Anaplastic lymphoma kinase expression and gene alterations in glioblastoma: correlations with clinical outcome
AimsTo study anaplastic lymphoma kinase (ALK) protein expression and possible underlying gene alterations in glioblastoma (GBM), correlating them with clinical outcome.MethodsWe studied ALK immunohistochemical expression and fluorescent in situ hybridisation (FISH)-detected ALK gene alterations in 5...
Gespeichert in:
| Veröffentlicht in: | Journal of clinical pathology 2017-07, Vol.70 (7), p.593-599 |
|---|---|
| Hauptverfasser: | , , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 599 |
|---|---|
| container_issue | 7 |
| container_start_page | 593 |
| container_title | Journal of clinical pathology |
| container_volume | 70 |
| creator | Karagkounis, George Stranjalis, George Argyrakos, Theodore Pantelaion, Varvara Mastoris, Konstantinos Rontogianni, Dimitra Komaitis, Spyridon Kalamatianos, Theodosis Sakas, Damianos Tiniakos, Dina |
| description | AimsTo study anaplastic lymphoma kinase (ALK) protein expression and possible underlying gene alterations in glioblastoma (GBM), correlating them with clinical outcome.MethodsWe studied ALK immunohistochemical expression and fluorescent in situ hybridisation (FISH)-detected ALK gene alterations in 51 GBMs (46 isocitrate dehydrogenase-1 (IDH1)R132H-negative and 5 IDH-mutant (IDH1R132H-positive)). We compared two anti-ALK antibodies and immunohistochemical detection systems (5Α4/Nichirei Biosciences, D5F3/Ventana). The results were correlated with tumour cell proliferation and clinical outcome.ResultsIntense granular cytoplasmic ALK immunostaining was observed in 10/51 (19.61%) GBM and correlated with high Ki67 proliferation index; only 1 in 10 ALK-positive cases displayed multiple alk gene signals by FISH. Moderate ALK immunostaining was observed in 21 (41.17%), weak immunostaining in 5 (9.80%) while 15 (29.42%) cases were negative. p53 was expressed in 26/51 GBM (50.9%) (10% cut-off). IDH1R132H-negative GBM showed higher ALK expression compared with IDH-mutant GBM (65.2% vs 20%). ALK overexpression was more common in older patients but did not correlate with other clinicopathological variables or patient overall survival.ConclusionsALK overexpression can be identified in up to 70% of GBMs and does not correlate with underlying alk gene amplification. Despite being more common in rapidly growing, clinically aggressive GBM, ALK overexpression did not show correlation with prognosis in this study. |
| doi_str_mv | 10.1136/jclinpath-2016-204102 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_1916378134</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1851294692</sourcerecordid><originalsourceid>FETCH-LOGICAL-b411t-6b221018912f722439e2a2a2f0fe84f73dc60d5437fce2dba68e4a2f7509539a3</originalsourceid><addsrcrecordid>eNqNkU9v1DAQxS1ERZfCRwBZ4sIl1GM7dsytqvgnVeoFzpGTTLpeHDvYiWi_fR3t0gMX0EgeyfN7T2M_Qt4A-wAg1OWh9y7MdtlXnIEqhwTGn5EdSM0rCVI9JzvGOFRGS3VOXuZ8YAyEBvGCnHNtjDBS7Ui4Cnb2Ni-up_5hmvdxsvSnCzYjxfs5Yc4uBmrDQO8wILV-wWSXcpepC_TOu9ht8iL7SPuYEvrT9Ldb9nRb0vXW07gufZzwFTkbrc_4-tQvyI_Pn75ff61ubr98u766qToJsFSq4xwYNAb4qDmXwiC3pUY2YiNHLYZesaGWQo898qGzqkFZxrpmphbGigvy_ug7p_hrxby0k8s9em8DxjW3YEAJ3YCQ_0abGnj5K8ML-u4v9BDXFMpDNkMulZL1RtVHqk8x54RjOyc32fTQAmu37Nqn7Notu_aYXdG9Pbmv3YTDk-pPWAVgR6CbDv_p-QjglafN</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1912466452</pqid></control><display><type>article</type><title>Anaplastic lymphoma kinase expression and gene alterations in glioblastoma: correlations with clinical outcome</title><source>MEDLINE</source><source>PubMed Central</source><creator>Karagkounis, George ; Stranjalis, George ; Argyrakos, Theodore ; Pantelaion, Varvara ; Mastoris, Konstantinos ; Rontogianni, Dimitra ; Komaitis, Spyridon ; Kalamatianos, Theodosis ; Sakas, Damianos ; Tiniakos, Dina</creator><creatorcontrib>Karagkounis, George ; Stranjalis, George ; Argyrakos, Theodore ; Pantelaion, Varvara ; Mastoris, Konstantinos ; Rontogianni, Dimitra ; Komaitis, Spyridon ; Kalamatianos, Theodosis ; Sakas, Damianos ; Tiniakos, Dina</creatorcontrib><description>AimsTo study anaplastic lymphoma kinase (ALK) protein expression and possible underlying gene alterations in glioblastoma (GBM), correlating them with clinical outcome.MethodsWe studied ALK immunohistochemical expression and fluorescent in situ hybridisation (FISH)-detected ALK gene alterations in 51 GBMs (46 isocitrate dehydrogenase-1 (IDH1)R132H-negative and 5 IDH-mutant (IDH1R132H-positive)). We compared two anti-ALK antibodies and immunohistochemical detection systems (5Α4/Nichirei Biosciences, D5F3/Ventana). The results were correlated with tumour cell proliferation and clinical outcome.ResultsIntense granular cytoplasmic ALK immunostaining was observed in 10/51 (19.61%) GBM and correlated with high Ki67 proliferation index; only 1 in 10 ALK-positive cases displayed multiple alk gene signals by FISH. Moderate ALK immunostaining was observed in 21 (41.17%), weak immunostaining in 5 (9.80%) while 15 (29.42%) cases were negative. p53 was expressed in 26/51 GBM (50.9%) (10% cut-off). IDH1R132H-negative GBM showed higher ALK expression compared with IDH-mutant GBM (65.2% vs 20%). ALK overexpression was more common in older patients but did not correlate with other clinicopathological variables or patient overall survival.ConclusionsALK overexpression can be identified in up to 70% of GBMs and does not correlate with underlying alk gene amplification. Despite being more common in rapidly growing, clinically aggressive GBM, ALK overexpression did not show correlation with prognosis in this study.</description><identifier>ISSN: 0021-9746</identifier><identifier>EISSN: 1472-4146</identifier><identifier>DOI: 10.1136/jclinpath-2016-204102</identifier><identifier>PMID: 27993946</identifier><language>eng</language><publisher>England: BMJ Publishing Group LTD</publisher><subject>Antigens ; Brain cancer ; Brain Neoplasms - enzymology ; Brain Neoplasms - genetics ; Brain Neoplasms - mortality ; Cell Proliferation ; Clinical outcomes ; Cloning ; Female ; Gangrene ; Glioblastoma - enzymology ; Glioblastoma - genetics ; Glioblastoma - mortality ; Humans ; In Situ Hybridization, Fluorescence ; Kaplan-Meier Estimate ; Kinases ; Lung cancer ; Lymphoma ; Male ; Middle Aged ; Mutation ; Mutation - genetics ; Neuroblastoma ; Prognosis ; Protein expression ; Proteins ; Receptor Protein-Tyrosine Kinases - genetics ; Receptor Protein-Tyrosine Kinases - metabolism ; Retrospective Studies ; Tumors</subject><ispartof>Journal of clinical pathology, 2017-07, Vol.70 (7), p.593-599</ispartof><rights>Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://www.bmj.com/company/products-services/rights-and-licensing</rights><rights>Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://www.bmj.com/company/products-services/rights-and-licensing/.