Proteomics uncover EPHA2 as a potential novel therapeutic target in colorectal cancer cell lines with acquired cetuximab resistance
Background In metastatic colorectal cancer (mCRC), acquired resistance against anti-EGFR targeted monoclonal antibodies, such as cetuximab (CET), was shown to be frequently caused by activating alterations in the RAS genes KRAS or NRAS . To this day, no efficient follow-up treatment option has emerg...
Gespeichert in:
| Veröffentlicht in: | Journal of cancer research and clinical oncology 2023-02, Vol.149 (2), p.669-682 |
|---|---|
| Hauptverfasser: | , , , , , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 682 |
|---|---|
| container_issue | 2 |
| container_start_page | 669 |
| container_title | Journal of cancer research and clinical oncology |
| container_volume | 149 |
| creator | Torlot, Lucien Jarzab, Anna Albert, Johanna Pók-Udvari, Ágnes Stahler, Arndt Holch, Julian Walter Gerlinger, Marco Heinemann, Volker Klauschen, Frederick Kirchner, Thomas Kumbrink, Jörg Küster, Bernhard Jung, Andreas |
| description | Background
In metastatic colorectal cancer (mCRC), acquired resistance against anti-EGFR targeted monoclonal antibodies, such as cetuximab (CET), was shown to be frequently caused by activating alterations in the
RAS
genes
KRAS
or
NRAS
. To this day, no efficient follow-up treatment option has emerged to treat mCRC in such a setting of resistance.
Methods
To uncover potential targets for second-line targeted therapies, we used mass-spectrometric proteomics to shed light on kinome reprogramming in an established cellular model of acquired,
KRAS
-associated CET resistance.
Results
This CET resistance was reflected by significant changes in the kinome, most of them individual to each cell line. Interestingly, all investigated resistant cell lines displayed upregulation of the Ephrin type-A receptor 2 (EPHA2), a well-known driver of traits of progression. Expectedly resistant cell lines displayed increased migration (
p
|
| doi_str_mv | 10.1007/s00432-022-04416-0 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_9931833</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2738192515</sourcerecordid><originalsourceid>FETCH-LOGICAL-c474t-630d9060623fe71150a9ecbdf321e41841b85b75e4f80acb720ed2c42cf611cb3</originalsourceid><addsrcrecordid>eNp9kTtvFDEUhUcIRJbAH6BAlmhoBnz9nG2QoigQpEikgNryeO7sOpq1N7YnQJ0_Hg8bwqOgsCz7fD6-R6dpXgJ9C5Tqd5lSwVlLWV1CgGrpo2YFyxVwLh83KwoaWslAHTXPcr6i9Sw1e9occSUoKK5Xze1ligXjzrtM5uDiDSZydnl-wojNxJJ9FUPxdiKhShMpW0x2j3PxjhSbNliID8TFKSZ0pWLOBlctHE4TmXzATL75siXWXc8-4VCFMn_3O9uThNnnsuDPmyejnTK-uN-Pm68fzr6cnrcXnz9-Oj25aJ3QorSK02FNFVWMj6gBJLVrdP0wcgYooBPQd7LXEsXYUet6zSgOzAnmRgXgen7cvD_47ud-h4OryZKdzD7VedIPE603fyvBb80m3pj1mkPHeTV4c2-Q4vWMuZidz0tUGzDO2TDNO1gzCbKir_9Br-KcQo1XKa06JSVdKHagXIo5JxwfhgFqlo7NoWNTOzY_Oza0Pnr1Z4yHJ79KrQA_ALlKYYPp99__sb0Dvfa0ZQ</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2776865505</pqid></control><display><type>article</type><title>Proteomics uncover EPHA2 as a potential novel therapeutic target in colorectal cancer cell lines with acquired cetuximab resistance</title><source>MEDLINE</source><source>SpringerNature Journals</source><creator>Torlot, Lucien ; Jarzab, Anna ; Albert, Johanna ; Pók-Udvari, Ágnes ; Stahler, Arndt ; Holch, Julian Walter ; Gerlinger, Marco ; Heinemann, Volker ; Klauschen, Frederick ; Kirchner, Thomas ; Kumbrink, Jörg ; Küster, Bernhard ; Jung, Andreas</creator><creatorcontrib>Torlot, Lucien ; Jarzab, Anna ; Albert, Johanna ; Pók-Udvari, Ágnes ; Stahler, Arndt ; Holch, Julian Walter ; Gerlinger, Marco ; Heinemann, Volker ; Klauschen, Frederick ; Kirchner, Thomas ; Kumbrink, Jörg ; Küster, Bernhard ; Jung, Andreas</creatorcontrib><description>Background
In metastatic colorectal cancer (mCRC), acquired resistance against anti-EGFR targeted monoclonal antibodies, such as cetuximab (CET), was shown to be frequently caused by activating alterations in the
RAS
genes
KRAS
or
NRAS
. To this day, no efficient follow-up treatment option has emerged to treat mCRC in such a setting of resistance.
