Adequacy of endosonography‐derived samples from peribronchial or periesophageal intrapulmonary lesions for the molecular profiling of lung cancer
Introduction and Objectives Endosonography is increasingly used for the diagnosis of centrally located, bronchoscopically invisible intrapulmonary lesions, but data regarding its utility for molecular profiling are lacking. We aimed to assess the suitability of endosonography samples obtained from i...
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Veröffentlicht in: | The clinical respiratory journal 2019-09, Vol.13 (9), p.590-597 |
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creator | Livi, Vanina Ardizzoni, Andrea Cancellieri, Alessandra Natali, Filippo Ferrari, Marco Paioli, Daniela Biase, Dario Capizzi, Elisa Tallini, Giovanni Fiorentino, Michelangelo Trisolini, Rocco |
description | Introduction and Objectives
Endosonography is increasingly used for the diagnosis of centrally located, bronchoscopically invisible intrapulmonary lesions, but data regarding its utility for molecular profiling are lacking. We aimed to assess the suitability of endosonography samples obtained from intrapulmonary lesions for cancer genotyping and programmed‐death ligand 1 (PD‐L1) testing.
Methods
A prospectively collected database regarding 99 consecutive patients undergoing endosonography for the diagnosis of an intrapulmonary lesion was retrospectively reviewed. Genotyping ± PD‐L1 testing was carried out in the 53 patients with advanced lung cancer and was classified as complete if all clinically indicated tests could be performed, incomplete if at least one test could not be carried out, and unsuccessful if the sample was unsuitable for molecular analysis.
Results
All clinically indicated biomarkers could be tested in 44 (83%) patients, whereas the molecular profiling was classified as incomplete in 6 (11.3%), and unsuccessful in 3 (5.7%). Thirty‐seven genetic alterations (KRAS mutation, 17; EGFR mutation, 17; ALK rearrangement, 3) and 2 cases of PD‐L1 expression >50% were found in 31 (58%) patients. EGFR was successfully analysed in 94.1% of cases, KRAS in 93.9%, ALK in 89%, ROS1 in 90% and PD‐L1 in 63.1%.
Conclusion
Endosonography‐derived samples from intrapulmonary lesions were suitable for a thorough molecular profiling in most patients. The few cases of incomplete accomplishment of the testing algorithm were related to the failure of PD‐L1 analysis due to the exhaustion of the sample or the lack of sufficient tumour cells in the paraffin‐embedded material. |
doi_str_mv | 10.1111/crj.13063 |
format | Article |
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Endosonography is increasingly used for the diagnosis of centrally located, bronchoscopically invisible intrapulmonary lesions, but data regarding its utility for molecular profiling are lacking. We aimed to assess the suitability of endosonography samples obtained from intrapulmonary lesions for cancer genotyping and programmed‐death ligand 1 (PD‐L1) testing.
Methods
A prospectively collected database regarding 99 consecutive patients undergoing endosonography for the diagnosis of an intrapulmonary lesion was retrospectively reviewed. Genotyping ± PD‐L1 testing was carried out in the 53 patients with advanced lung cancer and was classified as complete if all clinically indicated tests could be performed, incomplete if at least one test could not be carried out, and unsuccessful if the sample was unsuitable for molecular analysis.
Results
All clinically indicated biomarkers could be tested in 44 (83%) patients, whereas the molecular profiling was classified as incomplete in 6 (11.3%), and unsuccessful in 3 (5.7%). Thirty‐seven genetic alterations (KRAS mutation, 17; EGFR mutation, 17; ALK rearrangement, 3) and 2 cases of PD‐L1 expression >50% were found in 31 (58%) patients. EGFR was successfully analysed in 94.1% of cases, KRAS in 93.9%, ALK in 89%, ROS1 in 90% and PD‐L1 in 63.1%.
