ALK gene amplification is associated with poor prognosis in colorectal carcinoma
Background: Recently, the anaplastic lymphoma kinase (ALK) has been found to be altered in several solid and haematological tumours. ALK gene copy number changes and mutations in colorectal cancers (CRCs) are not well characterised. We aimed to study the prevalence of ALK copy number changes, transl...
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creator | Bavi, P Jehan, Z Bu, R Prabhakaran, S Al-Sanea, N Al-Dayel, F Al-Assiri, M Al-Halouly, T Sairafi, R Uddin, S Al-Kuraya, K S |
description | Background:
Recently, the anaplastic lymphoma kinase (ALK) has been found to be altered in several solid and haematological tumours.
ALK
gene copy number changes and mutations in colorectal cancers (CRCs) are not well characterised. We aimed to study the prevalence of ALK copy number changes, translocations, gene mutations and protein expression in 770 CRC patients, and correlate these findings with molecular and clinico-pathological data.
Methods:
ALK
gene copy number variations and ALK expression were evaluated by fluorescence
in situ
hybridisation (FISH) and immunohistochemistry, respectively.
Results:
Translocations of the
ALK
gene were not observed; 3.4% (26 out of 756) of the CRC patients tested had an increase in
ALK
gene copy number either amplification or gain. Interestingly, increased
ALK
gene copy number alteration was associated with poor prognosis (
P
=0.0135) and was an independent prognostic marker in multivariate Cox proportional hazards model. The study reveals a significant impact of
ALK
gene copy number alterations on the outcome of patients with CRC.
Conclusion:
The findings of our study highlight a potential role of targeting ALK in advanced CRCs by using ALK FISH and ALK IHC as a screening tool to detect ALK alterations. Based on these findings, a potential role of ALK inhibitor as a therapeutic agent in a subset of CRC merits further investigation. |
doi_str_mv | 10.1038/bjc.2013.641 |
format | Article |
fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_3833224</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1534843972</sourcerecordid><originalsourceid>FETCH-LOGICAL-c513t-8f77a55bd41575e23007e51f653304a7ea1d76ae0d619a8ba8db385b2b3562083</originalsourceid><addsrcrecordid>eNptkd1rFDEUxUOptOvqW59LoBR8cNZ8TjIvhVL8wgV90OdwJ5PZZplJxmS24n9vll1rFZ9COD_OPfcehC4oWVHC9Zt2a1eMUL6qBT1BCyo5q6hm6hQtCCGqIg0j5-h5ztvybYhWZ-icCcoaJsQCfbldf8IbFxyGcRp87y3MPgbsM4aco_Uwuw7_8PM9nmJMeEpxE2Iusg_YxiEmZ2cYsIVkfYgjvEDPehiye3l8l-jbu7df7z5U68_vP97drisrKZ8r3SsFUradoFJJx3iJ6iTta8k5EaAc0E7V4EhX0wZ0C7pruZYta7msGdF8iW4OvtOuHV1nXZgTDGZKfoT000Tw5m8l-HuziQ-Ga84ZE8Xg1dEgxe87l2cz-mzdMEBwcZdNOaTQgjeKFfTqH3QbdymU9QwVkjCu61LFEr0-UDbFnJPrH8NQYvZVmVKV2VdlSlUFv3y6wCP8u5sCXB8ByBaGPkGwPv_hVCOZYvu51YHLRQobl56k-9_gXzXfqpY</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1450238610</pqid></control><display><type>article</type><title>ALK gene amplification is associated with poor prognosis in colorectal carcinoma</title><source>MEDLINE</source><source>SpringerLink Journals</source><source>Nature</source><source>EZB-FREE-00999 freely available EZB journals</source><source>PubMed Central</source><creator>Bavi, P ; Jehan, Z ; Bu, R ; Prabhakaran, S ; Al-Sanea, N ; Al-Dayel, F ; Al-Assiri, M ; Al-Halouly, T ; Sairafi, R ; Uddin, S ; Al-Kuraya, K S</creator><creatorcontrib>Bavi, P ; Jehan, Z ; Bu, R ; Prabhakaran, S ; Al-Sanea, N ; Al-Dayel, F ; Al-Assiri, M ; Al-Halouly, T ; Sairafi, R ; Uddin, S ; Al-Kuraya, K S</creatorcontrib><description>Background:
Recently, the anaplastic lymphoma kinase (ALK) has been found to be altered in several solid and haematological tumours.