Methods
To uncover potential targets for second-line targeted therapies, we used mass-spectrometric proteomics to shed light on kinome reprogramming in an established cellular model of acquired,
KRAS
-associated CET resistance.
Results
This CET resistance was reflected by significant changes in the kinome, most of them individual to each cell line. Interestingly, all investigated resistant cell lines displayed upregulation of the Ephrin type-A receptor 2 (EPHA2), a well-known driver of traits of progression. Expectedly resistant cell lines displayed increased migration (
p
< 0.01) that was significantly reduced by targeting the EPHA2 signalling axis using RNA interference (RNAi) (
p
< 0.001), ephrin-A1 stimulation (
p
< 0.001), dasatinib (
p
< 0.01), or anti-EPHA2 antibody treatment (
p
< 0.001), identifying it as an actionable target in mCRC with acquired CET resistance.
Conclusion
These results highlight EPHA2 and its role in mCRC with
KRAS
-gene mutated acquired CET resistance and support its use as a potential actionable target for the development of future precision medicine therapies.</description><identifier>ISSN: 0171-5216</identifier><identifier>EISSN: 1432-1335</identifier><identifier>DOI: 10.1007/s00432-022-04416-0</identifier><identifier>PMID: 36401637</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer Berlin Heidelberg</publisher><subject>Antineoplastic Agents - therapeutic use ; Cancer Research ; Cell Line, Tumor ; Cell migration ; Cetuximab - pharmacology ; Colorectal cancer ; Colorectal carcinoma ; Colorectal Neoplasms - drug therapy ; Colorectal Neoplasms - genetics ; Colorectal Neoplasms - pathology ; Drug Resistance, Neoplasm - genetics ; EphA2 protein ; ErbB Receptors - genetics ; Hematology ; Humans ; Internal Medicine ; Medicine ; Medicine & Public Health ; Metastases ; Monoclonal antibodies ; Mutation ; Oncology ; Original Article – Cancer Research ; Original – Cancer Research ; Precision medicine ; Proteomics ; Proto-Oncogene Proteins p21(ras) - genetics ; RNA-mediated interference ; Targeted cancer therapy ; Therapeutic targets ; Tumor cell lines</subject><ispartof>Journal of cancer research and clinical oncology, 2023-02, Vol.149 (2), p.669-682</ispartof><rights>The Author(s) 2022</rights><rights>2022. The Author(s).</rights><rights>The Author(s) 2022. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c474t-630d9060623fe71150a9ecbdf321e41841b85b75e4f80acb720ed2c42cf611cb3</citedby><cites>FETCH-LOGICAL-c474t-630d9060623fe71150a9ecbdf321e41841b85b75e4f80acb720ed2c42cf611cb3</cites><orcidid>0000-0001-5270-9108</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00432-022-04416-0$$EPDF$$P50$$Gspringer$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00432-022-04416-0$$EHTML$$P50$$Gspringer$$Hfree_for_read</linktohtml><link.rule.ids>230,314,780,784,885,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/36401637$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Torlot, Lucien</creatorcontrib><creatorcontrib>Jarzab, Anna</creatorcontrib><creatorcontrib>Albert, Johanna</creatorcontrib><creatorcontrib>Pók-Udvari, Ágnes</creatorcontrib><creatorcontrib>Stahler, Arndt</creatorcontrib><creatorcontrib>Holch, Julian Walter</creatorcontrib><creatorcontrib>Gerlinger, Marco</creatorcontrib><creatorcontrib>Heinemann, Volker</creatorcontrib><creatorcontrib>Klauschen, Frederick</creatorcontrib><creatorcontrib>Kirchner, Thomas</creatorcontrib><creatorcontrib>Kumbrink, Jörg</creatorcontrib><creatorcontrib>Küster, Bernhard</creatorcontrib><creatorcontrib>Jung, Andreas</creatorcontrib><title>Proteomics uncover EPHA2 as a potential novel therapeutic target in colorectal cancer cell lines with acquired cetuximab resistance</title><title>Journal of cancer research and clinical oncology</title><addtitle>J Cancer Res Clin Oncol</addtitle><addtitle>J Cancer Res Clin Oncol</addtitle><description>Background
In metastatic colorectal cancer (mCRC), acquired resistance against anti-EGFR targeted monoclonal antibodies, such as cetuximab (CET), was shown to be frequently caused by activating alterations in the
RAS
genes
KRAS
or
NRAS
. To this day, no efficient follow-up treatment option has emerged to treat mCRC in such a setting of resistance.
