proofreading mutation. Furthermore, DNA was analyzed for hotspot mutations in 13 additional genes (BRAF, CDKNA2, CTNNB1, FBXW7, FGFR2, FGFR3, FOXL2, HRAS, KRAS, NRAS, PIK3CA, PPP2R1A, and PTEN) and protein expression of ER, PR, PTEN, and ARID1a was analyzed. Rates of distant metastasis, recurrence-free, and overall survival were calculated using the Kaplan-Meier method and log-rank test. In total, samples of 116 high-risk endometrial cancer patients were included: 86 endometrioid; 12 serous; and 18 clear cell. For endometrioid, serous, and clear cell cancers, 5-year recurrence-free survival rates were 68%, 27%, and 50% (P=0.014) and distant metastasis rates 23%, 64%, and 50% (P=0.001), respectively. Four prognostic subgroups were identified: (1) a group of p53-mutant tumors; (2) microsatellite instable tumors; (3) POLE proofreading-mutant tumors; and (4) a group with no specific molecular profile (NSMP). In group 3 (POLE-mutant; n=14) and group 2 (microsatellite instable; n=19) patients, no distant metastasis occurred, compared with 50% distant metastasis rate in group 1 (p53-mutant; n=36) and 39% in group 4 (NSMP; P<0.001). Five-year recurrence-free survival was 93% and 95% for group 3 (POLE-mutant) and group 2 (microsatellite instable) vs 42% (group 1, p53-mutant) and 52% (group 4, NSMP; P<0.001). Targetable FBXW7 and FGFR2 mutations (6%), alterations in the PI3K-AKT pathway (60%) and hormone receptor positivity (45%) were frequently found. In conclusion, molecular analysis of high-risk endometrial cancer identifies four distinct prognostic subgroups, with potential therapeutic implications. High frequencies of targetable alterations were identified and may serve as targets for individualized treatment.
DOI: 10.1038/modpathol.2015.43
PubMed: 25720322
Links to Exploration step
pubmed:25720322Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Refining prognosis and identifying targetable pathways for high-risk endometrial cancer; a TransPORTEC initiative.</title><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="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><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 Clinical Oncology, Leiden University Medical Center, Leiden, The Netherlands.</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, ON, Canada.</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="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 of Groningen, University Medical Center Groningen, Groningen, The Netherlands.</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="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="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="Crosbie, Emma J" sort="Crosbie, Emma J" uniqKey="Crosbie E" first="Emma J" last="Crosbie">Emma J. Crosbie</name><affiliation><nlm:affiliation>Institute of Cancer Sciences, University of Manchester, St Marys Hospital, Manchester, UK.</nlm:affiliation></affiliation></author><author><name sortKey="Kitchener, Henry C" sort="Kitchener, Henry C" uniqKey="Kitchener H" first="Henry C" last="Kitchener">Henry C. Kitchener</name><affiliation><nlm:affiliation>Institute of Cancer Sciences, University of Manchester, St Marys Hospital, Manchester, 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="Pollock, Pamela M" sort="Pollock, Pamela M" uniqKey="Pollock P" first="Pamela M" last="Pollock">Pamela M. Pollock</name><affiliation><nlm:affiliation>Institute of Health and Biomedical Innovation, Queensland University of Technology, Brisbane, QLD, Australia.</nlm:affiliation></affiliation></author><author><name sortKey="Smit, Vincent T" sort="Smit, Vincent T" uniqKey="Smit V" first="Vincent T" last="Smit">Vincent T. Smit</name><affiliation><nlm:affiliation>Department of Pathology, Leiden University Medical Center, Leiden, The Netherlands.</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 Clinical Oncology, Leiden University Medical Center, Leiden, The Netherlands.</nlm:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2015">2015</date><idno type="RBID">pubmed:25720322</idno><idno type="pmid">25720322</idno><idno type="doi">10.1038/modpathol.2015.43</idno><idno type="wicri:Area/PubMed/Corpus">002D32</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">002D32</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Refining prognosis and identifying targetable pathways for high-risk endometrial cancer; a TransPORTEC initiative.</title><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="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><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 Clinical Oncology, Leiden University Medical Center, Leiden, The Netherlands.</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, ON, Canada.</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="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 of Groningen, University Medical Center Groningen, Groningen, The Netherlands.</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="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="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="Crosbie, Emma J" sort="Crosbie, Emma J" uniqKey="Crosbie E" first="Emma J" last="Crosbie">Emma J. Crosbie</name><affiliation><nlm:affiliation>Institute of Cancer Sciences, University of Manchester, St Marys Hospital, Manchester, UK.