ALK
gene copy number changes and mutations in colorectal cancers (CRCs) are not well characterised. We aimed to study the prevalence of ALK copy number changes, translocations, gene mutations and protein expression in 770 CRC patients, and correlate these findings with molecular and clinico-pathological data.
Methods:
ALK
gene copy number variations and ALK expression were evaluated by fluorescence
in situ
hybridisation (FISH) and immunohistochemistry, respectively.
Results:
Translocations of the
ALK
gene were not observed; 3.4% (26 out of 756) of the CRC patients tested had an increase in
ALK
gene copy number either amplification or gain. Interestingly, increased
ALK
gene copy number alteration was associated with poor prognosis (
P
=0.0135) and was an independent prognostic marker in multivariate Cox proportional hazards model. The study reveals a significant impact of
ALK
gene copy number alterations on the outcome of patients with CRC.
Conclusion:
The findings of our study highlight a potential role of targeting ALK in advanced CRCs by using ALK FISH and ALK IHC as a screening tool to detect ALK alterations. Based on these findings, a potential role of ALK inhibitor as a therapeutic agent in a subset of CRC merits further investigation.</description><identifier>ISSN: 0007-0920</identifier><identifier>EISSN: 1532-1827</identifier><identifier>DOI: 10.1038/bjc.2013.641</identifier><identifier>PMID: 24129244</identifier><identifier>CODEN: BJCAAI</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>692/699/67/1504/1885 ; 692/700/1750 ; Aged ; Biological and medical sciences ; Biomarkers, Tumor - genetics ; Biomarkers, Tumor - metabolism ; Biomedical and Life Sciences ; Biomedicine ; Cancer Research ; Cancer therapies ; Chemotherapy ; Cohort Studies ; Colorectal cancer ; Colorectal Neoplasms - diagnosis ; Colorectal Neoplasms - genetics ; Colorectal Neoplasms - mortality ; Drug Resistance ; Epidemiology ; Female ; Gastroenterology. Liver. Pancreas. Abdomen ; Gene Amplification ; Gene Dosage ; Gene Expression Regulation, Neoplastic ; Genetics and Genomics ; Humans ; Immunohistochemistry ; In Situ Hybridization, Fluorescence ; Kinases ; Lymphoma ; Male ; Medical prognosis ; Medical research ; Medical sciences ; Middle Aged ; Molecular Medicine ; Multiple tumors. Solid tumors. Tumors in childhood (general aspects) ; Mutation ; Oncology ; Pathology ; Prognosis ; Receptor Protein-Tyrosine Kinases - genetics ; Research centers ; Stomach. Duodenum. Small intestine. Colon. Rectum. Anus ; Surgery ; Survival analysis ; Tissue Array Analysis ; Tumors</subject><ispartof>British journal of cancer, 2013-11, Vol.109 (10), p.2735-2743</ispartof><rights>The Author(s) 2013</rights><rights>2015 INIST-CNRS</rights><rights>Copyright Nature Publishing Group Nov 12, 2013</rights><rights>Copyright © 2013 Cancer Research UK 2013 Cancer Research UK</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c513t-8f77a55bd41575e23007e51f653304a7ea1d76ae0d619a8ba8db385b2b3562083</citedby><cites>FETCH-LOGICAL-c513t-8f77a55bd41575e23007e51f653304a7ea1d76ae0d619a8ba8db385b2b3562083</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3833224/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3833224/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,41464,42533,51294,53766,53768</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=27952720$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24129244$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Bavi, P</creatorcontrib><creatorcontrib>Jehan, Z</creatorcontrib><creatorcontrib>Bu, R</creatorcontrib><creatorcontrib>Prabhakaran, S</creatorcontrib><creatorcontrib>Al-Sanea, N</creatorcontrib><creatorcontrib>Al-Dayel, F</creatorcontrib><creatorcontrib>Al-Assiri, M</creatorcontrib><creatorcontrib>Al-Halouly, T</creatorcontrib><creatorcontrib>Sairafi, R</creatorcontrib><creatorcontrib>Uddin, S</creatorcontrib><creatorcontrib>Al-Kuraya, K S</creatorcontrib><title>ALK gene amplification is associated with poor prognosis in colorectal carcinoma</title><title>British journal of cancer</title><addtitle>Br J Cancer</addtitle><addtitle>Br J Cancer</addtitle><description>Background:
Recently, the anaplastic lymphoma kinase (ALK) has been found to be altered in several solid and haematological tumours.
