Promoter methylation status of VEGF receptor genes: A possible epigenetic biomarker to anticipate the efficacy of intracellular-acting VEGF-targeted drugs in cancer cells
We evaluated whether the inhibitory effects of vascular endothelial growth factor (VEGF)-targeted drugs on the proliferation of cancer cells differed according to VEGF receptor (VEGFR) genes, Flt1 and KDR, promoter methylation status. Five hyper-VEGFR-methylation and six no-VEGFR-methylation cancer...
Gespeichert in:
| Veröffentlicht in: | Epigenetics 2012-02, Vol.7 (2), p.191-200 |
|---|---|
| Hauptverfasser: | , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 200 |
|---|---|
| container_issue | 2 |
| container_start_page | 191 |
| container_title | Epigenetics |
| container_volume | 7 |
| creator | Kim, Jeeyeon Hwang, Junha Jeong, Hyeseon Song, Hee-Jung Shin, Jieun Hur, Gangmin Park, Young Woo Lee, Suk Hoon Kim, Jei |
| description | We evaluated whether the inhibitory effects of vascular endothelial growth factor (VEGF)-targeted drugs on the proliferation of cancer cells differed according to VEGF receptor (VEGFR) genes, Flt1 and KDR, promoter methylation status. Five hyper-VEGFR-methylation and six no-VEGFR-methylation cancer cells were used for the present study, together with human umbilical endothelial cells (HUVECs) as a control. No-VEGFR-methylation cancer cells showed higher expression of Flt1 and KDR than hyper-VEGFR-methylation cancer cells. Hyper-VEGFR-methylation cancer cells only showed increased expression and protein levels of Flt1 and KDR after treatment with the demethylase 5-aza-2'-deoxycytidine. Two drugs (a VEGF-specific-antibody, bevacizumab, and a KDR-specific-antibody) targeting extracellular VEGF-VEGFR signaling and two VEGF-specific-tyrosine kinase inhibitors (PTK/ZK and sunitinib) targeting intracellular VEGFR signaling were used in the cell proliferation assay. HUVECs showed dose- and time-dependent proliferation decrease with all tested drugs over a 72 h incubation period. No- or hyper-VEGFR-methylation cancer cells showed no significant proliferation differences after treatment with VEGF-specific-antibody or VEGFR2-specific-antibody. After PTK/ZK or sunitinib treatment, no-VEGFR-methylation cancer cells showed dose- or time-dependent decreases in proliferation. Hyper-VEGFR-methylation cancer cells also showed proliferation inhibition by VEGF-specific-tyrosine kinase inhibitors after demethylation of Flt1 and KDR. Proliferation inhibition synergistically increased after combination of demethylation with PTK/ZK in hyper-VEGF-methylation cancer cells. We observed that intracellular targeting of VEGF-VEGFR signaling could be more effective than extracellular targeting of the pathway in the suppression of proliferation of some cancer cells. In particular, the efficacy of intracellular targeting of VEGF-specific-tyrosine kinase inhibitors might be influenced by the epigenetic alteration of VEGFRs. |
| doi_str_mv | 10.4161/epi.7.2.18973 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_926878949</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>926878949</sourcerecordid><originalsourceid>FETCH-LOGICAL-c534t-8b7c0b850b9f1ccffa000769f4033d52a1207426871e5ba81d39f88293d737103</originalsourceid><addsrcrecordid>eNqFkU1v1DAQhiMEoqVw5Ip845TFH_mwuVXVtlRUogfgak2c8daQxMF2hPYv8Stxuu32gsRprNEz74zftyjeMrqpWMM-4Ow27YZvmFSteFacsrpWJRdUPn98c1WdFK9i_EFpJRqlXhYnnAtVV406Lf7cBj_6hIGMmO72AyTnJxITpCUSb8n37dUlCWhwTj6QHU4YP5JzMvsYXTcgyevXZnKGdM6PEH5mqeQJTLnlZkhI0l3GrHUGzH6VdFMKYHAYlgFCCSa5aXe_p0wQdpiwJ31YdjGDxMBksuBKx9fFCwtDxDcP9az4drn9evGpvPlydX1xflOaWlSplF1raCdr2inLjLEWKKVto2xFhehrDozTtuKNbBnWHUjWC2Wl5Er0rWgZFWfF-4PuHPyvBWPSo4vrBTChX6JW66xUlcpkeSBNyH4EtHoOLnuw14zqNR2d7dGt5vo-ncy_e1BeuhH7I_0Yx5Ng3tVjzI5G4zBbcEQ_u3F7e71Kzr3NvPoP_5RP1BByGfB4jDzMusn6MMJvH4ZeJ9gPPtiQfXdRi3__4y_58cd8</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>926878949</pqid></control><display><type>article</type><title>Promoter