Src inhibitors in early breast cancer: a methodology, feasibility and variability study
Early clinical trials of anticancer agents may be enriched by robust biomarkers of activity. Surrogate measures used in trials of cytotoxic agents, such as tumor size regression, may not be informative when investigating targeted agents that act principally to inhibit invasion or proliferation. This...
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| Veröffentlicht in: | Breast cancer research and treatment 2009-03, Vol.114 (2), p.211-221 |
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| creator | Jones, R. J Young, O Renshaw, L Jacobs, V Fennell, M Marshall, A Green, T. P Elvin, P Womack, C Clack, G Dixon, J. M |
| description | Early clinical trials of anticancer agents may be enriched by robust biomarkers of activity. Surrogate measures used in trials of cytotoxic agents, such as tumor size regression, may not be informative when investigating targeted agents that act principally to inhibit invasion or proliferation. This study aimed to determine the validity of invasion-related biomarkers of activity for AZD0530, a potent Src inhibitor currently in clinical development. Focal adhesion kinase (FAK) and paxillin are downstream phosphorylation substrates of Src and mediate tumor cell adhesion and invasiveness. These were therefore selected as biologically relevant markers of Src inhibition. Early breast cancer was chosen as a model as multiple samples can be collected during standard treatment and there is an intervening period in which experimental intervention can be applied. Tumor tissue was collected from diagnostic core biopsies and subsequent surgical tumor excision samples in 29 women with early breast cancer attending a single center. Protein levels were assessed quantitatively by Luminex® and qualitatively by immunohistochemistry. AZD0530 inhibited tumor growth in a manner independent of dose and inhibited phosphorylation of FAK and paxillin in a dose-dependent manner in a Calu-6 xenograft model. In the clinical study, agreement of within-visit and also of between-visit measurements was high and the estimated number of patients required to detect a drug effect would be low enough to allow use of these markers as endpoints in future dose selection studies. |
| doi_str_mv | 10.1007/s10549-008-9997-1 |
| format | Article |
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J ; Young, O ; Renshaw, L ; Jacobs, V ; Fennell, M ; Marshall, A ; Green, T. P ; Elvin, P ; Womack, C ; Clack, G ; Dixon, J. M</creator><creatorcontrib>Jones, R. J ; Young, O ; Renshaw, L ; Jacobs, V ; Fennell, M ; Marshall, A ; Green, T. P ; Elvin, P ; Womack, C ; Clack, G ; Dixon, J. M</creatorcontrib><description>Early clinical trials of anticancer agents may be enriched by robust biomarkers of activity. Surrogate measures used in trials of cytotoxic agents, such as tumor size regression, may not be informative when investigating targeted agents that act principally to inhibit invasion or proliferation. This study aimed to determine the validity of invasion-related biomarkers of activity for AZD0530, a potent Src inhibitor currently in clinical development. Focal adhesion kinase (FAK) and paxillin are downstream phosphorylation substrates of Src and mediate tumor cell adhesion and invasiveness. These were therefore selected as biologically relevant markers of Src inhibition. Early breast cancer was chosen as a model as multiple samples can be collected during standard treatment and there is an intervening period in which experimental intervention can be applied. Tumor tissue was collected from diagnostic core biopsies and subsequent surgical tumor excision samples in 29 women with early breast cancer attending a single center. Protein levels were assessed quantitatively by Luminex® and qualitatively by immunohistochemistry. AZD0530 inhibited tumor growth in a manner independent of dose and inhibited phosphorylation of FAK and paxillin in a dose-dependent manner in a Calu-6 xenograft model. In the clinical study, agreement of within-visit and also of between-visit measurements was high and the estimated number of patients required to detect a drug effect would be low enough to allow use of these markers as endpoints in future dose selection studies.