Conclusion
Endosonography‐derived samples from intrapulmonary lesions were suitable for a thorough molecular profiling in most patients. The few cases of incomplete accomplishment of the testing algorithm were related to the failure of PD‐L1 analysis due to the exhaustion of the sample or the lack of sufficient tumour cells in the paraffin‐embedded material.</description><identifier>ISSN: 1752-6981</identifier><identifier>EISSN: 1752-699X</identifier><identifier>DOI: 10.1111/crj.13063</identifier><identifier>PMID: 31343834</identifier><language>eng</language><publisher>England: John Wiley & Sons, Inc</publisher><subject>Aged ; Aged, 80 and over ; anaplastic lymphoma kinase ; Anaplastic Lymphoma Kinase - genetics ; B7-H1 Antigen - genetics ; Biomarkers ; Bronchoscopy - instrumentation ; endobronchial ultrasound ; Endosonography - methods ; epidermal growth factor receptor ; ErbB Receptors - genetics ; Esophagus - diagnostic imaging ; Esophagus - pathology ; Female ; Genotype ; Humans ; Lung cancer ; Lung Neoplasms - diagnostic imaging ; Lung Neoplasms - genetics ; Lung Neoplasms - pathology ; Male ; Medical diagnosis ; Middle Aged ; Mutation ; Neoplasm Staging ; programmed‐death ligand 1 ; Protein-Tyrosine Kinases - genetics ; Proto-Oncogene Proteins - genetics ; Proto-Oncogene Proteins p21(ras) - genetics ; rapid onsite evaluation ; Retrospective Studies</subject><ispartof>The clinical respiratory journal, 2019-09, Vol.13 (9), p.590-597</ispartof><rights>2019 John Wiley & Sons Ltd</rights><rights>2019 John Wiley & Sons Ltd.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3533-e7d6a9aa40f62975deaece2e046a29a645d9d210236668a010c99f183509a3ee3</citedby><cites>FETCH-LOGICAL-c3533-e7d6a9aa40f62975deaece2e046a29a645d9d210236668a010c99f183509a3ee3</cites><orcidid>0000-0002-1067-4696</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fcrj.13063$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fcrj.13063$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,11541,27901,27902,45550,45551,46027,46451</link.rule.ids><linktorsrc>$$Uhttps://onlinelibrary.wiley.com/doi/abs/10.1111%2Fcrj.13063$$EView_record_in_Wiley-Blackwell$$FView_record_in_$$GWiley-Blackwell</linktorsrc><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31343834$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Livi, Vanina</creatorcontrib><creatorcontrib>Ardizzoni, Andrea</creatorcontrib><creatorcontrib>Cancellieri, Alessandra</creatorcontrib><creatorcontrib>Natali, Filippo</creatorcontrib><creatorcontrib>Ferrari, Marco</creatorcontrib><creatorcontrib>Paioli, Daniela</creatorcontrib><creatorcontrib>Biase, Dario</creatorcontrib><creatorcontrib>Capizzi, Elisa</creatorcontrib><creatorcontrib>Tallini, Giovanni</creatorcontrib><creatorcontrib>Fiorentino, Michelangelo</creatorcontrib><creatorcontrib>Trisolini, Rocco</creatorcontrib><title>Adequacy of endosonography‐derived samples from peribronchial or periesophageal intrapulmonary lesions for the molecular profiling of lung cancer</title><title>The clinical respiratory journal</title><addtitle>Clin Respir J</addtitle><description>Introduction and Objectives
Endosonography is increasingly used for the diagnosis of centrally located, bronchoscopically invisible intrapulmonary lesions, but data regarding its utility for molecular profiling are lacking. We aimed to assess the suitability of endosonography samples obtained from intrapulmonary lesions for cancer genotyping and programmed‐death ligand 1 (PD‐L1) testing.
Methods
A prospectively collected database regarding 99 consecutive patients undergoing endosonography for the diagnosis of an intrapulmonary lesion was retrospectively reviewed. Genotyping ± PD‐L1 testing was carried out in the 53 patients with advanced lung cancer and was classified as complete if all clinically indicated tests could be performed, incomplete if at least one test could not be carried out, and unsuccessful if the sample was unsuitable for molecular analysis.
Results
All clinically indicated biomarkers could be tested in 44 (83%) patients, whereas the molecular profiling was classified as incomplete in 6 (11.3%), and unsuccessful in 3 (5.7%). Thirty‐seven genetic alterations (KRAS mutation, 17; EGFR mutation, 17; ALK rearrangement, 3) and 2 cases of PD‐L1 expression >50% were found in 31 (58%) patients. EGFR was successfully analysed in 94.1% of cases, KRAS in 93.9%, ALK in 89%, ROS1 in 90% and PD‐L1 in 63.1%.