</nlm:affiliation></affiliation></author><author><name sortKey="Kitchener, Henry C" sort="Kitchener, Henry C" uniqKey="Kitchener H" first="Henry C" last="Kitchener">Henry C. Kitchener</name><affiliation><nlm:affiliation>Institute of Cancer Sciences, University of Manchester, St Marys Hospital, Manchester, 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="Pollock, Pamela M" sort="Pollock, Pamela M" uniqKey="Pollock P" first="Pamela M" last="Pollock">Pamela M. Pollock</name><affiliation><nlm:affiliation>Institute of Health and Biomedical Innovation, Queensland University of Technology, Brisbane, QLD, Australia.</nlm:affiliation></affiliation></author><author><name sortKey="Smit, Vincent T" sort="Smit, Vincent T" uniqKey="Smit V" first="Vincent T" last="Smit">Vincent T. Smit</name><affiliation><nlm:affiliation>Department of Pathology, Leiden University Medical Center, Leiden, The Netherlands.</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 Clinical Oncology, 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="2015" type="published">2015</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adult</term><term>Aged</term><term>Biomarkers, Tumor (analysis)</term><term>DNA Mutational Analysis</term><term>Endometrial Neoplasms (classification)</term><term>Endometrial Neoplasms (genetics)</term><term>Endometrial Neoplasms (pathology)</term><term>Female</term><term>Humans</term><term>Immunohistochemistry</term><term>Kaplan-Meier Estimate</term><term>Middle Aged</term><term>Polymerase Chain Reaction</term><term>Prognosis</term><term>Risk Factors</term><term>Tissue Array Analysis</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analysis" xml:lang="en"><term>Biomarkers, Tumor</term></keywords><keywords scheme="MESH" qualifier="classification" xml:lang="en"><term>Endometrial Neoplasms</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Endometrial Neoplasms</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Endometrial Neoplasms</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adult</term><term>Aged</term><term>DNA Mutational Analysis</term><term>Female</term><term>Humans</term><term>Immunohistochemistry</term><term>Kaplan-Meier Estimate</term><term>Middle Aged</term><term>Polymerase Chain Reaction</term><term>Prognosis</term><term>Risk Factors</term><term>Tissue Array Analysis</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">This study aimed to investigate whether molecular analysis can be used to refine risk assessment, direct adjuvant therapy, and identify actionable alterations in high-risk endometrial cancer. TransPORTEC, an international consortium related to the PORTEC3 trial, was established for translational research in high-risk endometrial cancer. In this explorative study, routine molecular analyses were used to detect prognostic subgroups: p53 immunohistochemistry, microsatellite instability and POLE proofreading mutation. Furthermore, DNA was analyzed for hotspot mutations in 13 additional genes (BRAF, CDKNA2, CTNNB1, FBXW7, FGFR2, FGFR3, FOXL2, HRAS, KRAS, NRAS, PIK3CA, PPP2R1A, and PTEN) and protein expression of ER, PR, PTEN, and ARID1a was analyzed. Rates of distant metastasis, recurrence-free, and overall survival were calculated using the Kaplan-Meier method and log-rank test. In total, samples of 116 high-risk endometrial cancer patients were included: 86 endometrioid; 12 serous; and 18 clear cell. For endometrioid, serous, and clear cell cancers, 5-year recurrence-free survival rates were 68%, 27%, and 50% (P=0.014) and distant metastasis rates 23%, 64%, and 50% (P=0.001), respectively. Four prognostic subgroups were identified: (1) a group of p53-mutant tumors; (2) microsatellite instable tumors; (3) POLE proofreading-mutant tumors; and (4) a group with no specific molecular profile (NSMP). In group 3 (POLE-mutant; n=14) and group 2 (microsatellite instable; n=19) patients, no distant metastasis occurred, compared with 50% distant metastasis rate in group 1 (p53-mutant; n=36) and 39% in group 4 (NSMP; P<0.001). Five-year recurrence-free survival was 93% and 95% for group 3 (POLE-mutant) and group 2 (microsatellite instable) vs 42% (group 1, p53-mutant) and 52% (group 4, NSMP; P<0.001). Targetable FBXW7 and FGFR2 mutations (6%), alterations in the PI3K-AKT pathway (60%) and hormone receptor positivity (45%) were frequently found. In conclusion, molecular analysis of high-risk endometrial cancer identifies four distinct prognostic subgroups, with potential therapeutic implications. High frequencies of targetable alterations were identified and may serve as targets for individualized treatment.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">25720322</PMID><DateCreated><Year>2015</Year><Month>05</Month><Day>30</Day></DateCreated><DateCompleted><Year>2016</Year><Month>03</Month><Day>25</Day></DateCompleted><DateRevised><Year>2017</Year><Month>09</Month><Day>22</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1530-0285</ISSN><JournalIssue CitedMedium="Internet"><Volume>28</Volume><Issue>6</Issue><PubDate><Year>2015</Year><Month>Jun</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>Refining prognosis and identifying targetable pathways for high-risk endometrial cancer; a TransPORTEC initiative.