</description><identifier>ISSN: 0167-6806</identifier><identifier>EISSN: 1573-7217</identifier><identifier>DOI: 10.1007/s10549-008-9997-1</identifier><identifier>PMID: 18409068</identifier><identifier>CODEN: BCTRD6</identifier><language>eng</language><publisher>Boston: Boston : Springer US</publisher><subject>Animals ; AZD0530 ; Benzodioxoles - pharmacology ; Biological and medical sciences ; Breast cancer ; Breast Neoplasms - drug therapy ; Breast Neoplasms - metabolism ; Breast Neoplasms - pathology ; Cancer research ; Cancer therapies ; Early breast cancer ; Feasibility Studies ; Female ; Focal adhesion kinase ; Focal Adhesion Kinase 1 - metabolism ; Genes ; Gynecology. Andrology. Obstetrics ; Humans ; Immunoenzyme Techniques ; immunohistochemistry ; Inhibitor drugs ; Lung Neoplasms - drug therapy ; Lung Neoplasms - metabolism ; Lung Neoplasms - pathology ; Mammary gland diseases ; Medical sciences ; Medicine ; Medicine & Public Health ; Oncology ; Paxillin ; Paxillin - metabolism ; phosphorylation ; Phosphorylation - drug effects ; Preclinical Study ; Protein-Tyrosine Kinases - antagonists & inhibitors ; Quinazolines - pharmacology ; Rats ; Rats, Nude ; Src kinase ; src-Family Kinases ; Tumor Cells, Cultured ; Tumors ; Xenograft Model Antitumor Assays</subject><ispartof>Breast cancer research and treatment, 2009-03, Vol.114 (2), p.211-221</ispartof><rights>Springer Science+Business Media, LLC. 2008</rights><rights>2009 INIST-CNRS</rights><rights>Springer Science+Business Media, LLC. 2009</rights><rights>Distributed under a Creative Commons Attribution 4.0 International License</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c500t-5b347e1cdea445d036005531dfdeed85cc7f5b5066efb6428f5abfe50c68692e3</citedby><cites>FETCH-LOGICAL-c500t-5b347e1cdea445d036005531dfdeed85cc7f5b5066efb6428f5abfe50c68692e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s10549-008-9997-1$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s10549-008-9997-1$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>230,314,780,784,885,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=21127832$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18409068$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://hal.science/hal-00478335$$DView record in HAL$$Hfree_for_read</backlink></links><search><creatorcontrib>Jones, R. J</creatorcontrib><creatorcontrib>Young, O</creatorcontrib><creatorcontrib>Renshaw, L</creatorcontrib><creatorcontrib>Jacobs, V</creatorcontrib><creatorcontrib>Fennell, M</creatorcontrib><creatorcontrib>Marshall, A</creatorcontrib><creatorcontrib>Green, T. P</creatorcontrib><creatorcontrib>Elvin, P</creatorcontrib><creatorcontrib>Womack, C</creatorcontrib><creatorcontrib>Clack, G</creatorcontrib><creatorcontrib>Dixon, J. M</creatorcontrib><title>Src inhibitors in early breast cancer: a methodology, feasibility and variability study</title><title>Breast cancer research and treatment</title><addtitle>Breast Cancer Res Treat</addtitle><addtitle>Breast Cancer Res Treat</addtitle><description>Early clinical trials of anticancer agents may be enriched by robust biomarkers of activity. Surrogate measures used in trials of cytotoxic agents, such as tumor size regression, may not be informative when investigating targeted agents that act principally to inhibit invasion or proliferation. This study aimed to determine the validity of invasion-related biomarkers of activity for AZD0530, a potent Src inhibitor currently in clinical development. Focal adhesion kinase (FAK) and paxillin are downstream phosphorylation substrates of Src and mediate tumor cell adhesion and invasiveness. These were therefore selected as biologically relevant markers of Src inhibition. Early breast cancer