</rights><rights>Copyright: 2016 Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://www.bmj.com/company/products-services/rights-and-licensing</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-b411t-6b221018912f722439e2a2a2f0fe84f73dc60d5437fce2dba68e4a2f7509539a3</citedby><cites>FETCH-LOGICAL-b411t-6b221018912f722439e2a2a2f0fe84f73dc60d5437fce2dba68e4a2f7509539a3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,781,785,27929,27930</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27993946$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Karagkounis, George</creatorcontrib><creatorcontrib>Stranjalis, George</creatorcontrib><creatorcontrib>Argyrakos, Theodore</creatorcontrib><creatorcontrib>Pantelaion, Varvara</creatorcontrib><creatorcontrib>Mastoris, Konstantinos</creatorcontrib><creatorcontrib>Rontogianni, Dimitra</creatorcontrib><creatorcontrib>Komaitis, Spyridon</creatorcontrib><creatorcontrib>Kalamatianos, Theodosis</creatorcontrib><creatorcontrib>Sakas, Damianos</creatorcontrib><creatorcontrib>Tiniakos, Dina</creatorcontrib><title>Anaplastic lymphoma kinase expression and gene alterations in glioblastoma: correlations with clinical outcome</title><title>Journal of clinical pathology</title><addtitle>J Clin Pathol</addtitle><description>AimsTo study anaplastic lymphoma kinase (ALK) protein expression and possible underlying gene alterations in glioblastoma (GBM), correlating them with clinical outcome.MethodsWe studied ALK immunohistochemical expression and fluorescent in situ hybridisation (FISH)-detected ALK gene alterations in 51 GBMs (46 isocitrate dehydrogenase-1 (IDH1)R132H-negative and 5 IDH-mutant (IDH1R132H-positive)). We compared two anti-ALK antibodies and immunohistochemical detection systems (5Α4/Nichirei Biosciences, D5F3/Ventana). The results were correlated with tumour cell proliferation and clinical outcome.ResultsIntense granular cytoplasmic ALK immunostaining was observed in 10/51 (19.61%) GBM and correlated with high Ki67 proliferation index; only 1 in 10 ALK-positive cases displayed multiple alk gene signals by FISH. Moderate ALK immunostaining was observed in 21 (41.17%), weak immunostaining in 5 (9.80%) while 15 (29.42%) cases were negative. p53 was expressed in 26/51 GBM (50.9%) (10% cut-off). IDH1R132H-negative GBM showed higher ALK expression compared with IDH-mutant GBM (65.2% vs 20%). ALK overexpression was more common in older patients but did not correlate with other clinicopathological variables or patient overall survival.ConclusionsALK overexpression can be identified in up to 70% of GBMs and does not correlate with underlying alk gene amplification. Despite being more common in rapidly growing, clinically aggressive GBM, ALK overexpression did not show correlation with prognosis in this study.</description><subject>Antigens</subject><subject>Brain cancer</subject><subject>Brain Neoplasms - enzymology</subject><subject>Brain Neoplasms - genetics</subject><subject>Brain Neoplasms - mortality</subject><subject>Cell Proliferation</subject><subject>Clinical outcomes</subject><subject>Cloning</subject><subject>Female</subject><subject>Gangrene</subject><subject>Glioblastoma - enzymology</subject><subject>Glioblastoma - genetics</subject><subject>Glioblastoma - mortality</subject><subject>Humans</subject><subject>In Situ Hybridization, Fluorescence</subject><subject>Kaplan-Meier Estimate</subject><subject>Kinases</subject><subject>Lung cancer</subject><subject>Lymphoma</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Mutation</subject><subject>Mutation - genetics</subject><subject>Neuroblastoma</subject><subject>Prognosis</subject><subject>Protein expression</subject><subject>Proteins</subject><subject>Receptor Protein-Tyrosine Kinases - genetics</subject><subject>Receptor Protein-Tyrosine Kinases - metabolism</subject><subject>Retrospective