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Prediction of BRCA1 status in patients with breast cancer using estroqen receptor and basal phenotype

Identifieur interne : 004848 ( PascalFrancis/Corpus ); précédent : 004847; suivant : 004849

Prediction of BRCA1 status in patients with breast cancer using estroqen receptor and basal phenotype

Auteurs : Sunil R. Lakhani ; Jorge S. Reis-Filho ; Laura Fulford ; Frederique Penault-Llorca ; Marc Van Dervijver ; Suzanne Parry ; Timothy Bishop ; Javier Benitez ; Carmen Rivas ; Yves-Jean Bignon ; Jenny Chang-Claude ; Ute Hamann ; Cees J. Cornelisse ; Peter Devilee ; Matthias W. Beckmann ; Carolin Nestle-Kr Mling ; Peter A. Daly ; Neva Haites ; Jenny Varley ; Fiona Lalloo ; Gareth Evans ; Christine Maugard ; Hanne Meijers-Heijboer ; Jan G. M. Klijn ; Edith Olah ; Barry A. Gusterson ; Silvana Pilotti ; Paolo Radice ; Siegfried Scherneck ; Hagay Sobol ; Jocelyne Jacquemier ; Teresa Wagner ; Julian Peto ; Michael R. Stratton ; Lesley Mcguffog ; Douglas F. Easton

Source :

RBID : Pascal:05-0335175

Descripteurs français

English descriptors

Abstract

Purpose:To investigate the proportion of breast cancers arising in patients with germ line BRCA1 and BRCA2 mutations expressing basal markers and developing predictive tests for identification of high-risk patients. Experimental Design: Histopathologic material from 182 tumors in BRCA1 mutation carriers, 63 BRCA2 carriers, and 109 controls, collected as part of the international Breast Cancer Linkage Consortium were immunohistochemically stained for CK14, CK5/6, CK17, epidermal growth factor receptor (EGFR), and osteonectin. Results: All five basal markers were commoner in BRCA1 tumors than in control tumors (CK14: 61% versus, 12%; CK5/6: 58% versus 7%; CK17: 53%versus10%; osteonectin: 43%versus19%; EGFR: 67% versus 21%; P < 0.0001 in each case). In a multivariate analysis, CK14, CK5/6, and estrogen receptor (ER) remained significant predictors of BRCA1 carrier status. In contrast, the frequency of basal markers in BRCA2 tumors did not differ significant from controls. Conclusion: The use of cytokeratin staining in combination with ER and morphology provides a more accurate predictor of BRCA1 mutation status than previously available, that may be useful in selecting patients for BRCA1 mutation testing. The high percentage of BRCA1 cases positive for EGFR suggests that specific anti-tyrosine kinase therapy may be of potential benefit in these patients.

Notice en format standard (ISO 2709)

Pour connaître la documentation sur le format Inist Standard.

