AMG 479, a fully human anti–insulin-like growth factor receptor type I monoclonal antibody, inhibits the growth and survival of pancreatic carcinoma cells
Pancreatic carcinoma is a leading cause of cancer deaths, and recent clinical trials of a number of oncology therapeutics have not substantially improved clinical outcomes. We have evaluated the therapeutic potential of AMG 479, a fully human monoclonal antibody against insulin-like growth factor (I...
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| Veröffentlicht in: | Molecular cancer therapeutics 2009-05, Vol.8 (5), p.1095-1105 |
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| creator | Beltran, Pedro J Mitchell, Petia Chung, Young-A Cajulis, Elaina Lu, John Belmontes, Brian Ho, Joanne Tsai, Mei Mei Zhu, Min Vonderfecht, Steven Baserga, Renato Kendall, Richard Radinsky, Robert Calzone, Frank J |
| description | Pancreatic carcinoma is a leading cause of cancer deaths, and recent clinical trials of a number of oncology therapeutics
have not substantially improved clinical outcomes. We have evaluated the therapeutic potential of AMG 479, a fully human monoclonal
antibody against insulin-like growth factor (IGF) type I receptor (IGF-IR), in two IGF-IR–expressing pancreatic carcinoma
cell lines, BxPC-3 and MiaPaCa2, which also differentially express insulin receptor (INSR). AMG 479 bound to IGF-IR ( K D 0.33 nmol/L) and blocked IGF-I and IGF-II binding (IC 50 < 0.6 nmol/L) without cross-reacting to INSR. AMG 479 completely inhibited ligand-induced (IGF-I, IGF-II, and insulin) activation
of IGF-IR homodimers and IGF-IR/INSR hybrids (but not INSR homodimers) leading to reduced cellular viability in serum-deprived
cultures. AMG 479 inhibited >80% of basal IGF-IR activity in BxPC-3 and MiaPaCa2 xenografts and prevented IGF-IR and IGF-IR/INSR
hybrid activation following challenge with supraphysiologic concentrations of IGF-I. As a single agent, AMG 479 inhibited
(∼80%) the growth of pancreatic carcinoma xenografts, and long-term treatment was associated with reduced IGF-IR signaling
activity and expression. Efficacy seemed to be the result of two distinct biological effects: proapoptotic in BxPC-3 and antimitogenic
in MiaPaCa2. The combination of AMG 479 with gemcitabine resulted in additive inhibitory activity both in vitro and in vivo . These results indicate that AMG 479 is a clinical candidate, both as a single agent and in combination with gemcitabine,
for the treatment of patients with pancreatic carcinoma.[Mol Cancer Ther 2009;8(5):1095–105] |
| doi_str_mv | 10.1158/1535-7163.MCT-08-1171 |
| format | Article |
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have not substantially improved clinical outcomes. We have evaluated the therapeutic potential of AMG 479, a fully human monoclonal
antibody against insulin-like growth factor (IGF) type I receptor (IGF-IR), in two IGF-IR–expressing pancreatic carcinoma
cell lines, BxPC-3 and MiaPaCa2, which also differentially express insulin receptor (INSR). AMG 479 bound to IGF-IR ( K D 0.33 nmol/L) and blocked IGF-I and IGF-II binding (IC 50 < 0.6 nmol/L) without cross-reacting to INSR. AMG 479 completely inhibited ligand-induced (IGF-I, IGF-II, and insulin) activation
of IGF-IR homodimers and IGF-IR/INSR hybrids (but not INSR homodimers) leading to reduced cellular viability in serum-deprived
cultures. AMG 479 inhibited >80% of basal IGF-IR activity in BxPC-3 and MiaPaCa2 xenografts and prevented IGF-IR and IGF-IR/INSR
hybrid activation following challenge with supraphysiologic concentrations of IGF-I. As a single agent, AMG 479 inhibited
(∼80%) the growth of pancreatic carcinoma xenografts, and long-term treatment was associated with reduced IGF-IR signaling
