Pulmonary atypical carcinoid : Predictors of survival in 106 cases
Identifieur interne : 000424 ( PascalFrancis/Curation ); précédent : 000423; suivant : 000425Pulmonary atypical carcinoid : Predictors of survival in 106 cases
Auteurs : Mary Beth Beasley [États-Unis, Pays-Bas, France, Royaume-Uni, Australie, Japon] ; Frederik B. J. M. Thunnissen ; Elisabeth Brambilla ; Philip Hasleton ; Richard Steele ; Samuel P. Hammar ; Thomas V. Colby ; Mary Sheppard ; Yukio Shimosato ; Michael N. Koss ; Roni Falk ; Willam D. TravisSource :
- Human pathology [ 0046-8177 ] ; 2000.
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- Pascal (Inist)
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- topic : Homme.
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Abstract
Pulmonary neuroendocrine tumors (NE) include a spectrum of tumors from typical carcinoid (TC) to atypical carcinoid (AC), large cell neuroendocrine carcinoma (LCNEC), and small cell carcinoma (SCLC). Little is known about prognostic predictors for AC because of its rarity. Survival analysis was performed on 106 ACs with clinical follow-up from the AFIP and the Pathology Panel of the International Association for the Study of Lung Cancer (IASLC). The tumors fulfilled the 1999 WHO/IASLC criteria for AC of a NE tumor with a mitotic rate of 2 to 10 per 2 mm2 of viable tumor or coagulative necrosis. Multiple clinical and histologic features were analyzed by Kaplan-Meier and Cox regression analysis. Of the clinical features, higher stage (P = .003) and a tumor size of 3.5 cm or greater (P = .003) were associated with a worse prognosis. Features that were histologically unfavorable by univariate analysis were mitotic rate (P = .002), pleomorphism (P = .018), and aerogenous spread (P = .007). Histologically favorable features by univariate analysis were the presence of palisading (P = .008), papillary (P = .039), pseudoglandular (P = .026), and rosette (P = .022) patterns. Female gender showed a trend toward a poorer prognosis (P = .085) and was included in the multivariate model. Multivariate analysis stratified for stage showed mitoses (P <.001), a tumor size of 3.5 cm or greater (P =.017), and female gender (P =.012) to be the only negative independent predictors of prognosis and the presence of rosettes (P =.016) to be the only independent positive predictor. We further divided the AC into subgroups of low (2 to 5 mitoses/2 mm2) and high (6 to 10 mitoses/2 mm2) mitotic rate and compared the survival with TC and with LCNEC. Within the category of AC, the patients with a higher mitotic rate had a significantly worse survival than those with a lower mitotic rate (P <.001) stratified for stage. Five- and 10-year survival rates for AC (61% and 35%, respectively) stratified for stage were significantly worse than for TC and better than that for LCNEC and SCLC. Chemotherapy or radiation therapy was given in 12 of 52 and 14 of 52 cases, respectively, but the data were insufficient to evaluate tumor response. We conclude that AC is an aggressive neuroendocrine neoplasm with survival intermediate between TC and LCNEC and SCLC. Higher mitotic rate, tumor size of 3.5 cm or greater, female gender, and presence of rosettes are the only independent predictors of survival. Surgical resection remains the treatment of choice, and the role of chemotherapy and radiation therapy remains to be proven.