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A01 01  1    @0 1078-0432
A03   1    @0 Clin. cancer res.
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A06       @2 14
A08 01  1  ENG  @1 Prediction of BRCA1 status in patients with breast cancer using estroqen receptor and basal phenotype
A11 01  1    @1 LAKHANI (Sunil R.)
A11 02  1    @1 REIS-FILHO (Jorge S.)
A11 03  1    @1 FULFORD (Laura)
A11 04  1    @1 PENAULT-LLORCA (Frederique)
A11 05  1    @1 VAN DERVIJVER (Marc)
A11 06  1    @1 PARRY (Suzanne)
A11 07  1    @1 BISHOP (Timothy)
A11 08  1    @1 BENITEZ (Javier)
A11 09  1    @1 RIVAS (Carmen)
A11 10  1    @1 BIGNON (Yves-Jean)
A11 11  1    @1 CHANG-CLAUDE (Jenny)
A11 12  1    @1 HAMANN (Ute)
A11 13  1    @1 CORNELISSE (Cees J.)
A11 14  1    @1 DEVILEE (Peter)
A11 15  1    @1 BECKMANN (Matthias W.)
A11 16  1    @1 NESTLE-KRÄMLING (Carolin)
A11 17  1    @1 DALY (Peter A.)
A11 18  1    @1 HAITES (Neva)
A11 19  1    @1 VARLEY (Jenny)
A11 20  1    @1 LALLOO (Fiona)
A11 21  1    @1 EVANS (Gareth)
A11 22  1    @1 MAUGARD (Christine)
A11 23  1    @1 MEIJERS-HEIJBOER (Hanne)
A11 24  1    @1 KLIJN (Jan G. M.)
A11 25  1    @1 OLAH (Edith)
A11 26  1    @1 GUSTERSON (Barry A.)
A11 27  1    @1 PILOTTI (Silvana)
A11 28  1    @1 RADICE (Paolo)
A11 29  1    @1 SCHERNECK (Siegfried)
A11 30  1    @1 SOBOL (Hagay)
A11 31  1    @1 JACQUEMIER (Jocelyne)
A11 32  1    @1 WAGNER (Teresa)
A11 33  1    @1 PETO (Julian)
A11 34  1    @1 STRATTON (Michael R.)
A11 35  1    @1 MCGUFFOG (Lesley)
A11 36  1    @1 EASTON (Douglas F.)
A14 01      @1 The Breakthrough Toby Robins Breast Cancer Research Centre, Institute of Cancer Research @2 London @3 GBR @Z 1 aut. @Z 2 aut. @Z 3 aut. @Z 6 aut.
A14 02      @1 Molecular and Cellular Pathology, University of Queensland @2 Brisbane @3 AUS @Z 1 aut.
A14 03      @1 Centre Jean Perrin @2 Clermont-Ferrand @3 FRA @Z 4 aut. @Z 10 aut.
A14 04      @1 The Netherlands Cancer Institute @2 Amsterdam @3 NLD @Z 5 aut.
A14 05      @1 Imperial Cancer Research Fund Genetic Epidemiology Laboratory, St. James University Hospital @2 Leeds @3 GBR @Z 7 aut.
A14 06      @1 Department of Genetics, Dpto Genetica Humana. Centro Nacional nvestigaciones Oncológicas @2 Madrid @3 ESP @Z 8 aut.
A14 07      @1 Department of Pathology, Fundación Jiménez Díaz, Autonomous University of Madrid @2 Madrid @3 ESP @Z 9 aut.
A14 08      @1 Deutsches Krebsforschungszentrum, Divisions of Epidemiology and Molecular Genome Analysis @2 Heidelberg @3 DEU @Z 11 aut. @Z 12 aut.
A14 09      @1 Department of Genetics and Pathology, Leiden University @2 Leiden @3 NLD @Z 13 aut. @Z 14 aut.
A14 10      @1 Departments of Obstetrics and Gynecology, Friedrich Alexander University @2 Erlangen @3 DEU @Z 15 aut. @Z 16 aut.
A14 11      @1 Department of Medicine, Trinity College Medical School, St James Hospital @2 Dublin @3 IRL @Z 17 aut.
A14 12      @1 Medical Genetics, Department of Medicine and Therapeutics, University of Aberdeen @2 Aberdeen @3 GBR @Z 18 aut.
A14 13      @1 CRUK Cancer Genetics Group, Paterson Institute for Cancer Research @2 Manchester @3 GBR @Z 19 aut.
A14 14      @1 Department of Medical Genetics, St. Mary's Hospital @2 Manchester @3 GBR @Z 20 aut. @Z 21 aut.
A14 15      @1 University Hospital @2 Nantes @3 FRA @Z 22 aut.
A14 16      @1 Department of Clinical Genetics and Medical Oncology, Daniel den Hoed Cancer Centre, Erasmus University Medical Centre Rotterdam @2 Rotterdam @3 NLD @Z 23 aut. @Z 24 aut.
A14 17      @1 Department of Molecular Biology, National Institute of Oncology @2 Budapest @3 HUN @Z 25 aut.
A14 18      @1 Department of Pathology, Western Infirmary, University of Glasgow @2 Scotland @3 GBR @Z 26 aut.
A14 19      @1 Department of Pathology, Istituto Nazionale Tumori @2 Milan @3 ITA @Z 27 aut.
A14 20      @1 Department of Experimental Oncology, Istituto Nazionale Tumori @2 Milan @3 ITA @Z 28 aut.
A14 21      @1 Max-Delbruck-Centrum fur Moleculare Medizin, Tumorgenetik @2 Berlin @3 DEU @Z 29 aut.
A14 22      @1 Department of Genetic Oncology and Cancer Control, Institut National de la Sante et de la Recherche Medicale EPI 9939, Paoli Calmettes Institute @2 Marseille @3 FRA @Z 30 aut. @Z 31 aut.
A14 23      @1 Department of Obstetrics and Gynaecology, General Hospital, University of Vienna @3 AUT @Z 32 aut.
A14 24      @1 Sections of Cancer Genetics and Epidemiology, Institute of Cancer Research, Haddow Laboratories @3 GBR @Z 33 aut. @Z 34 aut.
A14 25      @1 London School of Hygiene and Tropical Medicine @2 London @3 GBR @Z 33 aut.
A17 01  1    @1 Breast Cancer Linkage Consortium @3 INC
A20       @1 5175-5180
A21       @1 2005
A23 01      @0 ENG
A43 01      @1 INIST @2 26073 @5 354000137962310150
A44       @0 0000 @1 © 2005 INIST-CNRS. All rights reserved.
A45       @0 28 ref.
A47 01  1    @0 05-0335175
A60       @1 P
A61       @0 A
A64 01  1    @0 Clinical cancer research
A66 01      @0 USA
C01 01    ENG  @0 Purpose:To investigate the proportion of breast cancers arising in patients with germ line BRCA1 and BRCA2 mutations expressing basal markers and developing predictive tests for identification of high-risk patients. Experimental Design: Histopathologic material from 182 tumors in BRCA1 mutation carriers, 63 BRCA2 carriers, and 109 controls, collected as part of the international Breast Cancer Linkage Consortium were immunohistochemically stained for CK14, CK5/6, CK17, epidermal growth factor receptor (EGFR), and osteonectin. Results: All five basal markers were commoner in BRCA1 tumors than in control tumors (CK14: 61% versus, 12%; CK5/6: 58% versus 7%; CK17: 53%versus10%; osteonectin: 43%versus19%; EGFR: 67% versus 21%; P < 0.0001 in each case). In a multivariate analysis, CK14, CK5/6, and estrogen receptor (ER) remained significant predictors of BRCA1 carrier status. In contrast, the frequency of basal markers in BRCA2 tumors did not differ significant from controls. Conclusion: The use of cytokeratin staining in combination with ER and morphology provides a more accurate predictor of BRCA1 mutation status than previously available, that may be useful in selecting patients for BRCA1 mutation testing. The high percentage of BRCA1 cases positive for EGFR suggests that specific anti-tyrosine kinase therapy may be of potential benefit in these patients.
C02 01  X    @0 002B02R
C03 01  X  FRE  @0 Prédiction @5 01
C03 01  X  ENG  @0 Prediction @5 01
C03 01  X  SPA  @0 Predicción @5 01
C03 02  X  FRE  @0 Facteur prédictif @5 02
C03 02  X  ENG  @0 Predictive factor @5 02
C03 02  X  SPA  @0 Factor predictivo @5 02
C03 03  X  FRE  @0 Gène suppresseur tumeur @5 03
C03 03  X  ENG  @0 Tumor suppressor gene @5 03
C03 03  X  SPA  @0 Gen supresor tumor @5 03
C03 04  X  FRE  @0 Gène BRCA1 @5 04
C03 04  X  ENG  @0 BRCA1 gene @5 04
C03 04  X  SPA  @0 Gen BRCA1 @5 04
C03 05  X  FRE  @0 Homme @5 05
C03 05  X  ENG  @0 Human @5 05
C03 05  X  SPA  @0 Hombre @5 05
C03 06  X  FRE  @0 Glande mammaire pathologie @2 NM @5 06
C03 06  X  ENG  @0 Mammary gland diseases @2 NM @5 06
C03 06  X  SPA  @0 Glándula mamaria patología @2 NM @5 06
C03 07  X  FRE  @0 Tumeur maligne @5 07
C03 07  X  ENG  @0 Malignant tumor @5 07
C03 07  X  SPA  @0 Tumor maligno @5 07
C03 08  X  FRE  @0 Récepteur biologique @5 08
C03 08  X  ENG  @0 Biological receptor @5 08
C03 08  X  SPA  @0 Receptor biológico @5 08
C03 09  X  FRE  @0 Phénotype @5 09
C03 09  X  ENG  @0 Phenotype @5 09
C03 09  X  SPA  @0 Fenotipo @5 09
C03 10  X  FRE  @0 Cancer sein @4 CD @5 96
C03 10  X  ENG  @0 Breast cancer @4 CD @5 96
C03 10  X  SPA  @0 Cáncer del pecho @4 CD @5 96
N21       @1 234
N44 01      @1 OTO
N82       @1 OTO

Format Inist (serveur)