Conclusion
Endosonography‐derived samples from intrapulmonary lesions were suitable for a thorough molecular profiling in most patients. The few cases of incomplete accomplishment of the testing algorithm were related to the failure of PD‐L1 analysis due to the exhaustion of the sample or the lack of sufficient tumour cells in the paraffin‐embedded material.</description><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>anaplastic lymphoma kinase</subject><subject>Anaplastic Lymphoma Kinase - genetics</subject><subject>B7-H1 Antigen - genetics</subject><subject>Biomarkers</subject><subject>Bronchoscopy - instrumentation</subject><subject>endobronchial ultrasound</subject><subject>Endosonography - methods</subject><subject>epidermal growth factor receptor</subject><subject>ErbB Receptors - genetics</subject><subject>Esophagus - diagnostic imaging</subject><subject>Esophagus - pathology</subject><subject>Female</subject><subject>Genotype</subject><subject>Humans</subject><subject>Lung cancer</subject><subject>Lung Neoplasms - diagnostic imaging</subject><subject>Lung Neoplasms - genetics</subject><subject>Lung Neoplasms - pathology</subject><subject>Male</subject><subject>Medical diagnosis</subject><subject>Middle Aged</subject><subject>Mutation</subject><subject>Neoplasm Staging</subject><subject>programmed‐death ligand 1</subject><subject>Protein-Tyrosine Kinases - genetics</subject><subject>Proto-Oncogene Proteins - genetics</subject><subject>Proto-Oncogene Proteins p21(ras) - genetics</subject><subject>rapid onsite evaluation</subject><subject>Retrospective Studies</subject><issn>1752-6981</issn><issn>1752-699X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kd9qFDEUxoMotq5e-AIy4I1ebJs_M5nJZVm0KgVBFLwbTpMzu1kyyTTZqeydjyD0DX0ST7u1F4K5OeHj93055GPspeAngs6pzdsTobhWj9ixaBu51MZ8f_xw78QRe1bKlvOma1XzlB0poWrVqfqY3Zw5vJrB7qs0VBhdKimmdYZps__985fD7K_RVQXGKWCphpzGaiLxMqdoNx5ClfKdgCVNG1gjKT7uyD-HMUXI-4p8PkXyErnbYDWmgHYOQL6cBh98XN--HWaaFqLF_Jw9GSAUfHE_F-zb-3dfVx-WF5_PP67OLpZWNUotsXUaDEDNBy1N2zgEtCiR1xqkAV03zjgpuFRa6w644NaYQXSq4QYUolqwN4dcWuRqxrLrR18shgAR01x6KXUtZWfIsmCv_0G3ac6RtiOqU22rOTdEvT1QNqdSMg79lP1In9AL3t821VNT_V1TxL66T5wvR3QP5N9qCDg9AD98wP3_k_rVl0-HyD9Dc6FT</recordid><startdate>201909</startdate><enddate>201909</enddate><creator>Livi, Vanina</creator><creator>Ardizzoni, Andrea</creator><creator>Cancellieri, Alessandra</creator><creator>Natali, Filippo</creator><creator>Ferrari, Marco</creator><creator>Paioli, Daniela</creator><creator>Biase, Dario</creator><creator>Capizzi, Elisa</creator><creator>Tallini, Giovanni</creator><creator>Fiorentino, Michelangelo</creator><creator>Trisolini, Rocco</creator><general>John Wiley & Sons, Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>K9.</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-1067-4696</orcidid></search><sort><creationdate>201909</creationdate><title>Adequacy of endosonography‐derived samples from peribronchial or periesophageal intrapulmonary lesions for the molecular profiling of lung cancer</title><author>Livi, Vanina ; Ardizzoni, Andrea ; Cancellieri, Alessandra ; Natali, Filippo ; Ferrari, Marco ; Paioli, Daniela ; Biase, Dario ; Capizzi, Elisa ; Tallini, Giovanni ; Fiorentino, Michelangelo ; Trisolini, Rocco</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3533-e7d6a9aa40f62975deaece2e046a29a645d9d210236668a010c99f183509a3ee3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>anaplastic lymphoma kinase</topic><topic>Anaplastic Lymphoma Kinase - genetics</topic><topic>B7-H1 Antigen - genetics</topic><topic>Biomarkers</topic><topic>Bronchoscopy - instrumentation</topic><topic>endobronchial ultrasound</topic><topic>Endosonography - methods</topic><topic>epidermal growth factor receptor</topic><topic>ErbB Receptors - genetics</topic><topic>Esophagus - diagnostic imaging</topic><topic>Esophagus - pathology</topic><topic>Female</topic><topic>Genotype</topic><topic>Humans</topic><topic>Lung cancer</topic><topic>Lung Neoplasms - diagnostic imaging</topic><topic>Lung Neoplasms - genetics</topic><topic>Lung Neoplasms - pathology</topic><topic>Male</topic><topic>Medical diagnosis</topic><topic>Middle Aged</topic><topic>Mutation</topic><topic>Neoplasm Staging</topic><topic>programmed‐death ligand 1</topic><topic>Protein-Tyrosine Kinases - genetics</topic><topic>Proto-Oncogene Proteins - genetics</topic><topic>Proto-Oncogene Proteins p21(ras) - genetics</topic><topic>rapid onsite