methylation status of VEGF receptor genes: A possible epigenetic biomarker to anticipate the efficacy of intracellular-acting VEGF-targeted drugs in cancer cells</title><source>MEDLINE</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>PubMed Central</source><creator>Kim, Jeeyeon ; Hwang, Junha ; Jeong, Hyeseon ; Song, Hee-Jung ; Shin, Jieun ; Hur, Gangmin ; Park, Young Woo ; Lee, Suk Hoon ; Kim, Jei</creator><creatorcontrib>Kim, Jeeyeon ; Hwang, Junha ; Jeong, Hyeseon ; Song, Hee-Jung ; Shin, Jieun ; Hur, Gangmin ; Park, Young Woo ; Lee, Suk Hoon ; Kim, Jei</creatorcontrib><description>We evaluated whether the inhibitory effects of vascular endothelial growth factor (VEGF)-targeted drugs on the proliferation of cancer cells differed according to VEGF receptor (VEGFR) genes, Flt1 and KDR, promoter methylation status. Five hyper-VEGFR-methylation and six no-VEGFR-methylation cancer cells were used for the present study, together with human umbilical endothelial cells (HUVECs) as a control. No-VEGFR-methylation cancer cells showed higher expression of Flt1 and KDR than hyper-VEGFR-methylation cancer cells. Hyper-VEGFR-methylation cancer cells only showed increased expression and protein levels of Flt1 and KDR after treatment with the demethylase 5-aza-2'-deoxycytidine. Two drugs (a VEGF-specific-antibody, bevacizumab, and a KDR-specific-antibody) targeting extracellular VEGF-VEGFR signaling and two VEGF-specific-tyrosine kinase inhibitors (PTK/ZK and sunitinib) targeting intracellular VEGFR signaling were used in the cell proliferation assay. HUVECs showed dose- and time-dependent proliferation decrease with all tested drugs over a 72 h incubation period. No- or hyper-VEGFR-methylation cancer cells showed no significant proliferation differences after treatment with VEGF-specific-antibody or VEGFR2-specific-antibody. After PTK/ZK or sunitinib treatment, no-VEGFR-methylation cancer cells showed dose- or time-dependent decreases in proliferation. Hyper-VEGFR-methylation cancer cells also showed proliferation inhibition by VEGF-specific-tyrosine kinase inhibitors after demethylation of Flt1 and KDR. Proliferation inhibition synergistically increased after combination of demethylation with PTK/ZK in hyper-VEGF-methylation cancer cells. We observed that intracellular targeting of VEGF-VEGFR signaling could be more effective than extracellular targeting of the pathway in the suppression of proliferation of some cancer cells. In particular, the efficacy of intracellular targeting of VEGF-specific-tyrosine kinase inhibitors might be influenced by the epigenetic alteration of VEGFRs.</description><identifier>ISSN: 1559-2294</identifier><identifier>EISSN: 1559-2308</identifier><identifier>DOI: 10.4161/epi.7.2.18973</identifier><identifier>PMID: 22395469</identifier><language>eng</language><publisher>United States: Taylor & Francis</publisher><subject>Antineoplastic Agents - pharmacology ; Antineoplastic Agents - therapeutic use ; Binding ; Biology ; Biomarkers, Tumor - genetics ; Bioscience ; Calcium ; Cancer ; Cell ; Cell Line, Tumor ; Cell Proliferation - drug effects ; CpG Islands - genetics ; Cycle ; DNA Methylation - drug effects ; DNA Methylation - genetics ; Epigenesis, Genetic - drug effects ; epigenetic change ; Extracellular Signal-Regulated MAP Kinases - metabolism ; Flt1 ; Human Umbilical Vein Endothelial Cells - metabolism ; Humans ; Intracellular Space - drug effects ; Intracellular Space - metabolism ; KDR ; Landes ; Molecular Targeted Therapy ; Neoplasms - drug therapy ; Neoplasms - enzymology ; Neoplasms - genetics ; Neoplasms - pathology ; Organogenesis ; Phosphorylation - drug effects ; promoter