ALK
gene copy number changes and mutations in colorectal cancers (CRCs) are not well characterised. We aimed to study the prevalence of ALK copy number changes, translocations, gene mutations and protein expression in 770 CRC patients, and correlate these findings with molecular and clinico-pathological data.
Methods:
ALK
gene copy number variations and ALK expression were evaluated by fluorescence
in situ
hybridisation (FISH) and immunohistochemistry, respectively.
Results:
Translocations of the
ALK
gene were not observed; 3.4% (26 out of 756) of the CRC patients tested had an increase in
ALK
gene copy number either amplification or gain. Interestingly, increased
ALK
gene copy number alteration was associated with poor prognosis (
P
=0.0135) and was an independent prognostic marker in multivariate Cox proportional hazards model. The study reveals a significant impact of
ALK
gene copy number alterations on the outcome of patients with CRC.
Conclusion:
The findings of our study highlight a potential role of targeting ALK in advanced CRCs by using ALK FISH and ALK IHC as a screening tool to detect ALK alterations. Based on these findings, a potential role of ALK inhibitor as a therapeutic agent in a subset of CRC merits further investigation.</description><subject>692/699/67/1504/1885</subject><subject>692/700/1750</subject><subject>Aged</subject><subject>Biological and medical sciences</subject><subject>Biomarkers, Tumor - genetics</subject><subject>Biomarkers, Tumor - metabolism</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cancer Research</subject><subject>Cancer therapies</subject><subject>Chemotherapy</subject><subject>Cohort Studies</subject><subject>Colorectal cancer</subject><subject>Colorectal Neoplasms - diagnosis</subject><subject>Colorectal Neoplasms - genetics</subject><subject>Colorectal Neoplasms - mortality</subject><subject>Drug Resistance</subject><subject>Epidemiology</subject><subject>Female</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>Gene Amplification</subject><subject>Gene Dosage</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Genetics and Genomics</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>In Situ Hybridization, Fluorescence</subject><subject>Kinases</subject><subject>Lymphoma</subject><subject>Male</subject><subject>Medical prognosis</subject><subject>Medical research</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Molecular Medicine</subject><subject>Multiple tumors. Solid tumors. Tumors in childhood (general aspects)</subject><subject>Mutation</subject><subject>Oncology</subject><subject>Pathology</subject><subject>Prognosis</subject><subject>Receptor Protein-Tyrosine Kinases - genetics</subject><subject>Research centers</subject><subject>Stomach. Duodenum. Small intestine. Colon. Rectum. Anus</subject><subject>Surgery</subject><subject>Survival analysis</subject><subject>Tissue Array Analysis</subject><subject>Tumors</subject><issn>0007-0920</issn><issn>1532-1827</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNptkd1rFDEUxUOptOvqW59LoBR8cNZ8TjIvhVL8wgV90OdwJ5PZZplJxmS24n9vll1rFZ9COD_OPfcehC4oWVHC9Zt2a1eMUL6qBT1BCyo5q6hm6hQtCCGqIg0j5-h5ztvybYhWZ-icCcoaJsQCfbldf8IbFxyGcRp87y3MPgbsM4aco_Uwuw7_8PM9nmJMeEpxE2Iusg_YxiEmZ2cYsIVkfYgjvEDPehiye3l8l-jbu7df7z5U68_vP97drisrKZ8r3SsFUradoFJJx3iJ6iTta8k5EaAc0E7V4EhX0wZ0C7pruZYta7msGdF8iW4OvtOuHV1nXZgTDGZKfoT000Tw5m8l-HuziQ-Ga84ZE8Xg1dEgxe87l2cz-mzdMEBwcZdNOaTQgjeKFfTqH3QbdymU9QwVkjCu61LFEr0-UDbFnJPrH8NQYvZVmVKV2VdlSlUFv3y6wCP8u5sCXB8ByBaGPkGwPv_hVCOZYvu51YHLRQobl56k-9_gXzXfqpY</recordid><startdate>20131112</startdate><enddate>20131112</enddate><creator>Bavi, P</creator><creator>Jehan, Z</creator><creator>Bu, R</creator><creator>Prabhakaran, S</creator><creator>Al-Sanea, N</creator><creator>Al-Dayel, F</creator><creator>Al-Assiri, M</creator><creator>Al-Halouly, T</creator><creator>Sairafi, R</creator><creator>Uddin, S</creator><creator>Al-Kuraya, K