NO : PASCAL 05-0335175 INIST
ET : Prediction of BRCA1 status in patients with breast cancer using estroqen receptor and basal phenotype
AU : LAKHANI (Sunil R.); REIS-FILHO (Jorge S.); FULFORD (Laura); PENAULT-LLORCA (Frederique); VAN DERVIJVER (Marc); PARRY (Suzanne); BISHOP (Timothy); BENITEZ (Javier); RIVAS (Carmen); BIGNON (Yves-Jean); CHANG-CLAUDE (Jenny); HAMANN (Ute); CORNELISSE (Cees J.); DEVILEE (Peter); BECKMANN (Matthias W.); NESTLE-KRÄMLING (Carolin); DALY (Peter A.); HAITES (Neva); VARLEY (Jenny); LALLOO (Fiona); EVANS (Gareth); MAUGARD (Christine); MEIJERS-HEIJBOER (Hanne); KLIJN (Jan G. M.); OLAH (Edith); GUSTERSON (Barry A.); PILOTTI (Silvana); RADICE (Paolo); SCHERNECK (Siegfried); SOBOL (Hagay); JACQUEMIER (Jocelyne); WAGNER (Teresa); PETO (Julian); STRATTON (Michael R.); MCGUFFOG (Lesley); EASTON (Douglas F.)
AF : The Breakthrough Toby Robins Breast Cancer Research Centre, Institute of Cancer Research/London/Royaume-Uni (1 aut., 2 aut., 3 aut., 6 aut.); Molecular and Cellular Pathology, University of Queensland/Brisbane/Australie (1 aut.); Centre Jean Perrin/Clermont-Ferrand/France (4 aut., 10 aut.); The Netherlands Cancer Institute/Amsterdam/Pays-Bas (5 aut.); Imperial Cancer Research Fund Genetic Epidemiology Laboratory, St. James University Hospital/Leeds/Royaume-Uni (7 aut.); Department of Genetics, Dpto Genetica Humana. Centro Nacional nvestigaciones Oncológicas/Madrid/Espagne (8 aut.); Department of Pathology, Fundación Jiménez Díaz, Autonomous University of Madrid/Madrid/Espagne (9 aut.); Deutsches Krebsforschungszentrum, Divisions of Epidemiology and Molecular Genome Analysis/Heidelberg/Allemagne (11 aut., 12 aut.); Department of Genetics and Pathology, Leiden University/Leiden/Pays-Bas (13 aut., 14 aut.); Departments of Obstetrics and Gynecology, Friedrich Alexander University/Erlangen/Allemagne (15 aut., 16 aut.); Department of Medicine, Trinity College Medical School, St James Hospital/Dublin/Irlande (17 aut.); Medical Genetics, Department of Medicine and Therapeutics, University of Aberdeen/Aberdeen/Royaume-Uni (18 aut.); CRUK Cancer Genetics Group, Paterson Institute for Cancer Research/Manchester/Royaume-Uni (19 aut.); Department of Medical Genetics, St. Mary's Hospital/Manchester/Royaume-Uni (20 aut., 21 aut.); University Hospital/Nantes/France (22 aut.); Department of Clinical Genetics and Medical Oncology, Daniel den Hoed Cancer Centre, Erasmus University Medical Centre Rotterdam/Rotterdam/Pays-Bas (23 aut., 24 aut.); Department of Molecular Biology, National Institute of Oncology/Budapest/Hongrie (25 aut.); Department of Pathology, Western Infirmary, University of Glasgow/Scotland/Royaume-Uni (26 aut.); Department of Pathology, Istituto Nazionale Tumori/Milan/Italie (27 aut.); Department of Experimental Oncology, Istituto Nazionale Tumori/Milan/Italie (28 aut.); Max-Delbruck-Centrum fur Moleculare Medizin, Tumorgenetik/Berlin/Allemagne (29 aut.); Department of Genetic Oncology and Cancer Control, Institut National de la Sante et de la Recherche Medicale EPI 9939, Paoli Calmettes Institute/Marseille/France (30 aut., 31 aut.); Department of Obstetrics and Gynaecology, General Hospital, University of Vienna/Autriche (32 aut.); Sections of Cancer Genetics and Epidemiology, Institute of Cancer Research, Haddow Laboratories/Royaume-Uni (33 aut., 34 aut.); London School of Hygiene and Tropical Medicine/London/Royaume-Uni (33 aut.)
DT : Publication en série; Niveau analytique
SO : Clinical cancer research; ISSN 1078-0432; Etats-Unis; Da. 2005; Vol. 11; No. 14; Pp. 5175-5180; Bibl. 28 ref.
LA : Anglais
EA : Purpose:To investigate the proportion of breast cancers arising in patients with germ line BRCA1 and BRCA2 mutations expressing basal markers and developing predictive tests for identification of high-risk patients. Experimental Design: Histopathologic material from 182 tumors in BRCA1 mutation carriers, 63 BRCA2 carriers, and 109 controls, collected as part of the international Breast Cancer Linkage Consortium were immunohistochemically stained for CK14, CK5/6, CK17, epidermal growth factor receptor (EGFR), and osteonectin. Results: All five basal markers were commoner in BRCA1 tumors than in control tumors (CK14: 61% versus, 12%; CK5/6: 58% versus 7%; CK17: 53%versus10%; osteonectin: 43%versus19%; EGFR: 67% versus 21%; P < 0.0001 in each case). In a multivariate analysis, CK14, CK5/6, and estrogen receptor (ER) remained significant predictors of BRCA1 carrier status. In contrast, the frequency of basal markers in BRCA2 tumors did not differ significant from controls. Conclusion: The use of cytokeratin staining in combination with ER and morphology provides a more accurate predictor of BRCA1 mutation status than previously available, that may be useful in selecting patients for BRCA1 mutation testing. The high percentage of BRCA1 cases positive for EGFR suggests that specific anti-tyrosine kinase therapy may be of potential benefit in these patients.
CC : 002B02R
FD : Prédiction; Facteur prédictif; Gène suppresseur tumeur; Gène BRCA1; Homme; Glande mammaire pathologie; Tumeur maligne; Récepteur biologique; Phénotype; Cancer sein
ED : Prediction; Predictive factor; Tumor suppressor gene; BRCA1 gene; Human; Mammary gland diseases; Malignant tumor; Biological receptor; Phenotype; Breast cancer
SD : Predicción; Factor predictivo; Gen supresor tumor; Gen BRCA1; Hombre; Glándula mamaria patología; Tumor maligno; Receptor biológico; Fenotipo; Cáncer del pecho
LO : INIST-26073.354000137962310150
ID : 05-0335175