hypermethylation ; Promoter Regions, Genetic - genetics ; Protein Kinase Inhibitors - pharmacology ; Protein Kinase Inhibitors - therapeutic use ; Proteins ; Proto-Oncogene Proteins c-akt - metabolism ; Receptors, Vascular Endothelial Growth Factor - genetics ; Treatment Outcome ; vascular endothelial growth factor (VEGF) ; Vascular Endothelial Growth Factor A - antagonists & inhibitors ; Vascular Endothelial Growth Factor A - metabolism ; VEGF receptor (VEGFR) ; VEGF-specific antibody ; VEGF-specific tyrosine kinase inhibitor ; VEGF-targeted drug ; VEGFR2-specific antibody</subject><ispartof>Epigenetics, 2012-02, Vol.7 (2), p.191-200</ispartof><rights>Copyright © 2012 Landes Bioscience 2012</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c534t-8b7c0b850b9f1ccffa000769f4033d52a1207426871e5ba81d39f88293d737103</citedby><cites>FETCH-LOGICAL-c534t-8b7c0b850b9f1ccffa000769f4033d52a1207426871e5ba81d39f88293d737103</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27923,27924</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22395469$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kim, Jeeyeon</creatorcontrib><creatorcontrib>Hwang, Junha</creatorcontrib><creatorcontrib>Jeong, Hyeseon</creatorcontrib><creatorcontrib>Song, Hee-Jung</creatorcontrib><creatorcontrib>Shin, Jieun</creatorcontrib><creatorcontrib>Hur, Gangmin</creatorcontrib><creatorcontrib>Park, Young Woo</creatorcontrib><creatorcontrib>Lee, Suk Hoon</creatorcontrib><creatorcontrib>Kim, Jei</creatorcontrib><title>Promoter methylation status of VEGF receptor genes: A possible epigenetic biomarker to anticipate the efficacy of intracellular-acting VEGF-targeted drugs in cancer cells</title><title>Epigenetics</title><addtitle>Epigenetics</addtitle><description>We evaluated whether the inhibitory effects of vascular endothelial growth factor (VEGF)-targeted drugs on the proliferation of cancer cells differed according to VEGF receptor (VEGFR) genes, Flt1 and KDR, promoter methylation status. Five hyper-VEGFR-methylation and six no-VEGFR-methylation cancer cells were used for the present study, together with human umbilical endothelial cells (HUVECs) as a control. No-VEGFR-methylation cancer cells showed higher expression of Flt1 and KDR than hyper-VEGFR-methylation cancer cells. Hyper-VEGFR-methylation cancer cells only showed increased expression and protein levels of Flt1 and KDR after treatment with the demethylase 5-aza-2'-deoxycytidine. Two drugs (a VEGF-specific-antibody, bevacizumab, and a KDR-specific-antibody) targeting extracellular VEGF-VEGFR signaling and two VEGF-specific-tyrosine kinase inhibitors (PTK/ZK and sunitinib) targeting intracellular VEGFR signaling were used in the cell proliferation assay. HUVECs showed dose- and time-dependent proliferation decrease with all tested drugs over a 72 h incubation period. No- or hyper-VEGFR-methylation cancer cells showed no significant proliferation differences after treatment with VEGF-specific-antibody or VEGFR2-specific-antibody. After PTK/ZK or sunitinib treatment, no-VEGFR-methylation cancer cells showed dose- or time-dependent decreases in proliferation. Hyper-VEGFR-methylation cancer cells also showed proliferation inhibition by VEGF-specific-tyrosine kinase inhibitors after demethylation of Flt1 and KDR. Proliferation inhibition synergistically increased after combination of demethylation with PTK/ZK in hyper-VEGF-methylation cancer cells. We observed that intracellular targeting of VEGF-VEGFR signaling could be more effective than extracellular targeting of the pathway in the suppression of proliferation of some cancer cells. In particular, the efficacy of intracellular targeting of VEGF-specific-tyrosine kinase inhibitors might be influenced by the epigenetic alteration of VEGFRs.