activity and expression. Efficacy seemed to be the result of two distinct biological effects: proapoptotic in BxPC-3 and antimitogenic
in MiaPaCa2. The combination of AMG 479 with gemcitabine resulted in additive inhibitory activity both in vitro and in vivo . These results indicate that AMG 479 is a clinical candidate, both as a single agent and in combination with gemcitabine,
for the treatment of patients with pancreatic carcinoma.[Mol Cancer Ther 2009;8(5):1095–105]</description><identifier>ISSN: 1535-7163</identifier><identifier>EISSN: 1538-8514</identifier><identifier>DOI: 10.1158/1535-7163.MCT-08-1171</identifier><identifier>PMID: 19366899</identifier><language>eng</language><publisher>United States: American Association for Cancer Research</publisher><subject>AMG 479 ; Animals ; Antibodies, Monoclonal - pharmacology ; Antimetabolites, Antineoplastic - pharmacology ; Caspase 3 - metabolism ; Cell Line, Tumor ; Cell Proliferation - drug effects ; Cell Survival - drug effects ; Deoxycytidine - analogs & derivatives ; Deoxycytidine - pharmacology ; Drug Synergism ; Female ; Humans ; hybrid receptors ; IGF-IR ; insulin receptor ; Insulin-Like Growth Factor I - metabolism ; Insulin-Like Growth Factor II - metabolism ; Mice ; Mice, Nude ; pancreatic carcinoma ; Pancreatic Neoplasms - pathology ; Protein Binding - drug effects ; Receptor, IGF Type 1 - antagonists & inhibitors ; Receptor, IGF Type 1 - metabolism ; Receptor, Insulin - metabolism ; Signal Transduction - drug effects ; Xenograft Model Antitumor Assays</subject><ispartof>Molecular cancer therapeutics, 2009-05, Vol.8 (5), p.1095-1105</ispartof><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c453t-f6c2e2c87ac0f244ef3b1080d1fad992833c4abadf63efb5936e62e5f42a9e3a3</citedby><cites>FETCH-LOGICAL-c453t-f6c2e2c87ac0f244ef3b1080d1fad992833c4abadf63efb5936e62e5f42a9e3a3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,3342,27903,27904</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19366899$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Beltran, Pedro J</creatorcontrib><creatorcontrib>Mitchell, Petia</creatorcontrib><creatorcontrib>Chung, Young-A</creatorcontrib><creatorcontrib>Cajulis, Elaina</creatorcontrib><creatorcontrib>Lu, John</creatorcontrib><creatorcontrib>Belmontes, Brian</creatorcontrib><creatorcontrib>Ho, Joanne</creatorcontrib><creatorcontrib>Tsai, Mei Mei</creatorcontrib><creatorcontrib>Zhu, Min</creatorcontrib><creatorcontrib>Vonderfecht, Steven</creatorcontrib><creatorcontrib>Baserga, Renato</creatorcontrib><creatorcontrib>Kendall, Richard</creatorcontrib><creatorcontrib>Radinsky, Robert</creatorcontrib><creatorcontrib>Calzone, Frank J</creatorcontrib><title>AMG 479, a fully human anti–insulin-like growth factor receptor type I monoclonal antibody, inhibits the growth and survival of pancreatic carcinoma cells</title><title>Molecular cancer therapeutics</title><addtitle>Mol Cancer Ther</addtitle><description>Pancreatic carcinoma is a leading cause of cancer deaths, and recent clinical trials of a number of oncology therapeutics
have not substantially improved clinical outcomes. We have evaluated the therapeutic potential of AMG 479, a fully human monoclonal
antibody against insulin-like growth factor (IGF) type I receptor (IGF-IR), in two IGF-IR–expressing pancreatic carcinoma
cell lines, BxPC-3 and MiaPaCa2, which also differentially express insulin receptor (INSR). AMG 479 bound to IGF-IR ( K D 0.33 nmol/L) and blocked IGF-I and IGF-II binding (IC 50 < 0.6 nmol/L) without cross-reacting to INSR. AMG 479 completely inhibited ligand-induced (IGF-I, IGF-II, and insulin) activation