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Pascal:05-0335175

Le document en format XML

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<name sortKey="Bignon, Yves Jean" sort="Bignon, Yves Jean" uniqKey="Bignon Y" first="Yves-Jean" last="Bignon">Yves-Jean Bignon</name>
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<name sortKey="Nestle Kr Mling, Carolin" sort="Nestle Kr Mling, Carolin" uniqKey="Nestle Kr Mling C" first="Carolin" last="Nestle-Kr Mling">Carolin Nestle-Kr Mling</name>
<affiliation>
<inist:fA14 i1="10">
<s1>Departments of Obstetrics and Gynecology, Friedrich Alexander University</s1>
<s2>Erlangen</s2>
<s3>DEU</s3>
<sZ>15 aut.</sZ>
<sZ>16 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author>
<name sortKey="Daly, Peter A" sort="Daly, Peter A" uniqKey="Daly P" first="Peter A." last="Daly">Peter A. Daly</name>
<affiliation>
<inist:fA14 i1="11">
<s1>Department of Medicine, Trinity College Medical School, St James Hospital</s1>
<s2>Dublin</s2>
<s3>IRL</s3>
<sZ>17 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author>
<name sortKey="Haites, Neva" sort="Haites, Neva" uniqKey="Haites N" first="Neva" last="Haites">Neva Haites</name>
<affiliation>
<inist:fA14 i1="12">
<s1>Medical Genetics, Department of Medicine and Therapeutics, University of Aberdeen</s1>
<s2>Aberdeen</s2>
<s3>GBR</s3>
<sZ>18 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author>
<name sortKey="Varley, Jenny" sort="Varley, Jenny" uniqKey="Varley J" first="Jenny" last="Varley">Jenny Varley</name>
<affiliation>
<inist:fA14 i1="13">
<s1>CRUK Cancer Genetics Group, Paterson Institute for Cancer Research</s1>
<s2>Manchester</s2>
<s3>GBR</s3>
<sZ>19 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author>
<name sortKey="Lalloo, Fiona" sort="Lalloo, Fiona" uniqKey="Lalloo F" first="Fiona" last="Lalloo">Fiona Lalloo</name>
<affiliation>
<inist:fA14 i1="14">
<s1>Department of Medical Genetics, St. Mary's Hospital</s1>
<s2>Manchester</s2>
<s3>GBR</s3>
<sZ>20 aut.</sZ>
<sZ>21 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author>
<name sortKey="Evans, Gareth" sort="Evans, Gareth" uniqKey="Evans G" first="Gareth" last="Evans">Gareth Evans</name>
<affiliation>
<inist:fA14 i1="14">
<s1>Department of Medical Genetics, St. Mary's Hospital</s1>
<s2>Manchester</s2>
<s3>GBR</s3>
<sZ>20 aut.</sZ>
<sZ>21 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author>
<name sortKey="Maugard, Christine" sort="Maugard, Christine" uniqKey="Maugard C" first="Christine" last="Maugard">Christine Maugard</name>
<affiliation>
<inist:fA14 i1="15">
<s1>University Hospital</s1>
<s2>Nantes</s2>
<s3>FRA</s3>
<sZ>22 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author>
<name sortKey="Meijers Heijboer, Hanne" sort="Meijers Heijboer, Hanne" uniqKey="Meijers Heijboer H" first="Hanne" last="Meijers-Heijboer">Hanne Meijers-Heijboer</name>
<affiliation>
<inist:fA14 i1="16">
<s1>Department of Clinical Genetics and Medical Oncology, Daniel den Hoed Cancer Centre, Erasmus University Medical Centre Rotterdam</s1>
<s2>Rotterdam</s2>
<s3>NLD</s3>
<sZ>23 aut.</sZ>
<sZ>24 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author>
<name sortKey="Klijn, Jan G M" sort="Klijn, Jan G M" uniqKey="Klijn J" first="Jan G. M." last="Klijn">Jan G. M. Klijn</name>
<affiliation>
<inist:fA14 i1="16">
<s1>Department of Clinical Genetics and Medical Oncology, Daniel den Hoed Cancer Centre, Erasmus University Medical Centre Rotterdam</s1>
<s2>Rotterdam</s2>
<s3>NLD</s3>
<sZ>23 aut.</sZ>
<sZ>24 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author>
<name sortKey="Olah, Edith" sort="Olah, Edith" uniqKey="Olah E" first="Edith" last="Olah">Edith Olah</name>
<affiliation>
<inist:fA14 i1="17">
<s1>Department of Molecular Biology, National Institute of Oncology</s1>
<s2>Budapest</s2>
<s3>HUN</s3>
<sZ>25 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author>
<name sortKey="Gusterson, Barry A" sort="Gusterson, Barry A" uniqKey="Gusterson B" first="Barry A." last="Gusterson">Barry A. Gusterson</name>
<affiliation>
<inist:fA14 i1="18">
<s1>Department of Pathology, Western Infirmary, University of Glasgow</s1>
<s2>Scotland</s2>
<s3>GBR</s3>
<sZ>26 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author>
<name sortKey="Pilotti, Silvana" sort="Pilotti, Silvana" uniqKey="Pilotti S" first="Silvana" last="Pilotti">Silvana Pilotti</name>
<affiliation>
<inist:fA14 i1="19">
<s1>Department of Pathology, Istituto Nazionale Tumori</s1>
<s2>Milan</s2>
<s3>ITA</s3>
<sZ>27 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author>
<name sortKey="Radice, Paolo" sort="Radice, Paolo" uniqKey="Radice P" first="Paolo" last="Radice">Paolo Radice</name>
<affiliation>
<inist:fA14 i1="20">
<s1>Department of Experimental Oncology, Istituto Nazionale Tumori</s1>
<s2>Milan</s2>
<s3>ITA</s3>
<sZ>28 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author>
<name sortKey="Scherneck, Siegfried" sort="Scherneck, Siegfried" uniqKey="Scherneck S" first="Siegfried" last="Scherneck">Siegfried Scherneck</name>
<affiliation>
<inist:fA14 i1="21">
<s1>Max-Delbruck-Centrum fur Moleculare Medizin, Tumorgenetik</s1>
<s2>Berlin</s2>
<s3>DEU</s3>
<sZ>29 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author>
<name sortKey="Sobol, Hagay" sort="Sobol, Hagay" uniqKey="Sobol H" first="Hagay" last="Sobol">Hagay Sobol</name>
<affiliation>
<inist:fA14 i1="22">
<s1>Department of Genetic Oncology and Cancer Control, Institut National de la Sante et de la Recherche Medicale EPI 9939, Paoli Calmettes Institute</s1>
<s2>Marseille</s2>
<s3>FRA</s3>
<sZ>30 aut.</sZ>
<sZ>31 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author>
<name sortKey="Jacquemier, Jocelyne" sort="Jacquemier, Jocelyne" uniqKey="Jacquemier J" first="Jocelyne" last="Jacquemier">Jocelyne Jacquemier</name>
<affiliation>
<inist:fA14 i1="22">
<s1>Department of Genetic Oncology and Cancer Control, Institut National de la Sante et de la Recherche Medicale EPI 9939, Paoli Calmettes Institute</s1>
<s2>Marseille</s2>
<s3>FRA</s3>
<sZ>30 aut.</sZ>
<sZ>31 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author>