was chosen as a model as multiple samples can be collected during standard treatment and there is an intervening period in which experimental intervention can be applied. Tumor tissue was collected from diagnostic core biopsies and subsequent surgical tumor excision samples in 29 women with early breast cancer attending a single center. Protein levels were assessed quantitatively by Luminex® and qualitatively by immunohistochemistry. AZD0530 inhibited tumor growth in a manner independent of dose and inhibited phosphorylation of FAK and paxillin in a dose-dependent manner in a Calu-6 xenograft model. In the clinical study, agreement of within-visit and also of between-visit measurements was high and the estimated number of patients required to detect a drug effect would be low enough to allow use of these markers as endpoints in future dose selection studies.</description><subject>Animals</subject><subject>AZD0530</subject><subject>Benzodioxoles - pharmacology</subject><subject>Biological and medical sciences</subject><subject>Breast cancer</subject><subject>Breast Neoplasms - drug therapy</subject><subject>Breast Neoplasms - metabolism</subject><subject>Breast Neoplasms - pathology</subject><subject>Cancer research</subject><subject>Cancer therapies</subject><subject>Early breast cancer</subject><subject>Feasibility Studies</subject><subject>Female</subject><subject>Focal adhesion kinase</subject><subject>Focal Adhesion Kinase 1 - metabolism</subject><subject>Genes</subject><subject>Gynecology. Andrology. Obstetrics</subject><subject>Humans</subject><subject>Immunoenzyme Techniques</subject><subject>immunohistochemistry</subject><subject>Inhibitor drugs</subject><subject>Lung Neoplasms - drug therapy</subject><subject>Lung Neoplasms - metabolism</subject><subject>Lung Neoplasms - pathology</subject><subject>Mammary gland diseases</subject><subject>Medical sciences</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Oncology</subject><subject>Paxillin</subject><subject>Paxillin - metabolism</subject><subject>phosphorylation</subject><subject>Phosphorylation - drug effects</subject><subject>Preclinical Study</subject><subject>Protein-Tyrosine Kinases - antagonists & inhibitors</subject><subject>Quinazolines - pharmacology</subject><subject>Rats</subject><subject>Rats, Nude</subject><subject>Src kinase</subject><subject>src-Family Kinases</subject><subject>Tumor Cells, Cultured</subject><subject>Tumors</subject><subject>Xenograft Model Antitumor Assays</subject><issn>0167-6806</issn><issn>1573-7217</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><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>eNp9kU1v1DAQhi0EotvCD-ACERJISARm7Pgj3KqqUKSVOJSKo-U49m6qbNzaSaX8e7xK1EocOPljnpl5Z15C3iB8QQD5NSHwqi4BVFnXtSzxGdkgl6yUFOVzsgEUshQKxAk5TekWAGoJ9UtygqqCGoTakD_X0RbdsO-abgwx5WvhTOznoonOpLGwZrAufitMcXDjPrShD7v5c-FzMKf03TgXZmiLBxM7s77TOLXzK_LCmz651-t5Rm6-X_6-uCq3v378vDjflpYDjCVvWCUd2taZquItMAHAOcPWt861ilsrPW84COF8IyqqPDeNdxysUKKmjp2RT0vdven1XewOJs46mE5fnW_18Q-gkoox_oCZ_biwdzHcTy6N-tAl6_reDC5MSQuhlADKMvj-H_A2THHIc2iKtMpyUGYIF8jGkFJ0_rE9gj7aoxd7sgKlj_boo4K3a-GpObj2KWP1IwMfVsAka3of8_q79MhRRJqnoZmjC5dyaNi5-KTwf93fLUneBG12MRe-uaaADJDXwPKW_gIhZ6_Y</recordid><startdate>20090301</startdate><enddate>20090301</enddate><creator>Jones, R. 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Obstetrics</topic><topic>Humans</topic><topic>Immunoenzyme Techniques</topic><topic>immunohistochemistry</topic><topic>Inhibitor drugs</topic><topic>Lung Neoplasms - drug therapy</topic><topic>Lung Neoplasms - metabolism</topic><topic>Lung Neoplasms - pathology</topic><topic>Mammary gland diseases</topic><topic>Medical sciences</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Oncology</topic><topic>Paxillin</topic><topic>Paxillin - metabolism</topic><topic>phosphorylation</topic><topic>Phosphorylation - drug effects</topic><topic>Preclinical Study</topic><topic>Protein-Tyrosine Kinases - antagonists & inhibitors</topic><topic>Quinazolines - pharmacology</topic><topic>Rats</topic><topic>Rats, Nude</topic><topic>Src kinase</topic><topic>src-Family Kinases</topic><topic>Tumor Cells, Cultured</topic><topic>Tumors</topic><topic>Xenograft Model Antitumor Assays</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Jones, R. 