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en" level="a">Pulmonary atypical carcinoid : Predictors of survival in 106 cases</title><author><name sortKey="Beasley, Mary Beth" sort="Beasley, Mary Beth" uniqKey="Beasley M" first="Mary Beth" last="Beasley">Mary Beth Beasley</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Department of Pulmonary and Mediastinal Pathology, Armed Forces Institute of Pathology</s1><s2>Washington, DC</s2><s3>USA</s3></inist:fA14><country>États-Unis</country></affiliation><affiliation wicri:level="1"><inist:fA14 i1="02"><s1>Canisius Wilhemina Hospital</s1><s2>Nymegen</s2><s3>NLD</s3></inist:fA14><country>Pays-Bas</country></affiliation><affiliation wicri:level="1"><inist:fA14 i1="03"><s1>Centre Hospitalier Universitaire de Grenoble</s1><s3>FRA</s3></inist:fA14><country>France</country></affiliation><affiliation wicri:level="1"><inist:fA14 i1="04"><s1>University of Manchester School of Medicine</s1><s2>Manchester</s2><s3>GBR</s3></inist:fA14><country>Royaume-Uni</country></affiliation><affiliation wicri:level="1"><inist:fA14 i1="05"><s1>Princess Alexandra Hospital</s1><s2>Woolloongabba</s2><s3>AUS</s3></inist:fA14><country>Australie</country></affiliation><affiliation wicri:level="1"><inist:fA14 i1="06"><s1>Diagnostic Specialties Laboratory</s1><s2>Bremerton, WA</s2><s3>USA</s3></inist:fA14><country>États-Unis</country></affiliation><affiliation wicri:level="1"><inist:fA14 i1="07"><s1>Mayo Clinic</s1><s2>Scottsdale, AZ</s2><s3>USA</s3></inist:fA14><country>États-Unis</country></affiliation><affiliation wicri:level="1"><inist:fA14 i1="08"><s1>Royal Brompton Hospital</s1><s2>London</s2><s3>GBR</s3></inist:fA14><country>Royaume-Uni</country></affiliation><affiliation wicri:level="1"><inist:fA14 i1="09"><s1>Keio University School of Medicine</s1><s2>Tokyo</s2><s3>JPN</s3></inist:fA14><country>Japon</country></affiliation><affiliation wicri:level="1"><inist:fA14 i1="10"><s1>Environmental Epidemiology Branch, National Cancer Institute, National Institutes of Health</s1><s2>Rockville, MD</s2><s3>USA</s3></inist:fA14><country>États-Unis</country></affiliation></author><author><name sortKey="Thunnissen, Frederik B J M" sort="Thunnissen, Frederik B J M" uniqKey="Thunnissen F" first="Frederik B. 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Travis</name></author></titleStmt><publicationStmt><idno type="wicri:source">INIST</idno><idno type="inist">01-0050117</idno><date when="2000">2000</date><idno type="stanalyst">PASCAL 01-0050117 INIST</idno><idno type="RBID">Pascal:01-0050117</idno><idno type="wicri:Area/PascalFrancis/Corpus">005D33</idno><idno type="wicri:Area/PascalFrancis/Curation">000424</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">Pulmonary atypical carcinoid : Predictors of survival in 106 cases</title><author><name sortKey="Beasley, Mary Beth" sort="Beasley, Mary Beth" uniqKey="Beasley M" first="Mary Beth" last="Beasley">Mary Beth Beasley</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Department of Pulmonary and Mediastinal Pathology, Armed Forces Institute of Pathology</s1><s2>Washington, DC</s2><s3>USA</s3></inist:fA14><country>États-Unis</country></affiliation><affiliation wicri:level="1"><inist:fA14 i1="02"><s1>Canisius Wilhemina Hospital</s1><s2>Nymegen</s2><s3>NLD</s3></inist:fA14><country>Pays-Bas</country></affiliation><affiliation wicri:level="1"><inist:fA14 i1="03"><s1>Centre Hospitalier Universitaire de Grenoble</s1><s3>FRA</s3></inist:fA14><country>France</country></affiliation><affiliation wicri:level="1"><inist:fA14 i1="04"><s1>University of Manchester School of Medicine</s1><s2>Manchester</s2><s3>GBR</s3></inist:fA14><country>Royaume-Uni</country></affiliation><affiliation wicri:level="1"><inist:fA14 i1="05"><s1>Princess Alexandra