<name sortKey="Wagner, Teresa" sort="Wagner, Teresa" uniqKey="Wagner T" first="Teresa" last="Wagner">Teresa Wagner</name>
<affiliation>
<inist:fA14 i1="23">
<s1>Department of Obstetrics and Gynaecology, General Hospital, University of Vienna</s1>
<s3>AUT</s3>
<sZ>32 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author>
<name sortKey="Peto, Julian" sort="Peto, Julian" uniqKey="Peto J" first="Julian" last="Peto">Julian Peto</name>
<affiliation>
<inist:fA14 i1="24">
<s1>Sections of Cancer Genetics and Epidemiology, Institute of Cancer Research, Haddow Laboratories</s1>
<s3>GBR</s3>
<sZ>33 aut.</sZ>
<sZ>34 aut.</sZ>
</inist:fA14>
</affiliation>
<affiliation>
<inist:fA14 i1="25">
<s1>London School of Hygiene and Tropical Medicine</s1>
<s2>London</s2>
<s3>GBR</s3>
<sZ>33 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author>
<name sortKey="Stratton, Michael R" sort="Stratton, Michael R" uniqKey="Stratton M" first="Michael R." last="Stratton">Michael R. Stratton</name>
<affiliation>
<inist:fA14 i1="24">
<s1>Sections of Cancer Genetics and Epidemiology, Institute of Cancer Research, Haddow Laboratories</s1>
<s3>GBR</s3>
<sZ>33 aut.</sZ>
<sZ>34 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author>
<name sortKey="Mcguffog, Lesley" sort="Mcguffog, Lesley" uniqKey="Mcguffog L" first="Lesley" last="Mcguffog">Lesley Mcguffog</name>
</author>
<author>
<name sortKey="Easton, Douglas F" sort="Easton, Douglas F" uniqKey="Easton D" first="Douglas F." last="Easton">Douglas F. Easton</name>
</author>
</titleStmt>
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<idno type="wicri:source">INIST</idno>
<idno type="inist">05-0335175</idno>
<date when="2005">2005</date>
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<idno type="RBID">Pascal:05-0335175</idno>
<idno type="wicri:Area/PascalFrancis/Corpus">004848</idno>
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<title xml:lang="en" level="a">Prediction of BRCA1 status in patients with breast cancer using estroqen receptor and basal phenotype</title>
<author>
<name sortKey="Lakhani, Sunil R" sort="Lakhani, Sunil R" uniqKey="Lakhani S" first="Sunil R." last="Lakhani">Sunil R. Lakhani</name>
<affiliation>
<inist:fA14 i1="01">
<s1>The Breakthrough Toby Robins Breast Cancer Research Centre, Institute of Cancer Research</s1>
<s2>London</s2>
<s3>GBR</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>6 aut.</sZ>
</inist:fA14>
</affiliation>
<affiliation>
<inist:fA14 i1="02">
<s1>Molecular and Cellular Pathology, University of Queensland</s1>
<s2>Brisbane</s2>
<s3>AUS</s3>
<sZ>1 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author>
<name sortKey="Reis Filho, Jorge S" sort="Reis Filho, Jorge S" uniqKey="Reis Filho J" first="Jorge S." last="Reis-Filho">Jorge S. Reis-Filho</name>
<affiliation>
<inist:fA14 i1="01">
<s1>The Breakthrough Toby Robins Breast Cancer Research Centre, Institute of Cancer Research</s1>
<s2>London</s2>
<s3>GBR</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>6 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author>
<name sortKey="Fulford, Laura" sort="Fulford, Laura" uniqKey="Fulford L" first="Laura" last="Fulford">Laura Fulford</name>
<affiliation>
<inist:fA14 i1="01">
<s1>The Breakthrough Toby Robins Breast Cancer Research Centre, Institute of Cancer Research</s1>
<s2>London</s2>
<s3>GBR</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>6 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author>
<name sortKey="Penault Llorca, Frederique" sort="Penault Llorca, Frederique" uniqKey="Penault Llorca F" first="Frederique" last="Penault-Llorca">Frederique Penault-Llorca</name>
<affiliation>
<inist:fA14 i1="03">
<s1>Centre Jean Perrin</s1>
<s2>Clermont-Ferrand</s2>
<s3>FRA</s3>
<sZ>4 aut.</sZ>
<sZ>10 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author>
<name sortKey="Van Dervijver, Marc" sort="Van Dervijver, Marc" uniqKey="Van Dervijver M" first="Marc" last="Van Dervijver">Marc Van Dervijver</name>
<affiliation>
<inist:fA14 i1="04">
<s1>The Netherlands Cancer Institute</s1>
<s2>Amsterdam</s2>
<s3>NLD</s3>
<sZ>5 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author>
<name sortKey="Parry, Suzanne" sort="Parry, Suzanne" uniqKey="Parry S" first="Suzanne" last="Parry">Suzanne Parry</name>
<affiliation>
<inist:fA14 i1="01">
<s1>The Breakthrough Toby Robins Breast Cancer Research Centre, Institute of Cancer Research</s1>
<s2>London</s2>
<s3>GBR</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>6 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author>
<name sortKey="Bishop, Timothy" sort="Bishop, Timothy" uniqKey="Bishop T" first="Timothy" last="Bishop">Timothy Bishop</name>
<affiliation>
<inist:fA14 i1="05">
<s1>Imperial Cancer Research Fund Genetic Epidemiology Laboratory, St. James University Hospital</s1>
<s2>Leeds</s2>
<s3>GBR</s3>
<sZ>7 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author>
<name sortKey="Benitez, Javier" sort="Benitez, Javier" uniqKey="Benitez J" first="Javier" last="Benitez">Javier Benitez</name>
<affiliation>
<inist:fA14 i1="06">
<s1>Department of Genetics, Dpto Genetica Humana. Centro Nacional nvestigaciones Oncológicas</s1>
<s2>Madrid</s2>
<s3>ESP</s3>
<sZ>8 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author>
<name sortKey="Rivas, Carmen" sort="Rivas, Carmen" uniqKey="Rivas C" first="Carmen" last="Rivas">Carmen Rivas</name>
<affiliation>
<inist:fA14 i1="07">
<s1>Department of Pathology, Fundación Jiménez Díaz, Autonomous University of Madrid</s1>
<s2>Madrid</s2>
<s3>ESP</s3>
<sZ>9 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author>
<name sortKey="Bignon, Yves Jean" sort="Bignon, Yves Jean" uniqKey="Bignon Y" first="Yves-Jean" last="Bignon">Yves-Jean Bignon</name>
<affiliation>
<inist:fA14 i1="03">
<s1>Centre Jean Perrin</s1>
<s2>Clermont-Ferrand</s2>
<s3>FRA</s3>
<sZ>4 aut.</sZ>
<sZ>10 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author>
<name sortKey="Chang Claude, Jenny" sort="Chang Claude, Jenny" uniqKey="Chang Claude J" first="Jenny" last="Chang-Claude">Jenny Chang-Claude</name>
<affiliation>
<inist:fA14 i1="08">