Methods
To uncover potential targets for second-line targeted therapies, we used mass-spectrometric proteomics to shed light on kinome reprogramming in an established cellular model of acquired,
KRAS
-associated CET resistance.
Results
This CET resistance was reflected by significant changes in the kinome, most of them individual to each cell line. Interestingly, all investigated resistant cell lines displayed upregulation of the Ephrin type-A receptor 2 (EPHA2), a well-known driver of traits of progression. Expectedly resistant cell lines displayed increased migration (
p
< 0.01) that was significantly reduced by targeting the EPHA2 signalling axis using RNA interference (RNAi) (
p
< 0.001), ephrin-A1 stimulation (
p
< 0.001), dasatinib (
p
< 0.01), or anti-EPHA2 antibody treatment (
p
< 0.001), identifying it as an actionable target in mCRC with acquired CET resistance.
Conclusion
These results highlight EPHA2 and its role in mCRC with
KRAS
-gene mutated acquired CET resistance and support its use as a potential actionable target for the development of future precision medicine therapies.</description><subject>Antineoplastic Agents - therapeutic use</subject><subject>Cancer Research</subject><subject>Cell Line, Tumor</subject><subject>Cell migration</subject><subject>Cetuximab - pharmacology</subject><subject>Colorectal cancer</subject><subject>Colorectal carcinoma</subject><subject>Colorectal Neoplasms - drug therapy</subject><subject>Colorectal Neoplasms - genetics</subject><subject>Colorectal Neoplasms - pathology</subject><subject>Drug Resistance, Neoplasm - genetics</subject><subject>EphA2 protein</subject><subject>ErbB Receptors - genetics</subject><subject>Hematology</subject><subject>Humans</subject><subject>Internal Medicine</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Metastases</subject><subject>Monoclonal antibodies</subject><subject>Mutation</subject><subject>Oncology</subject><subject>Original Article – Cancer Research</subject><subject>Original – Cancer Research</subject><subject>Precision medicine</subject><subject>Proteomics</subject><subject>Proto-Oncogene Proteins p21(ras) - genetics</subject><subject>RNA-mediated interference</subject><subject>Targeted cancer therapy</subject><subject>Therapeutic targets</subject><subject>Tumor cell lines</subject><issn>0171-5216</issn><issn>1432-1335</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNp9kTtvFDEUhUcIRJbAH6BAlmhoBnz9nG2QoigQpEikgNryeO7sOpq1N7YnQJ0_Hg8bwqOgsCz7fD6-R6dpXgJ9C5Tqd5lSwVlLWV1CgGrpo2YFyxVwLh83KwoaWslAHTXPcr6i9Sw1e9occSUoKK5Xze1ligXjzrtM5uDiDSZydnl-wojNxJJ9FUPxdiKhShMpW0x2j3PxjhSbNliID8TFKSZ0pWLOBlctHE4TmXzATL75siXWXc8-4VCFMn_3O9uThNnnsuDPmyejnTK-uN-Pm68fzr6cnrcXnz9-Oj25aJ3QorSK02FNFVWMj6gBJLVrdP0wcgYooBPQd7LXEsXYUet6zSgOzAnmRgXgen7cvD_47ud-h4OryZKdzD7VedIPE603fyvBb80m3pj1mkPHeTV4c2-Q4vWMuZidz0tUGzDO2TDNO1gzCbKir_9Br-KcQo1XKa06JSVdKHagXIo5JxwfhgFqlo7NoWNTOzY_Oza0Pnr1Z4yHJ79KrQA_ALlKYYPp99__sb0Dvfa0ZQ</recordid><startdate>20230201</startdate><enddate>20230201</enddate><creator>Torlot, Lucien</creator><creator>Jarzab, Anna</creator><creator>Albert, Johanna</creator><creator>Pók-Udvari, Ágnes</creator><creator>Stahler, Arndt</creator><creator>Holch, Julian Walter</creator><creator>Gerlinger, Marco</creator><creator>Heinemann, Volker</creator><creator>Klauschen, Frederick</creator><creator>Kirchner, Thomas</creator><creator>Kumbrink, Jörg</creator><creator>Küster, Bernhard</creator><creator>Jung, Andreas</creator><general>Springer Berlin Heidelberg</general><general>Springer Nature B.V</general><scope>C6C</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>7TO</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0001-5270-9108</orcidid></search><sort><creationdate>20230201</creationdate><title>Proteomics uncover EPHA2 as a potential novel therapeutic target in colorectal cancer cell lines with acquired cetuximab resistance</title><author>Torlot, Lucien ; Jarzab, Anna ; Albert, Johanna ; Pók-Udvari, Ágnes ; Stahler, Arndt ; Holch, Julian Walter ; Gerlinger, Marco ; Heinemann, Volker ; Klauschen, Frederick ; Kirchner, Thomas ; Kumbrink, Jörg ; Küster, Bernhard ; Jung, Andreas</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c474t-630d9060623fe71150a9ecbdf321e41841b85b75e4f80acb720ed2c42cf611cb3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Antineoplastic Agents - therapeutic use</topic><topic>Cancer Research</topic><topic>Cell Line, Tumor</topic><topic>Cell migration</topic><topic>Cetuximab - pharmacology</topic><topic>Colorectal cancer</topic><topic>Colorectal carcinoma</topic><topic>Colorectal Neoplasms - drug therapy</topic><topic>Colorectal Neoplasms - genetics</topic><topic>Colorectal Neoplasms - pathology</topic><topic>Drug Resistance, Neoplasm - genetics</topic><topic>EphA2 protein</topic><topic>ErbB Receptors - genetics</topic><topic>Hematology</topic><topic>Humans</topic><topic>Internal Medicine</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Metastases</topic><topic>Monoclonal antibodies</topic><topic>Mutation</topic><topic>Oncology</topic><topic>Original Article – Cancer Research</topic><topic>Original – Cancer Research</topic><topic>Precision medicine</topic><topic>Proteomics</topic><topic>Proto-Oncogene Proteins p21(ras) - genetics</topic><topic>RNA-mediated interference</topic><topic>Targeted cancer therapy</topic><topic>Therapeutic targets</topic><topic>Tumor cell lines</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Torlot, Lucien</creatorcontrib><creatorcontrib>Jarzab, Anna</creatorcontrib><creatorcontrib>Albert, Johanna</creatorcontrib><creatorcontrib>Pók-Udvari, Ágnes</creatorcontrib><creatorcontrib>Stahler, Arndt</creatorcontrib><creatorcontrib>Holch, Julian Walter</creatorcontrib><creatorcontrib>Gerlinger, Marco</creatorcontrib><creatorcontrib>Heinemann, Volker</creatorcontrib><creatorcontrib>Klauschen, Frederick</creatorcontrib><creatorcontrib>Kirchner, Thomas</creatorcontrib><creatorcontrib>Kumbrink, Jörg</creatorcontrib><creatorcontrib>Küster, Bernhard</creatorcontrib><creatorcontrib>Jung, Andreas</creatorcontrib><collection>Springer Nature OA/Free Journals</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>Oncogenes and Growth Factors 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>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</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>Research Library Prep</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Research Library (Corporate)</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>PubMed Central (Full Participant titles)</collection><jtitle>Journal of cancer research and clinical oncology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Torlot, Lucien</au><au>Jarzab, Anna</au><au>Albert, Johanna</au><au>Pók-Udvari, Ágnes</au><au>Stahler, Arndt</au><au>Holch, Julian Walter</au><au>Gerlinger, Marco</au><au>Heinemann, Volker</au><au>Klauschen, Frederick</au><au>Kirchner, Thomas</au><au>Kumbrink, Jörg</au><au>Küster, Bernhard</au><au>Jung, Andreas</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Proteomics uncover EPHA2 as a potential novel therapeutic target in colorectal cancer cell lines with acquired cetuximab resistance</atitle><jtitle>Journal of cancer research and clinical oncology</jtitle><stitle>J Cancer Res Clin Oncol</stitle><addtitle>J Cancer Res Clin Oncol</addtitle><date>2023-02-01</date><risdate>2023</risdate><volume>149</volume><issue>2</issue><spage>669</spage><epage>682</epage><pages>669-682</pages><issn>0171-5216</issn><eissn>1432-1335</eissn><abstract>Background
In metastatic colorectal cancer (mCRC), acquired resistance against anti-EGFR targeted monoclonal antibodies, such as cetuximab (CET), was shown to be frequently caused by activating alterations in the
RAS
genes
KRAS
or
NRAS
. To this day, no efficient follow-up treatment option has emerged to treat mCRC in such a setting of resistance.