Hospital</s1><s2>Woolloongabba</s2><s3>AUS</s3></inist:fA14><country>Australie</country></affiliation><affiliation wicri:level="1"><inist:fA14 i1="06"><s1>Diagnostic Specialties Laboratory</s1><s2>Bremerton, WA</s2><s3>USA</s3></inist:fA14><country>États-Unis</country></affiliation><affiliation wicri:level="1"><inist:fA14 i1="07"><s1>Mayo Clinic</s1><s2>Scottsdale, AZ</s2><s3>USA</s3></inist:fA14><country>États-Unis</country></affiliation><affiliation wicri:level="1"><inist:fA14 i1="08"><s1>Royal Brompton Hospital</s1><s2>London</s2><s3>GBR</s3></inist:fA14><country>Royaume-Uni</country></affiliation><affiliation wicri:level="1"><inist:fA14 i1="09"><s1>Keio University School of Medicine</s1><s2>Tokyo</s2><s3>JPN</s3></inist:fA14><country>Japon</country></affiliation><affiliation wicri:level="1"><inist:fA14 i1="10"><s1>Environmental Epidemiology Branch, National Cancer Institute, National Institutes of Health</s1><s2>Rockville, MD</s2><s3>USA</s3></inist:fA14><country>États-Unis</country></affiliation></author><author><name sortKey="Thunnissen, Frederik B J M" sort="Thunnissen, Frederik B J M" uniqKey="Thunnissen F" first="Frederik B. J. M." last="Thunnissen">Frederik B. J. M. Thunnissen</name></author><author><name sortKey="Brambilla, Elisabeth" sort="Brambilla, Elisabeth" uniqKey="Brambilla E" first="Elisabeth" last="Brambilla">Elisabeth Brambilla</name></author><author><name sortKey="Hasleton, Philip" sort="Hasleton, Philip" uniqKey="Hasleton P" first="Philip" last="Hasleton">Philip Hasleton</name></author><author><name sortKey="Steele, Richard" sort="Steele, Richard" uniqKey="Steele R" first="Richard" last="Steele">Richard Steele</name></author><author><name sortKey="Hammar, Samuel P" sort="Hammar, Samuel P" uniqKey="Hammar S" first="Samuel P." last="Hammar">Samuel P. Hammar</name></author><author><name sortKey="Colby, Thomas V" sort="Colby, Thomas V" uniqKey="Colby T" first="Thomas V." last="Colby">Thomas V. Colby</name></author><author><name sortKey="Sheppard, Mary" sort="Sheppard, Mary" uniqKey="Sheppard M" first="Mary" last="Sheppard">Mary Sheppard</name></author><author><name sortKey="Shimosato, Yukio" sort="Shimosato, Yukio" uniqKey="Shimosato Y" first="Yukio" last="Shimosato">Yukio Shimosato</name></author><author><name sortKey="Koss, Michael N" sort="Koss, Michael N" uniqKey="Koss M" first="Michael N." last="Koss">Michael N. Koss</name></author><author><name sortKey="Falk, Roni" sort="Falk, Roni" uniqKey="Falk R" first="Roni" last="Falk">Roni Falk</name></author><author><name sortKey="Travis, Willam D" sort="Travis, Willam D" uniqKey="Travis W" first="Willam D." last="Travis">Willam D. Travis</name></author></analytic><series><title level="j" type="main">Human pathology</title><title level="j" type="abbreviated">Human pathol.</title><idno type="ISSN">0046-8177</idno><imprint><date when="2000">2000</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">Human pathology</title><title level="j" type="abbreviated">Human pathol.</title><idno type="ISSN">0046-8177</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Atypical</term><term>Bronchopulmonary</term><term>Carcinoid tumor</term><term>Dimension</term><term>Human</term><term>Immunohistochemistry</term><term>Mitotic index</term><term>Neuroendocrine tumor</term><term>Predictive factor</term><term>Prognosis</term><term>Survival</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Tumeur carcinoïde</term><term>Bronchopulmonaire</term><term>Atypique</term><term>Immunohistochimie</term><term>Facteur prédictif</term><term>Survie</term><term>Indice mitotique</term><term>Dimension</term><term>Tumeur neuroendocrinienne</term><term>Pronostic</term><term>Homme</term></keywords><keywords scheme="Wicri" type="topic" xml:lang="fr"><term>Homme</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Pulmonary