<s1>Deutsches Krebsforschungszentrum, Divisions of Epidemiology and Molecular Genome Analysis</s1>
<s2>Heidelberg</s2>
<s3>DEU</s3>
<sZ>11 aut.</sZ>
<sZ>12 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author>
<name sortKey="Hamann, Ute" sort="Hamann, Ute" uniqKey="Hamann U" first="Ute" last="Hamann">Ute Hamann</name>
<affiliation>
<inist:fA14 i1="08">
<s1>Deutsches Krebsforschungszentrum, Divisions of Epidemiology and Molecular Genome Analysis</s1>
<s2>Heidelberg</s2>
<s3>DEU</s3>
<sZ>11 aut.</sZ>
<sZ>12 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author>
<name sortKey="Cornelisse, Cees J" sort="Cornelisse, Cees J" uniqKey="Cornelisse C" first="Cees J." last="Cornelisse">Cees J. Cornelisse</name>
<affiliation>
<inist:fA14 i1="09">
<s1>Department of Genetics and Pathology, Leiden University</s1>
<s2>Leiden</s2>
<s3>NLD</s3>
<sZ>13 aut.</sZ>
<sZ>14 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author>
<name sortKey="Devilee, Peter" sort="Devilee, Peter" uniqKey="Devilee P" first="Peter" last="Devilee">Peter Devilee</name>
<affiliation>
<inist:fA14 i1="09">
<s1>Department of Genetics and Pathology, Leiden University</s1>
<s2>Leiden</s2>
<s3>NLD</s3>
<sZ>13 aut.</sZ>
<sZ>14 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author>
<name sortKey="Beckmann, Matthias W" sort="Beckmann, Matthias W" uniqKey="Beckmann M" first="Matthias W." last="Beckmann">Matthias W. Beckmann</name>
<affiliation>
<inist:fA14 i1="10">
<s1>Departments of Obstetrics and Gynecology, Friedrich Alexander University</s1>
<s2>Erlangen</s2>
<s3>DEU</s3>
<sZ>15 aut.</sZ>
<sZ>16 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author>
<name sortKey="Nestle Kr Mling, Carolin" sort="Nestle Kr Mling, Carolin" uniqKey="Nestle Kr Mling C" first="Carolin" last="Nestle-Kr Mling">Carolin Nestle-Kr Mling</name>
<affiliation>
<inist:fA14 i1="10">
<s1>Departments of Obstetrics and Gynecology, Friedrich Alexander University</s1>
<s2>Erlangen</s2>
<s3>DEU</s3>
<sZ>15 aut.</sZ>
<sZ>16 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author>
<name sortKey="Daly, Peter A" sort="Daly, Peter A" uniqKey="Daly P" first="Peter A." last="Daly">Peter A. Daly</name>
<affiliation>
<inist:fA14 i1="11">
<s1>Department of Medicine, Trinity College Medical School, St James Hospital</s1>
<s2>Dublin</s2>
<s3>IRL</s3>
<sZ>17 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author>
<name sortKey="Haites, Neva" sort="Haites, Neva" uniqKey="Haites N" first="Neva" last="Haites">Neva Haites</name>
<affiliation>
<inist:fA14 i1="12">
<s1>Medical Genetics, Department of Medicine and Therapeutics, University of Aberdeen</s1>
<s2>Aberdeen</s2>
<s3>GBR</s3>
<sZ>18 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author>
<name sortKey="Varley, Jenny" sort="Varley, Jenny" uniqKey="Varley J" first="Jenny" last="Varley">Jenny Varley</name>
<affiliation>
<inist:fA14 i1="13">
<s1>CRUK Cancer Genetics Group, Paterson Institute for Cancer Research</s1>
<s2>Manchester</s2>
<s3>GBR</s3>
<sZ>19 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author>
<name sortKey="Lalloo, Fiona" sort="Lalloo, Fiona" uniqKey="Lalloo F" first="Fiona" last="Lalloo">Fiona Lalloo</name>
<affiliation>
<inist:fA14 i1="14">
<s1>Department of Medical Genetics, St. Mary's Hospital</s1>
<s2>Manchester</s2>
<s3>GBR</s3>
<sZ>20 aut.</sZ>
<sZ>21 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author>
<name sortKey="Evans, Gareth" sort="Evans, Gareth" uniqKey="Evans G" first="Gareth" last="Evans">Gareth Evans</name>
<affiliation>
<inist:fA14 i1="14">
<s1>Department of Medical Genetics, St. Mary's Hospital</s1>
<s2>Manchester</s2>
<s3>GBR</s3>
<sZ>20 aut.</sZ>
<sZ>21 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author>
<name sortKey="Maugard, Christine" sort="Maugard, Christine" uniqKey="Maugard C" first="Christine" last="Maugard">Christine Maugard</name>
<affiliation>
<inist:fA14 i1="15">
<s1>University Hospital</s1>
<s2>Nantes</s2>
<s3>FRA</s3>
<sZ>22 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author>
<name sortKey="Meijers Heijboer, Hanne" sort="Meijers Heijboer, Hanne" uniqKey="Meijers Heijboer H" first="Hanne" last="Meijers-Heijboer">Hanne Meijers-Heijboer</name>
<affiliation>
<inist:fA14 i1="16">
<s1>Department of Clinical Genetics and Medical Oncology, Daniel den Hoed Cancer Centre, Erasmus University Medical Centre Rotterdam</s1>
<s2>Rotterdam</s2>
<s3>NLD</s3>
<sZ>23 aut.</sZ>
<sZ>24 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author>
<name sortKey="Klijn, Jan G M" sort="Klijn, Jan G M" uniqKey="Klijn J" first="Jan G. M." last="Klijn">Jan G. M. Klijn</name>
<affiliation>
<inist:fA14 i1="16">
<s1>Department of Clinical Genetics and Medical Oncology, Daniel den Hoed Cancer Centre, Erasmus University Medical Centre Rotterdam</s1>
<s2>Rotterdam</s2>
<s3>NLD</s3>
<sZ>23 aut.</sZ>
<sZ>24 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author>
<name sortKey="Olah, Edith" sort="Olah, Edith" uniqKey="Olah E" first="Edith" last="Olah">Edith Olah</name>
<affiliation>
<inist:fA14 i1="17">
<s1>Department of Molecular Biology, National Institute of Oncology</s1>
<s2>Budapest</s2>
<s3>HUN</s3>
<sZ>25 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author>
<name sortKey="Gusterson, Barry A" sort="Gusterson, Barry A" uniqKey="Gusterson B" first="Barry A." last="Gusterson">Barry A. Gusterson</name>
<affiliation>
<inist:fA14 i1="18">
<s1>Department of Pathology, Western Infirmary, University of Glasgow</s1>
<s2>Scotland</s2>
<s3>GBR</s3>
<sZ>26 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author>
<name sortKey="Pilotti, Silvana" sort="Pilotti, Silvana" uniqKey="Pilotti S" first="Silvana" last="Pilotti">Silvana Pilotti</name>
<affiliation>
<inist:fA14 i1="19">
<s1>Department of Pathology, Istituto Nazionale Tumori</s1>
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<name sortKey="Sobol, Hagay" sort="Sobol, Hagay" uniqKey="Sobol H" first="Hagay" last="Sobol">Hagay Sobol</name>
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</affiliation>
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<title level="j" type="main">Clinical cancer research</title>