S</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><scope>C6C</scope><scope>IQODW</scope><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>7RV</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB0</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>NAPCQ</scope><scope>PHGZM</scope><scope>PHGZT</scope><scope>PJZUB</scope><scope>PKEHL</scope><scope>PPXIY</scope><scope>PQEST</scope><scope>PQGLB</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope><scope>5PM</scope></search><sort><creationdate>20131112</creationdate><title>ALK gene amplification is associated with poor prognosis in colorectal carcinoma</title><author>Bavi, P ; Jehan, Z ; Bu, R ; Prabhakaran, S ; Al-Sanea, N ; Al-Dayel, F ; Al-Assiri, M ; Al-Halouly, T ; Sairafi, R ; Uddin, S ; Al-Kuraya, K S</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c513t-8f77a55bd41575e23007e51f653304a7ea1d76ae0d619a8ba8db385b2b3562083</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>692/699/67/1504/1885</topic><topic>692/700/1750</topic><topic>Aged</topic><topic>Biological and medical sciences</topic><topic>Biomarkers, Tumor - genetics</topic><topic>Biomarkers, Tumor - metabolism</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Cancer Research</topic><topic>Cancer therapies</topic><topic>Chemotherapy</topic><topic>Cohort Studies</topic><topic>Colorectal cancer</topic><topic>Colorectal Neoplasms - diagnosis</topic><topic>Colorectal Neoplasms - genetics</topic><topic>Colorectal Neoplasms - mortality</topic><topic>Drug Resistance</topic><topic>Epidemiology</topic><topic>Female</topic><topic>Gastroenterology. Liver. Pancreas. Abdomen</topic><topic>Gene Amplification</topic><topic>Gene Dosage</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Genetics and Genomics</topic><topic>Humans</topic><topic>Immunohistochemistry</topic><topic>In Situ Hybridization, Fluorescence</topic><topic>Kinases</topic><topic>Lymphoma</topic><topic>Male</topic><topic>Medical prognosis</topic><topic>Medical research</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Molecular Medicine</topic><topic>Multiple tumors. Solid tumors. Tumors in childhood (general aspects)</topic><topic>Mutation</topic><topic>Oncology</topic><topic>Pathology</topic><topic>Prognosis</topic><topic>Receptor Protein-Tyrosine Kinases - genetics</topic><topic>Research centers</topic><topic>Stomach. Duodenum. Small intestine. Colon. Rectum. Anus</topic><topic>Surgery</topic><topic>Survival analysis</topic><topic>Tissue Array Analysis</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Bavi, P</creatorcontrib><creatorcontrib>Jehan, Z</creatorcontrib><creatorcontrib>Bu, R</creatorcontrib><creatorcontrib>Prabhakaran, S</creatorcontrib><creatorcontrib>Al-Sanea, N</creatorcontrib><creatorcontrib>Al-Dayel, F</creatorcontrib><creatorcontrib>Al-Assiri, M</creatorcontrib><creatorcontrib>Al-Halouly, T</creatorcontrib><creatorcontrib>Sairafi, R</creatorcontrib><creatorcontrib>Uddin, S</creatorcontrib><creatorcontrib>Al-Kuraya, K S</creatorcontrib><collection>Springer Nature OA Free Journals</collection><collection>Pascal-Francis</collection><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>Nursing & Allied Health Database</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</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>British Nursing Database</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection (ProQuest)</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>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>Nursing & Allied Health Premium</collection><collection>ProQuest Central (New)</collection><collection>ProQuest One Academic (New)</collection><collection>ProQuest Health & Medical Research Collection</collection><collection>ProQuest One Academic Middle East (New)</collection><collection>ProQuest One Health & Nursing</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Applied & Life Sciences</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>British journal of cancer</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Bavi, P</au><au>Jehan, Z</au><au>Bu, R</au><au>Prabhakaran, S</au><au>Al-Sanea, N</au><au>Al-Dayel, F</au><au>Al-Assiri, M</au><au>Al-Halouly, T</au><au>Sairafi, R</au><au>Uddin, S</au><au>Al-Kuraya, K S</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>ALK gene amplification is associated with poor prognosis in colorectal carcinoma</atitle><jtitle>British journal of cancer</jtitle><stitle>Br J Cancer</stitle><addtitle>Br J Cancer</addtitle><date>2013-11-12</date><risdate>2013</risdate><volume>109</volume><issue>10</issue><spage>2735</spage><epage>2743</epage><pages>2735-2743</pages><issn>0007-0920</issn><eissn>1532-1827</eissn><coden>BJCAAI</coden><abstract>Background:
Recently, the anaplastic lymphoma kinase (ALK) has been found to be altered in several solid and haematological tumours.
ALK
gene copy number changes and mutations in colorectal cancers (CRCs) are not well characterised. We aimed to study the prevalence of ALK copy number changes, translocations, gene mutations and protein expression in 770 CRC patients, and correlate these findings with molecular and clinico-pathological data.
Methods:
ALK
gene copy number variations and ALK expression were evaluated by fluorescence
in situ
hybridisation (FISH) and immunohistochemistry, respectively.
Results:
Translocations of the
ALK
gene were not observed; 3.4% (26 out of 756) of the CRC patients tested had an increase in
ALK
gene copy number either amplification or gain. Interestingly, increased
ALK
gene copy number alteration was associated with poor prognosis (
P
=0.0135) and was an independent prognostic marker in multivariate Cox proportional hazards model. The study reveals a significant impact of
ALK
gene copy number alterations on the outcome of patients with CRC.
Conclusion:
The findings of our study highlight a potential role of targeting ALK in advanced CRCs by using ALK FISH and ALK IHC as a screening tool to detect ALK alterations. Based on these findings, a potential role of ALK inhibitor as a therapeutic agent in a subset of CRC merits further investigation.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>24129244</pmid><doi>10.1038/bjc.2013.641</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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subjects | 692/699/67/1504/1885 692/700/1750 Aged Biological and medical sciences Biomarkers, Tumor - genetics Biomarkers, Tumor - metabolism Biomedical and Life Sciences Biomedicine Cancer Research Cancer therapies Chemotherapy Cohort Studies Colorectal cancer Colorectal Neoplasms - diagnosis Colorectal Neoplasms - genetics Colorectal Neoplasms - mortality Drug Resistance Epidemiology Female Gastroenterology. Liver. Pancreas. Abdomen Gene Amplification Gene Dosage Gene Expression Regulation, Neoplastic Genetics and Genomics Humans Immunohistochemistry In Situ Hybridization, Fluorescence Kinases Lymphoma Male Medical prognosis Medical research Medical sciences Middle Aged Molecular Medicine Multiple tumors. Solid tumors. Tumors in childhood (general aspects) Mutation Oncology Pathology Prognosis Receptor Protein-Tyrosine Kinases - genetics Research centers Stomach. Duodenum. Small intestine. Colon. Rectum. Anus Surgery Survival analysis Tissue Array Analysis Tumors |
title | ALK gene amplification is associated with poor prognosis in colorectal carcinoma |
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