</ArticleTitle><Pagination><MedlinePgn>836-44</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1038/modpathol.2015.43</ELocationID><Abstract><AbstractText>This study aimed to investigate whether molecular analysis can be used to refine risk assessment, direct adjuvant therapy, and identify actionable alterations in high-risk endometrial cancer. TransPORTEC, an international consortium related to the PORTEC3 trial, was established for translational research in high-risk endometrial cancer. In this explorative study, routine molecular analyses were used to detect prognostic subgroups: p53 immunohistochemistry, microsatellite instability and POLE proofreading mutation. Furthermore, DNA was analyzed for hotspot mutations in 13 additional genes (BRAF, CDKNA2, CTNNB1, FBXW7, FGFR2, FGFR3, FOXL2, HRAS, KRAS, NRAS, PIK3CA, PPP2R1A, and PTEN) and protein expression of ER, PR, PTEN, and ARID1a was analyzed. Rates of distant metastasis, recurrence-free, and overall survival were calculated using the Kaplan-Meier method and log-rank test. In total, samples of 116 high-risk endometrial cancer patients were included: 86 endometrioid; 12 serous; and 18 clear cell. For endometrioid, serous, and clear cell cancers, 5-year recurrence-free survival rates were 68%, 27%, and 50% (P=0.014) and distant metastasis rates 23%, 64%, and 50% (P=0.001), respectively. Four prognostic subgroups were identified: (1) a group of p53-mutant tumors; (2) microsatellite instable tumors; (3) POLE proofreading-mutant tumors; and (4) a group with no specific molecular profile (NSMP). In group 3 (POLE-mutant; n=14) and group 2 (microsatellite instable; n=19) patients, no distant metastasis occurred, compared with 50% distant metastasis rate in group 1 (p53-mutant; n=36) and 39% in group 4 (NSMP; P<0.001). Five-year recurrence-free survival was 93% and 95% for group 3 (POLE-mutant) and group 2 (microsatellite instable) vs 42% (group 1, p53-mutant) and 52% (group 4, NSMP; P<0.001). Targetable FBXW7 and FGFR2 mutations (6%), alterations in the PI3K-AKT pathway (60%) and hormone receptor positivity (45%) were frequently found. In conclusion, molecular analysis of high-risk endometrial cancer identifies four distinct prognostic subgroups, with potential therapeutic implications. High frequencies of targetable alterations were identified and may serve as targets for individualized treatment.</AbstractText></Abstract><AuthorList CompleteYN="Y"><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>Bosse</LastName><ForeName>Tjalling</ForeName><Initials>T</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 Clinical Oncology, Leiden University Medical Center, Leiden, The Netherlands.</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, ON, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Church</LastName><ForeName>David N</ForeName><Initials>DN</Initials><AffiliationInfo><Affiliation>Molecular and Population Genetics Laboratory, The Wellcome Trust Centre for Human Genetics, University of Oxford, Oxford, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Nijman</LastName><ForeName>Hans W</ForeName><Initials>HW</Initials><AffiliationInfo><Affiliation>Department of Gynecology, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.</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>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>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>Crosbie</LastName><ForeName>Emma J</ForeName><Initials>EJ</Initials><AffiliationInfo><Affiliation>Institute of Cancer Sciences, University of Manchester, St Marys Hospital, Manchester, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kitchener</LastName><ForeName>Henry C</ForeName><Initials>HC</Initials><AffiliationInfo><Affiliation>Institute of Cancer Sciences, University of Manchester, St Marys Hospital, Manchester, 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>Pollock</LastName><ForeName>Pamela M</ForeName><Initials>PM</Initials><AffiliationInfo><Affiliation>Institute of Health and Biomedical Innovation, Queensland University of Technology, Brisbane, QLD, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Smit</LastName><ForeName>Vincent T</ForeName><Initials>VT</Initials><AffiliationInfo><Affiliation>Department of Pathology, Leiden University Medical Center, Leiden, The Netherlands.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Creutzberg</LastName><ForeName>Carien L</ForeName><Initials>CL</Initials><AffiliationInfo><Affiliation>Department of Clinical Oncology, Leiden University Medical Center, Leiden, The Netherlands.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>NIHR-CS-012-009</GrantID><Agency>Department of Health</Agency><Country>United Kingdom</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2015</Year><Month>02</Month><Day>27</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 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