Studies</subject><subject>Tumors</subject><issn>0021-9746</issn><issn>1472-4146</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqNkU9v1DAQxS1ERZfCRwBZ4sIl1GM7dsytqvgnVeoFzpGTTLpeHDvYiWi_fR3t0gMX0EgeyfN7T2M_Qt4A-wAg1OWh9y7MdtlXnIEqhwTGn5EdSM0rCVI9JzvGOFRGS3VOXuZ8YAyEBvGCnHNtjDBS7Ui4Cnb2Ni-up_5hmvdxsvSnCzYjxfs5Yc4uBmrDQO8wILV-wWSXcpepC_TOu9ht8iL7SPuYEvrT9Ldb9nRb0vXW07gufZzwFTkbrc_4-tQvyI_Pn75ff61ubr98u766qToJsFSq4xwYNAb4qDmXwiC3pUY2YiNHLYZesaGWQo898qGzqkFZxrpmphbGigvy_ug7p_hrxby0k8s9em8DxjW3YEAJ3YCQ_0abGnj5K8ML-u4v9BDXFMpDNkMulZL1RtVHqk8x54RjOyc32fTQAmu37Nqn7Notu_aYXdG9Pbmv3YTDk-pPWAVgR6CbDv_p-QjglafN</recordid><startdate>20170701</startdate><enddate>20170701</enddate><creator>Karagkounis, George</creator><creator>Stranjalis, George</creator><creator>Argyrakos, Theodore</creator><creator>Pantelaion, Varvara</creator><creator>Mastoris, Konstantinos</creator><creator>Rontogianni, Dimitra</creator><creator>Komaitis, Spyridon</creator><creator>Kalamatianos, Theodosis</creator><creator>Sakas, Damianos</creator><creator>Tiniakos, Dina</creator><general>BMJ Publishing Group LTD</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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</scope><scope>8AF</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>BTHHO</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>7T5</scope><scope>H94</scope></search><sort><creationdate>20170701</creationdate><title>Anaplastic lymphoma kinase expression and gene alterations in glioblastoma: correlations with clinical outcome</title><author>Karagkounis, George ; Stranjalis, George ; Argyrakos, Theodore ; Pantelaion, Varvara ; Mastoris, Konstantinos ; Rontogianni, Dimitra ; Komaitis, Spyridon ; Kalamatianos, Theodosis ; Sakas, Damianos ; Tiniakos, Dina</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b411t-6b221018912f722439e2a2a2f0fe84f73dc60d5437fce2dba68e4a2f7509539a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Antigens</topic><topic>Brain cancer</topic><topic>Brain Neoplasms - enzymology</topic><topic>Brain Neoplasms - genetics</topic><topic>Brain Neoplasms - mortality</topic><topic>Cell Proliferation</topic><topic>Clinical outcomes</topic><topic>Cloning</topic><topic>Female</topic><topic>Gangrene</topic><topic>Glioblastoma - enzymology</topic><topic>Glioblastoma - genetics</topic><topic>Glioblastoma - mortality</topic><topic>Humans</topic><topic>In Situ Hybridization, Fluorescence</topic><topic>Kaplan-Meier Estimate</topic><topic>Kinases</topic><topic>Lung cancer</topic><topic>Lymphoma</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Mutation</topic><topic>Mutation - genetics</topic><topic>Neuroblastoma</topic><topic>Prognosis</topic><topic>Protein expression</topic><topic>Proteins</topic><topic>Receptor Protein-Tyrosine Kinases - genetics</topic><topic>Receptor Protein-Tyrosine Kinases - metabolism</topic><topic>Retrospective Studies</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Karagkounis, George</creatorcontrib><creatorcontrib>Stranjalis, George</creatorcontrib><creatorcontrib>Argyrakos, Theodore</creatorcontrib><creatorcontrib>Pantelaion, Varvara</creatorcontrib><creatorcontrib>Mastoris, Konstantinos</creatorcontrib><creatorcontrib>Rontogianni, Dimitra</creatorcontrib><creatorcontrib>Komaitis, Spyridon</creatorcontrib><creatorcontrib>Kalamatianos, Theodosis</creatorcontrib><creatorcontrib>Sakas, Damianos</creatorcontrib><creatorcontrib>Tiniakos, Dina</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 Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>STEM Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>BMJ Journals</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><jtitle>Journal of clinical pathology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Karagkounis, George</au><au>Stranjalis, George</au><au>Argyrakos, Theodore</au><au>Pantelaion, Varvara</au><au>Mastoris, Konstantinos</au><au>Rontogianni, Dimitra</au><au>Komaitis, Spyridon</au><au>Kalamatianos, Theodosis</au><au>Sakas, Damianos</au><au>Tiniakos, Dina</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Anaplastic