<title level="j" type="abbreviated">Clin. cancer res.</title>
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<title level="j" type="main">Clinical cancer research</title>
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<term>BRCA1 gene</term>
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<term>Human</term>
<term>Malignant tumor</term>
<term>Mammary gland diseases</term>
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<term>Gène BRCA1</term>
<term>Homme</term>
<term>Glande mammaire pathologie</term>
<term>Tumeur maligne</term>
<term>Récepteur biologique</term>
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<div type="abstract" xml:lang="en">Purpose:To investigate the proportion of breast cancers arising in patients with germ line BRCA1 and BRCA2 mutations expressing basal markers and developing predictive tests for identification of high-risk patients. Experimental Design: Histopathologic material from 182 tumors in BRCA1 mutation carriers, 63 BRCA2 carriers, and 109 controls, collected as part of the international Breast Cancer Linkage Consortium were immunohistochemically stained for CK14, CK5/6, CK17, epidermal growth factor receptor (EGFR), and osteonectin. Results: All five basal markers were commoner in BRCA1 tumors than in control tumors (CK14: 61% versus, 12%; CK5/6: 58% versus 7%; CK17: 53%versus10%; osteonectin: 43%versus19%; EGFR: 67% versus 21%; P < 0.0001 in each case). In a multivariate analysis, CK14, CK5/6, and estrogen receptor (ER) remained significant predictors of BRCA1 carrier status. In contrast, the frequency of basal markers in BRCA2 tumors did not differ significant from controls. Conclusion: The use of cytokeratin staining in combination with ER and morphology provides a more accurate predictor of BRCA1 mutation status than previously available, that may be useful in selecting patients for BRCA1 mutation testing. The high percentage of BRCA1 cases positive for EGFR suggests that specific anti-tyrosine kinase therapy may be of potential benefit in these patients.</div>
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<s1>Centre Jean Perrin</s1>
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<s1>Department of Genetics, Dpto Genetica Humana. Centro Nacional nvestigaciones Oncológicas</s1>
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<s1>Department of Pathology, Fundación Jiménez Díaz, Autonomous University of Madrid</s1>
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<s1>Deutsches Krebsforschungszentrum, Divisions of Epidemiology and Molecular Genome Analysis</s1>
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<fA14 i1="09">
<s1>Department of Genetics and Pathology, Leiden University</s1>
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<s1>Department of Medicine, Trinity College Medical School, St James Hospital</s1>
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<s1>Medical Genetics, Department of Medicine and Therapeutics, University of Aberdeen</s1>
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<s1>CRUK Cancer Genetics Group, Paterson Institute for Cancer Research</s1>
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<fA14 i1="14">
<s1>Department of Medical Genetics, St. Mary's Hospital</s1>
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<sZ>23 aut.</sZ>
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<s1>Department of Molecular Biology, National Institute of Oncology</s1>
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<sZ>25 aut.</sZ>
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<fA14 i1="18">
<s1>Department of Pathology, Western Infirmary, University of Glasgow</s1>
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<s3>GBR</s3>
<sZ>26 aut.</sZ>
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<fA14 i1="19">
<s1>Department of Pathology, Istituto Nazionale Tumori</s1>
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<sZ>27 aut.</sZ>
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<fA14 i1="20">
<s1>Department of Experimental Oncology, Istituto Nazionale Tumori</s1>
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<sZ>28 aut.</sZ>
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<fA14 i1="21">
<s1>Max-Delbruck-Centrum fur Moleculare Medizin, Tumorgenetik</s1>
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<s1>Department of Genetic Oncology and Cancer Control, Institut National de la Sante et de la Recherche Medicale EPI 9939, Paoli Calmettes Institute</s1>
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<s0>Purpose:To investigate the proportion of breast cancers arising in patients with germ line BRCA1 and BRCA2 mutations expressing basal markers and developing predictive tests for identification of high-risk patients. Experimental Design: Histopathologic material from 182 tumors in BRCA1 mutation carriers, 63 BRCA2 carriers, and 109 controls, collected as part of the international Breast Cancer Linkage Consortium were immunohistochemically stained for CK14, CK5/6, CK17, epidermal growth factor receptor (EGFR), and osteonectin. Results: All five basal markers were commoner in BRCA1 tumors than in control tumors (CK14: 61% versus, 12%; CK5/6: 58% versus 7%; CK17: 53%versus10%; osteonectin: 43%versus19%; EGFR: 67% versus 21%; P < 0.0001 in each case). In a multivariate analysis, CK14, CK5/6, and estrogen receptor (ER) remained significant predictors of BRCA1 carrier status. In contrast, the frequency of basal markers in BRCA2 tumors did not differ significant from controls. Conclusion: The use of cytokeratin staining in combination with ER and morphology provides a more accurate predictor of BRCA1 mutation status than previously available, that may be useful in selecting patients for BRCA1 mutation testing. The high percentage of BRCA1 cases positive for EGFR suggests that specific anti-tyrosine kinase therapy may be of potential benefit in these patients.</s0>
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<s0>Phenotype</s0>
<s5>09</s5>
</fC03>
<fC03 i1="09" i2="X" l="SPA">