neuroendocrine tumors (NE) include a spectrum of tumors from typical carcinoid (TC) to atypical carcinoid (AC), large cell neuroendocrine carcinoma (LCNEC), and small cell carcinoma (SCLC). Little is known about prognostic predictors for AC because of its rarity. Survival analysis was performed on 106 ACs with clinical follow-up from the AFIP and the Pathology Panel of the International Association for the Study of Lung Cancer (IASLC). The tumors fulfilled the 1999 WHO/IASLC criteria for AC of a NE tumor with a mitotic rate of 2 to 10 per 2 mm<sup>2</sup> of viable tumor or coagulative necrosis. Multiple clinical and histologic features were analyzed by Kaplan-Meier and Cox regression analysis. Of the clinical features, higher stage (P = .003) and a tumor size of 3.5 cm or greater (P = .003) were associated with a worse prognosis. Features that were histologically unfavorable by univariate analysis were mitotic rate (P = .002), pleomorphism (P = .018), and aerogenous spread (P = .007). Histologically favorable features by univariate analysis were the presence of palisading (P = .008), papillary (P = .039), pseudoglandular (P = .026), and rosette (P = .022) patterns. Female gender showed a trend toward a poorer prognosis (P = .085) and was included in the multivariate model. Multivariate analysis stratified for stage showed mitoses (P <.001), a tumor size of 3.5 cm or greater (P =.017), and female gender (P =.012) to be the only negative independent predictors of prognosis and the presence of rosettes (P =.016) to be the only independent positive predictor. We further divided the AC into subgroups of low (2 to 5 mitoses/2 mm<sup>2</sup>) and high (6 to 10 mitoses/2 mm<sup>2</sup>) mitotic rate and compared the survival with TC and with LCNEC. Within the category of AC, the patients with a higher mitotic rate had a significantly worse survival than those with a lower mitotic rate (P <.001) stratified for stage. Five- and 10-year survival rates for AC (61% and 35%, respectively) stratified for stage were significantly worse than for TC and better than that for LCNEC and SCLC. Chemotherapy or radiation therapy was given in 12 of 52 and 14 of 52 cases, respectively, but the data were insufficient to evaluate tumor response. We conclude that AC is an aggressive neuroendocrine neoplasm with survival intermediate between TC and LCNEC and SCLC. Higher mitotic rate, tumor size of 3.5 cm or greater, female gender, and presence of rosettes are the only independent predictors of survival. Surgical resection remains the treatment of choice, and the role of chemotherapy and radiation therapy remains to be proven.</div></front></TEI><inist><standard h6="B"><pA><fA01 i1="01" i2="1"><s0>0046-8177</s0></fA01><fA02 i1="01"><s0>HPCQA4</s0></fA02><fA03 i2="1"><s0>Human pathol.</s0></fA03><fA05><s2>31</s2></fA05><fA06><s2>10</s2></fA06><fA08 i1="01" i2="1" l="ENG"><s1>Pulmonary atypical carcinoid : Predictors of survival in 106 cases</s1></fA08><fA11 i1="01" i2="1"><s1>BEASLEY (Mary Beth)</s1></fA11><fA11 i1="02" i2="1"><s1>THUNNISSEN (Frederik B. J. M.)</s1></fA11><fA11 i1="03" i2="1"><s1>BRAMBILLA (Elisabeth)</s1></fA11><fA11 i1="04" i2="1"><s1>HASLETON (Philip)</s1></fA11><fA11 i1="05" i2="1"><s1>STEELE (Richard)</s1></fA11><fA11 i1="06" i2="1"><s1>HAMMAR (Samuel P.)</s1></fA11><fA11 i1="07" i2="1"><s1>COLBY (Thomas V.)</s1></fA11><fA11 i1="08" i2="1"><s1>SHEPPARD (Mary)</s1></fA11><fA11 i1="09" i2="1"><s1>SHIMOSATO (Yukio)</s1></fA11><fA11 i1="10" i2="1"><s1>KOSS (Michael N.)</s1></fA11><fA11 i1="11" i2="1"><s1>FALK (Roni)</s1></fA11><fA11 i1="12" i2="1"><s1>TRAVIS (Willam D.)