lymphoma kinase expression and gene alterations in glioblastoma: correlations with clinical outcome</atitle><jtitle>Journal of clinical pathology</jtitle><addtitle>J Clin Pathol</addtitle><date>2017-07-01</date><risdate>2017</risdate><volume>70</volume><issue>7</issue><spage>593</spage><epage>599</epage><pages>593-599</pages><issn>0021-9746</issn><eissn>1472-4146</eissn><abstract>AimsTo study anaplastic lymphoma kinase (ALK) protein expression and possible underlying gene alterations in glioblastoma (GBM), correlating them with clinical outcome.MethodsWe studied ALK immunohistochemical expression and fluorescent in situ hybridisation (FISH)-detected ALK gene alterations in 51 GBMs (46 isocitrate dehydrogenase-1 (IDH1)R132H-negative and 5 IDH-mutant (IDH1R132H-positive)). We compared two anti-ALK antibodies and immunohistochemical detection systems (5Α4/Nichirei Biosciences, D5F3/Ventana). The results were correlated with tumour cell proliferation and clinical outcome.ResultsIntense granular cytoplasmic ALK immunostaining was observed in 10/51 (19.61%) GBM and correlated with high Ki67 proliferation index; only 1 in 10 ALK-positive cases displayed multiple alk gene signals by FISH. Moderate ALK immunostaining was observed in 21 (41.17%), weak immunostaining in 5 (9.80%) while 15 (29.42%) cases were negative. p53 was expressed in 26/51 GBM (50.9%) (10% cut-off). IDH1R132H-negative GBM showed higher ALK expression compared with IDH-mutant GBM (65.2% vs 20%). ALK overexpression was more common in older patients but did not correlate with other clinicopathological variables or patient overall survival.ConclusionsALK overexpression can be identified in up to 70% of GBMs and does not correlate with underlying alk gene amplification. Despite being more common in rapidly growing, clinically aggressive GBM, ALK overexpression did not show correlation with prognosis in this study.</abstract><cop>England</cop><pub>BMJ Publishing Group LTD</pub><pmid>27993946</pmid><doi>10.1136/jclinpath-2016-204102</doi><tpages>7</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0021-9746 |
| ispartof | Journal of clinical pathology, 2017-07, Vol.70 (7), p.593-599 |
| issn | 0021-9746 1472-4146 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_1916378134 |
| source | MEDLINE; PubMed Central |
| subjects | Antigens Brain cancer Brain Neoplasms - enzymology Brain Neoplasms - genetics Brain Neoplasms - mortality Cell Proliferation Clinical outcomes Cloning Female Gangrene Glioblastoma - enzymology Glioblastoma - genetics Glioblastoma - mortality Humans In Situ Hybridization, Fluorescence Kaplan-Meier Estimate Kinases Lung cancer Lymphoma Male Middle Aged Mutation Mutation - genetics Neuroblastoma Prognosis Protein expression Proteins Receptor Protein-Tyrosine Kinases - genetics Receptor Protein-Tyrosine Kinases - metabolism Retrospective Studies Tumors |
| title | Anaplastic lymphoma kinase expression and gene alterations in glioblastoma: correlations with clinical outcome |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-15T16%3A50%3A12IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Anaplastic%20lymphoma%20kinase%20expression%20and%20gene%20alterations%20in%20glioblastoma:%20correlations%20with%20clinical%20outcome&rft.jtitle=Journal%20of%20clinical%20pathology&rft.au=Karagkounis,%20George&rft.date=2017-07-01&rft.volume=70&rft.issue=7&rft.spage=593&rft.epage=599&rft.pages=593-599&rft.issn=0021-9746&rft.eissn=1472-4146&rft_id=info:doi/10.1136/jclinpath-2016-204102&rft_dat=%3Cproquest_cross%3E1851294692%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1912466452&rft_id=info:pmid/27993946&rfr_iscdi=true |