</description><subject>Antineoplastic Agents - pharmacology</subject><subject>Antineoplastic Agents - therapeutic use</subject><subject>Binding</subject><subject>Biology</subject><subject>Biomarkers, Tumor - genetics</subject><subject>Bioscience</subject><subject>Calcium</subject><subject>Cancer</subject><subject>Cell</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation - drug effects</subject><subject>CpG Islands - genetics</subject><subject>Cycle</subject><subject>DNA Methylation - drug effects</subject><subject>DNA Methylation - genetics</subject><subject>Epigenesis, Genetic - drug effects</subject><subject>epigenetic change</subject><subject>Extracellular Signal-Regulated MAP Kinases - metabolism</subject><subject>Flt1</subject><subject>Human Umbilical Vein Endothelial Cells - metabolism</subject><subject>Humans</subject><subject>Intracellular Space - drug effects</subject><subject>Intracellular Space - metabolism</subject><subject>KDR</subject><subject>Landes</subject><subject>Molecular Targeted Therapy</subject><subject>Neoplasms - drug therapy</subject><subject>Neoplasms - enzymology</subject><subject>Neoplasms - genetics</subject><subject>Neoplasms - pathology</subject><subject>Organogenesis</subject><subject>Phosphorylation - drug effects</subject><subject>promoter hypermethylation</subject><subject>Promoter Regions, Genetic - genetics</subject><subject>Protein Kinase Inhibitors - pharmacology</subject><subject>Protein Kinase Inhibitors - therapeutic use</subject><subject>Proteins</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Receptors, Vascular Endothelial Growth Factor - genetics</subject><subject>Treatment Outcome</subject><subject>vascular endothelial growth factor (VEGF)</subject><subject>Vascular Endothelial Growth Factor A - antagonists & inhibitors</subject><subject>Vascular Endothelial Growth Factor A - metabolism</subject><subject>VEGF receptor (VEGFR)</subject><subject>VEGF-specific antibody</subject><subject>VEGF-specific tyrosine kinase inhibitor</subject><subject>VEGF-targeted drug</subject><subject>VEGFR2-specific antibody</subject><issn>1559-2294</issn><issn>1559-2308</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkU1v1DAQhiMEoqVw5Ip845TFH_mwuVXVtlRUogfgak2c8daQxMF2hPYv8Stxuu32gsRprNEz74zftyjeMrqpWMM-4Ow27YZvmFSteFacsrpWJRdUPn98c1WdFK9i_EFpJRqlXhYnnAtVV406Lf7cBj_6hIGMmO72AyTnJxITpCUSb8n37dUlCWhwTj6QHU4YP5JzMvsYXTcgyevXZnKGdM6PEH5mqeQJTLnlZkhI0l3GrHUGzH6VdFMKYHAYlgFCCSa5aXe_p0wQdpiwJ31YdjGDxMBksuBKx9fFCwtDxDcP9az4drn9evGpvPlydX1xflOaWlSplF1raCdr2inLjLEWKKVto2xFhehrDozTtuKNbBnWHUjWC2Wl5Er0rWgZFWfF-4PuHPyvBWPSo4vrBTChX6JW66xUlcpkeSBNyH4EtHoOLnuw14zqNR2d7dGt5vo-ncy_e1BeuhH7I_0Yx5Ng3tVjzI5G4zBbcEQ_u3F7e71Kzr3NvPoP_5RP1BByGfB4jDzMusn6MMJvH4ZeJ9gPPtiQfXdRi3__4y_58cd8</recordid><startdate>20120201</startdate><enddate>20120201</enddate><creator>Kim, Jeeyeon</creator><creator>Hwang, Junha</creator><creator>Jeong, Hyeseon</creator><creator>Song, Hee-Jung</creator><creator>Shin, Jieun</creator><creator>Hur, Gangmin</creator><creator>Park, Young Woo</creator><creator>Lee, Suk Hoon</creator><creator>Kim, Jei</creator><general>Taylor & Francis</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>7X8</scope></search><sort><creationdate>20120201</creationdate><title>Promoter methylation status of VEGF receptor genes: A possible epigenetic biomarker to anticipate the efficacy of intracellular-acting VEGF-targeted drugs in cancer cells</title><author>Kim, Jeeyeon ; Hwang, Junha ; Jeong, Hyeseon ; Song, Hee-Jung ; Shin, Jieun ; Hur, Gangmin ; Park, Young Woo ; Lee, Suk Hoon ; Kim, Jei</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c534t-8b7c0b850b9f1ccffa000769f4033d52a1207426871e5ba81d39f88293d737103</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Antineoplastic Agents - pharmacology</topic><topic>Antineoplastic Agents - therapeutic use</topic><topic>Binding</topic><topic>Biology</topic><topic>Biomarkers, Tumor - genetics</topic><topic>Bioscience</topic><topic>Calcium</topic><topic>Cancer</topic><topic>Cell</topic><topic>Cell Line, Tumor</topic><topic>Cell Proliferation - drug effects</topic><topic>CpG Islands - genetics</topic><topic>Cycle</topic><topic>DNA Methylation - drug effects</topic><topic>DNA Methylation - genetics</topic><topic>Epigenesis, Genetic - drug effects</topic><topic>epigenetic change</topic><topic>Extracellular Signal-Regulated MAP Kinases - metabolism</topic><topic>Flt1</topic><topic>Human Umbilical Vein Endothelial Cells - metabolism</topic><topic>Humans</topic><topic>Intracellular Space - drug effects</topic><topic>Intracellular Space - metabolism</topic><topic>KDR</topic><topic>Landes</topic><topic>Molecular Targeted Therapy</topic><topic>Neoplasms - drug therapy</topic><topic>Neoplasms - enzymology</topic><topic>Neoplasms - genetics</topic><topic>Neoplasms - pathology</topic><topic>Organogenesis</topic><topic>Phosphorylation - drug effects</topic><topic>promoter hypermethylation</topic><topic>Promoter Regions, Genetic - genetics</topic><topic>Protein Kinase Inhibitors - pharmacology</topic><topic>Protein Kinase Inhibitors - therapeutic use</topic><topic>Proteins</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>Receptors, Vascular Endothelial Growth Factor - genetics</topic><topic>Treatment Outcome</topic><topic>vascular endothelial growth factor (VEGF)</topic><topic>Vascular Endothelial Growth Factor A - antagonists & inhibitors</topic><topic>Vascular Endothelial Growth Factor A - metabolism</topic><topic>VEGF receptor (VEGFR)</topic><topic>VEGF-specific antibody</topic><topic>VEGF-specific tyrosine kinase inhibitor</topic><topic>VEGF-targeted drug</topic><topic>VEGFR2-specific antibody</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kim, Jeeyeon</creatorcontrib><creatorcontrib>Hwang, Junha</creatorcontrib><creatorcontrib>Jeong, Hyeseon</creatorcontrib><creatorcontrib>Song, Hee-Jung</creatorcontrib><creatorcontrib>Shin, Jieun</creatorcontrib><creatorcontrib>Hur, Gangmin</creatorcontrib><creatorcontrib>Park, Young Woo</creatorcontrib><creatorcontrib>Lee, Suk Hoon</creatorcontrib><creatorcontrib>Kim, Jei</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Epigenetics</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kim, Jeeyeon</au><au>Hwang, Junha</au><au>Jeong, Hyeseon</au><au>Song, Hee-Jung</au><au>Shin, Jieun</au><au>Hur, Gangmin</au><au>Park, Young Woo</au><au>Lee, Suk Hoon</au><au>Kim, Jei</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Promoter methylation status of VEGF receptor genes: A possible epigenetic biomarker to anticipate the efficacy of intracellular-acting VEGF-targeted drugs in cancer cells</atitle><jtitle>Epigenetics</jtitle><addtitle>Epigenetics</addtitle><date>2012-02-01</date><risdate>2012</risdate><volume>7</volume><issue>2</issue><spage>191</spage><epage>200</epage><pages>191-200</pages><issn>1559-2294</issn><eissn>1559-2308</eissn><abstract>We evaluated whether the inhibitory effects of vascular endothelial growth factor (VEGF)-targeted drugs on the proliferation of cancer cells differed according to VEGF receptor (VEGFR) genes, Flt1 and KDR, promoter methylation status. Five hyper-VEGFR-methylation and six no-VEGFR-methylation cancer cells were used for the present study, together with human umbilical endothelial cells (HUVECs) as a control. No-VEGFR-methylation cancer cells showed higher expression of Flt1 and KDR than hyper-VEGFR-methylation cancer cells. Hyper-VEGFR-methylation cancer cells only showed increased expression and protein levels of Flt1 and KDR after treatment with the demethylase 5-aza-2'-deoxycytidine. Two drugs (a VEGF-specific-antibody, bevacizumab, and a