evaluation</topic><topic>Retrospective Studies</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Livi, Vanina</creatorcontrib><creatorcontrib>Ardizzoni, Andrea</creatorcontrib><creatorcontrib>Cancellieri, Alessandra</creatorcontrib><creatorcontrib>Natali, Filippo</creatorcontrib><creatorcontrib>Ferrari, Marco</creatorcontrib><creatorcontrib>Paioli, Daniela</creatorcontrib><creatorcontrib>Biase, Dario</creatorcontrib><creatorcontrib>Capizzi, Elisa</creatorcontrib><creatorcontrib>Tallini, Giovanni</creatorcontrib><creatorcontrib>Fiorentino, Michelangelo</creatorcontrib><creatorcontrib>Trisolini, Rocco</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><jtitle>The clinical respiratory journal</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext_linktorsrc</fulltext></delivery><addata><au>Livi, Vanina</au><au>Ardizzoni, Andrea</au><au>Cancellieri, Alessandra</au><au>Natali, Filippo</au><au>Ferrari, Marco</au><au>Paioli, Daniela</au><au>Biase, Dario</au><au>Capizzi, Elisa</au><au>Tallini, Giovanni</au><au>Fiorentino, Michelangelo</au><au>Trisolini, Rocco</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Adequacy of endosonography‐derived samples from peribronchial or periesophageal intrapulmonary lesions for the molecular profiling of lung cancer</atitle><jtitle>The clinical respiratory journal</jtitle><addtitle>Clin Respir J</addtitle><date>2019-09</date><risdate>2019</risdate><volume>13</volume><issue>9</issue><spage>590</spage><epage>597</epage><pages>590-597</pages><issn>1752-6981</issn><eissn>1752-699X</eissn><abstract>Introduction and Objectives
Endosonography is increasingly used for the diagnosis of centrally located, bronchoscopically invisible intrapulmonary lesions, but data regarding its utility for molecular profiling are lacking. We aimed to assess the suitability of endosonography samples obtained from intrapulmonary lesions for cancer genotyping and programmed‐death ligand 1 (PD‐L1) testing.
Methods
A prospectively collected database regarding 99 consecutive patients undergoing endosonography for the diagnosis of an intrapulmonary lesion was retrospectively reviewed. Genotyping ± PD‐L1 testing was carried out in the 53 patients with advanced lung cancer and was classified as complete if all clinically indicated tests could be performed, incomplete if at least one test could not be carried out, and unsuccessful if the sample was unsuitable for molecular analysis.
Results
All clinically indicated biomarkers could be tested in 44 (83%) patients, whereas the molecular profiling was classified as incomplete in 6 (11.3%), and unsuccessful in 3 (5.7%). Thirty‐seven genetic alterations (KRAS mutation, 17; EGFR mutation, 17; ALK rearrangement, 3) and 2 cases of PD‐L1 expression >50% were found in 31 (58%) patients. EGFR was successfully analysed in 94.1% of cases, KRAS in 93.9%, ALK in 89%, ROS1 in 90% and PD‐L1 in 63.1%.
Conclusion
Endosonography‐derived samples from intrapulmonary lesions were suitable for a thorough molecular profiling in most patients. The few cases of incomplete accomplishment of the testing algorithm were related to the failure of PD‐L1 analysis due to the exhaustion of the sample or the lack of sufficient tumour cells in the paraffin‐embedded material.</abstract><cop>England</cop><pub>John Wiley & Sons, Inc</pub><pmid>31343834</pmid><doi>10.1111/crj.13063</doi><tpages>8</tpages><orcidid>https://orcid.org/0000-0002-1067-4696</orcidid></addata></record> |
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subjects | Aged Aged, 80 and over anaplastic lymphoma kinase Anaplastic Lymphoma Kinase - genetics B7-H1 Antigen - genetics Biomarkers Bronchoscopy - instrumentation endobronchial ultrasound Endosonography - methods epidermal growth factor receptor ErbB Receptors - genetics Esophagus - diagnostic imaging Esophagus - pathology Female Genotype Humans Lung cancer Lung Neoplasms - diagnostic imaging Lung Neoplasms - genetics Lung Neoplasms - pathology Male Medical diagnosis Middle Aged Mutation Neoplasm Staging programmed‐death ligand 1 Protein-Tyrosine Kinases - genetics Proto-Oncogene Proteins - genetics Proto-Oncogene Proteins p21(ras) - genetics rapid onsite evaluation Retrospective Studies |
title | Adequacy of endosonography‐derived samples from peribronchial or periesophageal intrapulmonary lesions for the molecular profiling of lung cancer |
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