</s1></fA11><fA14 i1="01"><s1>Department of Pulmonary and Mediastinal Pathology, Armed Forces Institute of Pathology</s1><s2>Washington, DC</s2><s3>USA</s3></fA14><fA14 i1="02"><s1>Canisius Wilhemina Hospital</s1><s2>Nymegen</s2><s3>NLD</s3></fA14><fA14 i1="03"><s1>Centre Hospitalier Universitaire de Grenoble</s1><s3>FRA</s3></fA14><fA14 i1="04"><s1>University of Manchester School of Medicine</s1><s2>Manchester</s2><s3>GBR</s3></fA14><fA14 i1="05"><s1>Princess Alexandra Hospital</s1><s2>Woolloongabba</s2><s3>AUS</s3></fA14><fA14 i1="06"><s1>Diagnostic Specialties Laboratory</s1><s2>Bremerton, WA</s2><s3>USA</s3></fA14><fA14 i1="07"><s1>Mayo Clinic</s1><s2>Scottsdale, AZ</s2><s3>USA</s3></fA14><fA14 i1="08"><s1>Royal Brompton Hospital</s1><s2>London</s2><s3>GBR</s3></fA14><fA14 i1="09"><s1>Keio University School of Medicine</s1><s2>Tokyo</s2><s3>JPN</s3></fA14><fA14 i1="10"><s1>Environmental Epidemiology Branch, National Cancer Institute, National Institutes of Health</s1><s2>Rockville, MD</s2><s3>USA</s3></fA14><fA20><s1>1255-1265</s1></fA20><fA21><s1>2000</s1></fA21><fA23 i1="01"><s0>ENG</s0></fA23><fA43 i1="01"><s1>INIST</s1><s2>16045</s2><s5>354000093370990120</s5></fA43><fA44><s0>0000</s0><s1>© 2001 INIST-CNRS. All rights reserved.</s1></fA44><fA45><s0>41 ref.</s0></fA45><fA47 i1="01" i2="1"><s0>01-0050117</s0></fA47><fA60><s1>P</s1></fA60><fA61><s0>A</s0></fA61><fA64 i1="01" i2="1"><s0>Human pathology</s0></fA64><fA66 i1="01"><s0>USA</s0></fA66><fC01 i1="01" l="ENG"><s0>Pulmonary neuroendocrine tumors (NE) include a spectrum of tumors from typical carcinoid (TC) to atypical carcinoid (AC), large cell neuroendocrine carcinoma (LCNEC), and small cell carcinoma (SCLC). Little is known about prognostic predictors for AC because of its rarity. Survival analysis was performed on 106 ACs with clinical follow-up from the AFIP and the Pathology Panel of the International Association for the Study of Lung Cancer (IASLC). The tumors fulfilled the 1999 WHO/IASLC criteria for AC of a NE tumor with a mitotic rate of 2 to 10 per 2 mm<sup>2</sup> of viable tumor or coagulative necrosis. Multiple clinical and histologic features were analyzed by Kaplan-Meier and Cox regression analysis. Of the clinical features, higher stage (P = .003) and a tumor size of 3.5 cm or greater (P = .003) were associated with a worse prognosis. Features that were histologically unfavorable by univariate analysis were mitotic rate (P = .002), pleomorphism (P = .018), and aerogenous spread (P = .007). Histologically favorable features by univariate analysis were the presence of palisading (P = .008), papillary (P = .039), pseudoglandular (P = .026), and rosette (P = .022) patterns. Female gender showed a trend toward a poorer prognosis (P = .085) and was included in the multivariate model. Multivariate analysis stratified for stage showed mitoses (P <.001), a tumor size of 3.5 cm or greater (P =.017), and female gender (P =.012) to be the only negative independent predictors of prognosis and the presence of rosettes (P =.016) to be the only independent positive predictor. We further divided the AC into subgroups of low (2 to 5 mitoses/2 mm<sup>2</sup>) and high (6 to 10 mitoses/2 mm<sup>2</sup>) mitotic rate and compared the survival with TC and with LCNEC. Within the category of AC, the patients with a higher mitotic rate had a significantly worse survival than those with a lower mitotic rate (P <.001) stratified for stage. Five- and 10-year survival rates for AC (61% and 35%, respectively) stratified for stage were significantly worse than for TC and better than that for LCNEC and SCLC. Chemotherapy or radiation therapy was given in 12 of 52 and 14 of 52 cases, respectively, but the data were insufficient to evaluate tumor response. We conclude that AC is an aggressive neuroendocrine neoplasm with survival intermediate between TC and LCNEC and SCLC. Higher mitotic rate, tumor size of 3.5 cm or greater, female gender, and presence of rosettes are the only independent predictors of survival. Surgical resection remains the treatment of choice, and the role of chemotherapy and radiation therapy remains to be proven.