<s0>Fenotipo</s0>
<s5>09</s5>
</fC03>
<fC03 i1="10" i2="X" l="FRE">
<s0>Cancer sein</s0>
<s4>CD</s4>
<s5>96</s5>
</fC03>
<fC03 i1="10" i2="X" l="ENG">
<s0>Breast cancer</s0>
<s4>CD</s4>
<s5>96</s5>
</fC03>
<fC03 i1="10" i2="X" l="SPA">
<s0>Cáncer del pecho</s0>
<s4>CD</s4>
<s5>96</s5>
</fC03>
<fN21>
<s1>234</s1>
</fN21>
<fN44 i1="01">
<s1>OTO</s1>
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<s1>OTO</s1>
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<NO>PASCAL 05-0335175 INIST</NO>
<ET>Prediction of BRCA1 status in patients with breast cancer using estroqen receptor and basal phenotype</ET>
<AU>LAKHANI (Sunil R.); REIS-FILHO (Jorge S.); FULFORD (Laura); PENAULT-LLORCA (Frederique); VAN DERVIJVER (Marc); PARRY (Suzanne); BISHOP (Timothy); BENITEZ (Javier); RIVAS (Carmen); BIGNON (Yves-Jean); CHANG-CLAUDE (Jenny); HAMANN (Ute); CORNELISSE (Cees J.); DEVILEE (Peter); BECKMANN (Matthias W.); NESTLE-KRÄMLING (Carolin); DALY (Peter A.); HAITES (Neva); VARLEY (Jenny); LALLOO (Fiona); EVANS (Gareth); MAUGARD (Christine); MEIJERS-HEIJBOER (Hanne); KLIJN (Jan G. M.); OLAH (Edith); GUSTERSON (Barry A.); PILOTTI (Silvana); RADICE (Paolo); SCHERNECK (Siegfried); SOBOL (Hagay); JACQUEMIER (Jocelyne); WAGNER (Teresa); PETO (Julian); STRATTON (Michael R.); MCGUFFOG (Lesley); EASTON (Douglas F.)</AU>
<AF>The Breakthrough Toby Robins Breast Cancer Research Centre, Institute of Cancer Research/London/Royaume-Uni (1 aut., 2 aut., 3 aut., 6 aut.); Molecular and Cellular Pathology, University of Queensland/Brisbane/Australie (1 aut.); Centre Jean Perrin/Clermont-Ferrand/France (4 aut., 10 aut.); The Netherlands Cancer Institute/Amsterdam/Pays-Bas (5 aut.); Imperial Cancer Research Fund Genetic Epidemiology Laboratory, St. James University Hospital/Leeds/Royaume-Uni (7 aut.); Department of Genetics, Dpto Genetica Humana. Centro Nacional nvestigaciones Oncológicas/Madrid/Espagne (8 aut.); Department of Pathology, Fundación Jiménez Díaz, Autonomous University of Madrid/Madrid/Espagne (9 aut.); Deutsches Krebsforschungszentrum, Divisions of Epidemiology and Molecular Genome Analysis/Heidelberg/Allemagne (11 aut., 12 aut.); Department of Genetics and Pathology, Leiden University/Leiden/Pays-Bas (13 aut., 14 aut.); Departments of Obstetrics and Gynecology, Friedrich Alexander University/Erlangen/Allemagne (15 aut., 16 aut.); Department of Medicine, Trinity College Medical School, St James Hospital/Dublin/Irlande (17 aut.); Medical Genetics, Department of Medicine and Therapeutics, University of Aberdeen/Aberdeen/Royaume-Uni (18 aut.); CRUK Cancer Genetics Group, Paterson Institute for Cancer Research/Manchester/Royaume-Uni (19 aut.); Department of Medical Genetics, St. Mary's Hospital/Manchester/Royaume-Uni (20 aut., 21 aut.); University Hospital/Nantes/France (22 aut.); Department of Clinical Genetics and Medical Oncology, Daniel den Hoed Cancer Centre, Erasmus University Medical Centre Rotterdam/Rotterdam/Pays-Bas (23 aut., 24 aut.); Department of Molecular Biology, National Institute of Oncology/Budapest/Hongrie (25 aut.); Department of Pathology, Western Infirmary, University of Glasgow/Scotland/Royaume-Uni (26 aut.); Department of Pathology, Istituto Nazionale Tumori/Milan/Italie (27 aut.); Department of Experimental Oncology, Istituto Nazionale Tumori/Milan/Italie (28 aut.); Max-Delbruck-Centrum fur Moleculare Medizin, Tumorgenetik/Berlin/Allemagne (29 aut.); Department of Genetic Oncology and Cancer Control, Institut National de la Sante et de la Recherche Medicale EPI 9939, Paoli Calmettes Institute/Marseille/France (30 aut., 31 aut.); Department of Obstetrics and Gynaecology, General Hospital, University of Vienna/Autriche (32 aut.); Sections of Cancer Genetics and Epidemiology, Institute of Cancer Research, Haddow Laboratories/Royaume-Uni (33 aut., 34 aut.); London School of Hygiene and Tropical Medicine/London/Royaume-Uni (33 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Clinical cancer research; ISSN 1078-0432; Etats-Unis; Da. 2005; Vol. 11; No. 14; Pp. 5175-5180; Bibl. 28 ref.</SO>
<LA>Anglais</LA>
<EA>Purpose:To investigate the proportion of breast cancers arising in patients with germ line BRCA1 and BRCA2 mutations expressing basal markers and developing predictive tests for identification of high-risk patients. Experimental Design: Histopathologic material from 182 tumors in BRCA1 mutation carriers, 63 BRCA2 carriers, and 109 controls, collected as part of the international Breast Cancer Linkage Consortium were immunohistochemically stained for CK14, CK5/6, CK17, epidermal growth factor receptor (EGFR), and osteonectin. Results: All five basal markers were commoner in BRCA1 tumors than in control tumors (CK14: 61% versus, 12%; CK5/6: 58% versus 7%; CK17: 53%versus10%; osteonectin: 43%versus19%; EGFR: 67% versus 21%; P < 0.0001 in each case). In a multivariate analysis, CK14, CK5/6, and estrogen receptor (ER) remained significant predictors of BRCA1 carrier status. In contrast, the frequency of basal markers in BRCA2 tumors did not differ significant from controls. Conclusion: The use of cytokeratin staining in combination with ER and morphology provides a more accurate predictor of BRCA1 mutation status than previously available, that may be useful in selecting patients for BRCA1 mutation testing. The high percentage of BRCA1 cases positive for EGFR suggests that specific anti-tyrosine kinase therapy may be of potential benefit in these patients.</EA>
<CC>002B02R</CC>
<FD>Prédiction; Facteur prédictif; Gène suppresseur tumeur; Gène BRCA1; Homme; Glande mammaire pathologie; Tumeur maligne; Récepteur biologique; Phénotype; Cancer sein</FD>
<ED>Prediction; Predictive factor; Tumor suppressor gene; BRCA1 gene; Human; Mammary gland diseases; Malignant tumor; Biological receptor; Phenotype; Breast cancer</ED>
<SD>Predicción; Factor predictivo; Gen supresor tumor; Gen BRCA1; Hombre; Glándula mamaria patología; Tumor maligno; Receptor biológico; Fenotipo; Cáncer del pecho</SD>
<LO>INIST-26073.354000137962310150</LO>
<ID>05-0335175</ID>
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