Methods
To uncover potential targets for second-line targeted therapies, we used mass-spectrometric proteomics to shed light on kinome reprogramming in an established cellular model of acquired,
KRAS
-associated CET resistance.
Results
This CET resistance was reflected by significant changes in the kinome, most of them individual to each cell line. Interestingly, all investigated resistant cell lines displayed upregulation of the Ephrin type-A receptor 2 (EPHA2), a well-known driver of traits of progression. Expectedly resistant cell lines displayed increased migration (
p
< 0.01) that was significantly reduced by targeting the EPHA2 signalling axis using RNA interference (RNAi) (
p
< 0.001), ephrin-A1 stimulation (
p
< 0.001), dasatinib (
p
< 0.01), or anti-EPHA2 antibody treatment (
p
< 0.001), identifying it as an actionable target in mCRC with acquired CET resistance.
Conclusion
These results highlight EPHA2 and its role in mCRC with
KRAS
-gene mutated acquired CET resistance and support its use as a potential actionable target for the development of future precision medicine therapies.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer Berlin Heidelberg</pub><pmid>36401637</pmid><doi>10.1007/s00432-022-04416-0</doi><tpages>14</tpages><orcidid>https://orcid.org/0000-0001-5270-9108</orcidid><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0171-5216 |
| ispartof | Journal of cancer research and clinical oncology, 2023-02, Vol.149 (2), p.669-682 |
| issn | 0171-5216 1432-1335 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_9931833 |
| source | MEDLINE; SpringerNature Journals |
| subjects | Antineoplastic Agents - therapeutic use Cancer Research Cell Line, Tumor Cell migration Cetuximab - pharmacology Colorectal cancer Colorectal carcinoma Colorectal Neoplasms - drug therapy Colorectal Neoplasms - genetics Colorectal Neoplasms - pathology Drug Resistance, Neoplasm - genetics EphA2 protein ErbB Receptors - genetics Hematology Humans Internal Medicine Medicine Medicine & Public Health Metastases Monoclonal antibodies Mutation Oncology Original Article – Cancer Research Original – Cancer Research Precision medicine Proteomics Proto-Oncogene Proteins p21(ras) - genetics RNA-mediated interference Targeted cancer therapy Therapeutic targets Tumor cell lines |
| title | Proteomics uncover EPHA2 as a potential novel therapeutic target in colorectal cancer cell lines with acquired cetuximab resistance |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-21T08%3A15%3A44IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Proteomics%20uncover%20EPHA2%20as%20a%20potential%20novel%20therapeutic%20target%20in%20colorectal%20cancer%20cell%20lines%20with%20acquired%20cetuximab%20resistance&rft.jtitle=Journal%20of%20cancer%20research%20and%20clinical%20oncology&rft.au=Torlot,%20Lucien&rft.date=2023-02-01&rft.volume=149&rft.issue=2&rft.spage=669&rft.epage=682&rft.pages=669-682&rft.issn=0171-5216&rft.eissn=1432-1335&rft_id=info:doi/10.1007/s00432-022-04416-0&rft_dat=%3Cproquest_pubme%3E2738192515%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2776865505&rft_id=info:pmid/36401637&rfr_iscdi=true |