KDR-specific-antibody) targeting extracellular VEGF-VEGFR signaling and two VEGF-specific-tyrosine kinase inhibitors (PTK/ZK and sunitinib) targeting intracellular VEGFR signaling were used in the cell proliferation assay. HUVECs showed dose- and time-dependent proliferation decrease with all tested drugs over a 72 h incubation period. No- or hyper-VEGFR-methylation cancer cells showed no significant proliferation differences after treatment with VEGF-specific-antibody or VEGFR2-specific-antibody. After PTK/ZK or sunitinib treatment, no-VEGFR-methylation cancer cells showed dose- or time-dependent decreases in proliferation. Hyper-VEGFR-methylation cancer cells also showed proliferation inhibition by VEGF-specific-tyrosine kinase inhibitors after demethylation of Flt1 and KDR. Proliferation inhibition synergistically increased after combination of demethylation with PTK/ZK in hyper-VEGF-methylation cancer cells. We observed that intracellular targeting of VEGF-VEGFR signaling could be more effective than extracellular targeting of the pathway in the suppression of proliferation of some cancer cells. In particular, the efficacy of intracellular targeting of VEGF-specific-tyrosine kinase inhibitors might be influenced by the epigenetic alteration of VEGFRs.</abstract><cop>United States</cop><pub>Taylor & Francis</pub><pmid>22395469</pmid><doi>10.4161/epi.7.2.18973</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1559-2294 |
| ispartof | Epigenetics, 2012-02, Vol.7 (2), p.191-200 |
| issn | 1559-2294 1559-2308 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_926878949 |
| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central |
| subjects | Antineoplastic Agents - pharmacology Antineoplastic Agents - therapeutic use Binding Biology Biomarkers, Tumor - genetics Bioscience Calcium Cancer Cell Cell Line, Tumor Cell Proliferation - drug effects CpG Islands - genetics Cycle DNA Methylation - drug effects DNA Methylation - genetics Epigenesis, Genetic - drug effects epigenetic change Extracellular Signal-Regulated MAP Kinases - metabolism Flt1 Human Umbilical Vein Endothelial Cells - metabolism Humans Intracellular Space - drug effects Intracellular Space - metabolism KDR Landes Molecular Targeted Therapy Neoplasms - drug therapy Neoplasms - enzymology Neoplasms - genetics Neoplasms - pathology Organogenesis Phosphorylation - drug effects promoter hypermethylation Promoter Regions, Genetic - genetics Protein Kinase Inhibitors - pharmacology Protein Kinase Inhibitors - therapeutic use Proteins Proto-Oncogene Proteins c-akt - metabolism Receptors, Vascular Endothelial Growth Factor - genetics Treatment Outcome vascular endothelial growth factor (VEGF) Vascular Endothelial Growth Factor A - antagonists & inhibitors Vascular Endothelial Growth Factor A - metabolism VEGF receptor (VEGFR) VEGF-specific antibody VEGF-specific tyrosine kinase inhibitor VEGF-targeted drug VEGFR2-specific antibody |
| title | Promoter methylation status of VEGF receptor genes: A possible epigenetic biomarker to anticipate the efficacy of intracellular-acting VEGF-targeted drugs in cancer cells |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-11T18%3A29%3A31IST&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=Promoter%20methylation%20status%20of%20VEGF%20receptor%20genes:%20A%20possible%20epigenetic%20biomarker%20to%20anticipate%20the%20efficacy%20of%20intracellular-acting%20VEGF-targeted%20drugs%20in%20cancer%20cells&rft.jtitle=Epigenetics&rft.au=Kim,%20Jeeyeon&rft.date=2012-02-01&rft.volume=7&rft.issue=2&rft.spage=191&rft.epage=200&rft.pages=191-200&rft.issn=1559-2294&rft.eissn=1559-2308&rft_id=info:doi/10.4161/epi.7.2.18973&rft_dat=%3Cproquest_cross%3E926878949%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=926878949&rft_id=info:pmid/22395469&rfr_iscdi=true |