</s0></fC01><fC02 i1="01" i2="X"><s0>002B11A</s0></fC02><fC03 i1="01" i2="X" l="FRE"><s0>Tumeur carcinoïde</s0><s5>01</s5></fC03><fC03 i1="01" i2="X" l="ENG"><s0>Carcinoid tumor</s0><s5>01</s5></fC03><fC03 i1="01" i2="X" l="SPA"><s0>Tumor carcinoide</s0><s5>01</s5></fC03><fC03 i1="02" i2="X" l="FRE"><s0>Bronchopulmonaire</s0><s5>02</s5></fC03><fC03 i1="02" i2="X" l="ENG"><s0>Bronchopulmonary</s0><s5>02</s5></fC03><fC03 i1="02" i2="X" l="SPA"><s0>Broncopulmonar</s0><s5>02</s5></fC03><fC03 i1="03" i2="X" l="FRE"><s0>Atypique</s0><s5>03</s5></fC03><fC03 i1="03" i2="X" l="ENG"><s0>Atypical</s0><s5>03</s5></fC03><fC03 i1="03" i2="X" l="SPA"><s0>Atípico</s0><s5>03</s5></fC03><fC03 i1="04" i2="X" l="FRE"><s0>Immunohistochimie</s0><s5>04</s5></fC03><fC03 i1="04" i2="X" l="ENG"><s0>Immunohistochemistry</s0><s5>04</s5></fC03><fC03 i1="04" i2="X" l="SPA"><s0>Inmunohistoquímica</s0><s5>04</s5></fC03><fC03 i1="05" i2="X" l="FRE"><s0>Facteur prédictif</s0><s5>05</s5></fC03><fC03 i1="05" i2="X" l="ENG"><s0>Predictive factor</s0><s5>05</s5></fC03><fC03 i1="05" i2="X" l="SPA"><s0>Factor predictivo</s0><s5>05</s5></fC03><fC03 i1="06" i2="X" l="FRE"><s0>Survie</s0><s5>06</s5></fC03><fC03 i1="06" i2="X" l="ENG"><s0>Survival</s0><s5>06</s5></fC03><fC03 i1="06" i2="X" l="SPA"><s0>Sobrevivencia</s0><s5>06</s5></fC03><fC03 i1="07" i2="X" l="FRE"><s0>Indice mitotique</s0><s5>07</s5></fC03><fC03 i1="07" i2="X" l="ENG"><s0>Mitotic index</s0><s5>07</s5></fC03><fC03 i1="07" i2="X" l="SPA"><s0>Indice mitótico</s0><s5>07</s5></fC03><fC03 i1="08" i2="X" l="FRE"><s0>Dimension</s0><s5>08</s5></fC03><fC03 i1="08" i2="X" l="ENG"><s0>Dimension</s0><s5>08</s5></fC03><fC03 i1="08" i2="X" l="SPA"><s0>Dimensión</s0><s5>08</s5></fC03><fC03 i1="09" i2="X" l="FRE"><s0>Tumeur neuroendocrinienne</s0><s5>10</s5></fC03><fC03 i1="09" i2="X" l="ENG"><s0>Neuroendocrine tumor</s0><s5>10</s5></fC03><fC03 i1="09" i2="X" l="SPA"><s0>Tumor neuroendocrino</s0><s5>10</s5></fC03><fC03 i1="10" i2="X" l="FRE"><s0>Pronostic</s0><s5>17</s5></fC03><fC03 i1="10" i2="X" l="ENG"><s0>Prognosis</s0><s5>17</s5></fC03><fC03 i1="10" i2="X" l="SPA"><s0>Pronóstico</s0><s5>17</s5></fC03><fC03 i1="11" i2="X" l="FRE"><s0>Homme</s0><s5>20</s5></fC03><fC03 i1="11" i2="X" l="ENG"><s0>Human</s0><s5>20</s5></fC03><fC03 i1="11" i2="X" l="SPA"><s0>Hombre</s0><s5>20</s5></fC03><fC07 i1="01" i2="X" l="FRE"><s0>Appareil respiratoire pathologie</s0><s5>37</s5></fC07><fC07 i1="01" i2="X" l="ENG"><s0>Respiratory disease</s0><s5>37</s5></fC07><fC07 i1="01" i2="X" l="SPA"><s0>Aparato respiratorio patología</s0><s5>37</s5></fC07><fC07 i1="02" i2="X" l="FRE"><s0>Poumon pathologie</s0><s5>38</s5></fC07><fC07 i1="02" i2="X" l="ENG"><s0>Lung disease</s0><s5>38</s5></fC07><fC07 i1="02" i2="X" l="SPA"><s0>Pulmón patología</s0><s5>38</s5></fC07><fC07 i1="03" i2="X" l="FRE"><s0>Bronche pathologie</s0><s5>39</s5></fC07><fC07 i1="03" i2="X" l="ENG"><s0>Bronchus disease</s0><s5>39</s5></fC07><fC07 i1="03" i2="X" l="SPA"><s0>Bronquio patología</s0><s5>39</s5></fC07><fC07 i1="04" i2="X" l="FRE"><s0>Tumeur</s0><s5>40</s5></fC07><fC07 i1="04" i2="X" l="ENG"><s0>Tumor</s0><s5>40</s5></fC07><fC07 i1="04" i2="X" l="SPA"><s0>Tumor</s0><s5>40</s5></fC07><fC07 i1="05" i2="X" l="FRE"><s0>Anatomopathologie</s0><s5>45</s5></fC07><fC07 i1="05" i2="X" l="ENG"><s0>Pathology</s0><s5>45</s5></fC07><fC07 i1="05" i2="X" l="SPA"><s0>Anatomía patológica</s0><s5>45</s5></fC07><fN21><s1>029</s1></fN21></pA></standard></inist></record>Pour manipuler ce document sous Unix (Dilib)
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