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J</au><au>Young, O</au><au>Renshaw, L</au><au>Jacobs, V</au><au>Fennell, M</au><au>Marshall, A</au><au>Green, T. P</au><au>Elvin, P</au><au>Womack, C</au><au>Clack, G</au><au>Dixon, J. M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Src inhibitors in early breast cancer: a methodology, feasibility and variability study</atitle><jtitle>Breast cancer research and treatment</jtitle><stitle>Breast Cancer Res Treat</stitle><addtitle>Breast Cancer Res Treat</addtitle><date>2009-03-01</date><risdate>2009</risdate><volume>114</volume><issue>2</issue><spage>211</spage><epage>221</epage><pages>211-221</pages><issn>0167-6806</issn><eissn>1573-7217</eissn><coden>BCTRD6</coden><abstract>Early clinical trials of anticancer agents may be enriched by robust biomarkers of activity. Surrogate measures used in trials of cytotoxic agents, such as tumor size regression, may not be informative when investigating targeted agents that act principally to inhibit invasion or proliferation. This study aimed to determine the validity of invasion-related biomarkers of activity for AZD0530, a potent Src inhibitor currently in clinical development. Focal adhesion kinase (FAK) and paxillin are downstream phosphorylation substrates of Src and mediate tumor cell adhesion and invasiveness. These were therefore selected as biologically relevant markers of Src inhibition. Early breast cancer was chosen as a model as multiple samples can be collected during standard treatment and there is an intervening period in which experimental intervention can be applied. Tumor tissue was collected from diagnostic core biopsies and subsequent surgical tumor excision samples in 29 women with early breast cancer attending a single center. Protein levels were assessed quantitatively by Luminex® and qualitatively by immunohistochemistry. AZD0530 inhibited tumor growth in a manner independent of dose and inhibited phosphorylation of FAK and paxillin in a dose-dependent manner in a Calu-6 xenograft model. In the clinical study, agreement of within-visit and also of between-visit measurements was high and the estimated number of patients required to detect a drug effect would be low enough to allow use of these markers as endpoints in future dose selection studies.</abstract><cop>Boston</cop><pub>Boston : Springer US</pub><pmid>18409068</pmid><doi>10.1007/s10549-008-9997-1</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Breast cancer research and treatment, 2009-03, Vol.114 (2), p.211-221 |
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| language | eng |
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| source | MEDLINE; SpringerLink Journals - AutoHoldings |
| subjects | Animals AZD0530 Benzodioxoles - pharmacology Biological and medical sciences Breast cancer Breast Neoplasms - drug therapy Breast Neoplasms - metabolism Breast Neoplasms - pathology Cancer research Cancer therapies Early breast cancer Feasibility Studies Female Focal adhesion kinase Focal Adhesion Kinase 1 - metabolism Genes Gynecology. Andrology. Obstetrics Humans Immunoenzyme Techniques immunohistochemistry Inhibitor drugs Lung Neoplasms - drug therapy Lung Neoplasms - metabolism Lung Neoplasms - pathology Mammary gland diseases Medical sciences Medicine Medicine & Public Health Oncology Paxillin Paxillin - metabolism phosphorylation Phosphorylation - drug effects Preclinical Study Protein-Tyrosine Kinases - antagonists & inhibitors Quinazolines - pharmacology Rats Rats, Nude Src kinase src-Family Kinases Tumor Cells, Cultured Tumors Xenograft Model Antitumor Assays |
| title | Src inhibitors in early breast cancer: a methodology, feasibility and variability study |
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