of IGF-IR homodimers and IGF-IR/INSR hybrids (but not INSR homodimers) leading to reduced cellular viability in serum-deprived
cultures. AMG 479 inhibited >80% of basal IGF-IR activity in BxPC-3 and MiaPaCa2 xenografts and prevented IGF-IR and IGF-IR/INSR
hybrid activation following challenge with supraphysiologic concentrations of IGF-I. As a single agent, AMG 479 inhibited
(∼80%) the growth of pancreatic carcinoma xenografts, and long-term treatment was associated with reduced IGF-IR signaling
activity and expression. Efficacy seemed to be the result of two distinct biological effects: proapoptotic in BxPC-3 and antimitogenic
in MiaPaCa2. The combination of AMG 479 with gemcitabine resulted in additive inhibitory activity both in vitro and in vivo . These results indicate that AMG 479 is a clinical candidate, both as a single agent and in combination with gemcitabine,
for the treatment of patients with pancreatic carcinoma.[Mol Cancer Ther 2009;8(5):1095–105]</description><subject>AMG 479</subject><subject>Animals</subject><subject>Antibodies, Monoclonal - pharmacology</subject><subject>Antimetabolites, Antineoplastic - pharmacology</subject><subject>Caspase 3 - metabolism</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation - drug effects</subject><subject>Cell Survival - drug effects</subject><subject>Deoxycytidine - analogs & derivatives</subject><subject>Deoxycytidine - pharmacology</subject><subject>Drug Synergism</subject><subject>Female</subject><subject>Humans</subject><subject>hybrid receptors</subject><subject>IGF-IR</subject><subject>insulin receptor</subject><subject>Insulin-Like Growth Factor I - metabolism</subject><subject>Insulin-Like Growth Factor II - metabolism</subject><subject>Mice</subject><subject>Mice, Nude</subject><subject>pancreatic carcinoma</subject><subject>Pancreatic Neoplasms - pathology</subject><subject>Protein Binding - drug effects</subject><subject>Receptor, IGF Type 1 - antagonists & inhibitors</subject><subject>Receptor, IGF Type 1 - metabolism</subject><subject>Receptor, Insulin - metabolism</subject><subject>Signal Transduction - drug effects</subject><subject>Xenograft Model Antitumor Assays</subject><issn>1535-7163</issn><issn>1538-8514</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFUctu1TAQtSoQLbd8QpF3bJoSx3HiLKurUiq1YtOurYkzbgyJHeyk1d3xD2z5Or4Ep_eKLkYzGp0zj3MIOWP5BWNCfmaCi6xmFb-4295nucwYq9kROUl9mUnByjcv9R5zTN7H-D3PmWwK9o4cs4ZXlWyaE_Ln8u6alnVzToGaZRh2tF9GcBTcbP_--m1dXAbrssH-QPoY_PPcUwN69oEG1DitxbybkN7Q0TuvB-9geCG3vtudU-t629o50rn_zwfX0biEJ_uUoN7QCZwOCLPVVEPQ1vkRqMZhiKfkrYEh4odD3pCHL1f326_Z7bfrm-3lbaZLwefMVLrAQssadG6KskTDW5bLvGMGuqYpJOe6hBY6U3E0rUjPY1WgMGUBDXLgG_JpP3cK_ueCcVajjesF4NAvUcmyLjlfY0PEHqmDjzGgUVOwI4SdYrlafVGr5mrVXCVfVJ4ayZfE-3jYsLQjdq-sgxGvJ_T2sX-2AZVOsmAIGDGJ0iupRNrRCP4PfOCbTw</recordid><startdate>20090501</startdate><enddate>20090501</enddate><creator>Beltran, Pedro J</creator><creator>Mitchell, Petia</creator><creator>Chung, Young-A</creator><creator>Cajulis, Elaina</creator><creator>Lu, John</creator><creator>Belmontes, Brian</creator><creator>Ho, Joanne</creator><creator>Tsai, Mei Mei</creator><creator>Zhu, Min</creator><creator>Vonderfecht, Steven</creator><creator>Baserga, Renato</creator><creator>Kendall, Richard</creator><creator>Radinsky, Robert</creator><creator>Calzone, Frank J</creator><general>American Association for Cancer Research</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>20090501</creationdate><title>AMG 479, a fully human anti–insulin-like growth factor receptor type I monoclonal antibody, inhibits the growth and survival of pancreatic carcinoma cells</title><author>Beltran, Pedro J ; Mitchell, Petia ; Chung, Young-A ; Cajulis, Elaina ; Lu, John ; Belmontes, Brian ; Ho, Joanne ; Tsai, Mei Mei ; Zhu, Min ; Vonderfecht, Steven ; Baserga, Renato ; Kendall, Richard ; Radinsky, Robert ; Calzone, Frank J</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c453t-f6c2e2c87ac0f244ef3b1080d1fad992833c4abadf63efb5936e62e5f42a9e3a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>AMG 479</topic><topic>Animals</topic><topic>Antibodies, Monoclonal - pharmacology</topic><topic>Antimetabolites, Antineoplastic - pharmacology</topic><topic>Caspase 3 - metabolism</topic><topic>Cell Line, Tumor</topic><topic>Cell Proliferation - drug effects</topic><topic>Cell Survival - drug effects</topic><topic>Deoxycytidine - analogs & derivatives</topic><topic>Deoxycytidine - pharmacology</topic><topic>Drug Synergism</topic><topic>Female</topic><topic>Humans</topic><topic>hybrid receptors</topic><topic>IGF-IR</topic><topic>insulin receptor</topic><topic>Insulin-Like Growth Factor I - metabolism</topic><topic>Insulin-Like Growth Factor II - metabolism</topic><topic>Mice</topic><topic>Mice, Nude</topic><topic>pancreatic carcinoma</topic><topic>Pancreatic Neoplasms - pathology</topic><topic>Protein Binding - drug effects</topic><topic>Receptor, IGF Type 1 - antagonists & inhibitors</topic><topic>Receptor, IGF Type 1 - metabolism</topic><topic>Receptor, Insulin - metabolism</topic><topic>Signal Transduction - drug effects</topic><topic>Xenograft Model Antitumor Assays</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Beltran, Pedro J</creatorcontrib><creatorcontrib>Mitchell, Petia</creatorcontrib><creatorcontrib>Chung, Young-A</creatorcontrib><creatorcontrib>Cajulis, Elaina</creatorcontrib><creatorcontrib>Lu, John</creatorcontrib><creatorcontrib>Belmontes, Brian</creatorcontrib><creatorcontrib>Ho, Joanne</creatorcontrib><creatorcontrib>Tsai, Mei Mei</creatorcontrib><creatorcontrib>Zhu, Min</creatorcontrib><creatorcontrib>Vonderfecht, Steven</creatorcontrib><creatorcontrib>Baserga, Renato</creatorcontrib><creatorcontrib>Kendall, Richard</creatorcontrib><creatorcontrib>Radinsky, Robert</creatorcontrib><creatorcontrib>Calzone, Frank J</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>Molecular cancer therapeutics</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Beltran, Pedro J</au><au>Mitchell, Petia</au><au>Chung, Young-A</au><au>Cajulis, Elaina</au><au>Lu, John</au><au>Belmontes, Brian</au><au>Ho, Joanne</au><au>Tsai, Mei Mei</au><au>Zhu, Min</au><au>Vonderfecht, Steven</au><au>Baserga, Renato</au><au>Kendall, Richard</au><au>Radinsky, Robert</au><au>Calzone, Frank J</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>AMG 479, a fully human anti–insulin-like growth factor receptor type I monoclonal antibody, inhibits the growth and survival of pancreatic carcinoma cells</atitle><jtitle>Molecular cancer therapeutics</jtitle><addtitle>Mol Cancer Ther</addtitle><date>2009-05-01</date><risdate>2009</risdate><volume>8</volume><issue>5</issue><spage>1095</spage><epage>1105</epage><pages>1095-1105</pages><issn>1535-7163</issn><eissn>1538-8514</eissn><abstract>Pancreatic carcinoma is a leading cause of cancer deaths, and recent clinical trials of a number of oncology therapeutics
have not substantially improved clinical outcomes. We have evaluated the therapeutic potential of AMG 479, a fully human monoclonal
antibody against insulin-like growth factor (IGF) type I receptor (IGF-IR), in two IGF-IR–expressing pancreatic carcinoma
cell lines, BxPC-3 and MiaPaCa2, which also differentially express insulin receptor (INSR). AMG 479 bound to IGF-IR ( K D 0.33 nmol/L) and blocked IGF-I and IGF-II binding (IC 50 < 0.6 nmol/L) without cross-reacting to INSR. AMG 479 completely inhibited ligand-induced (IGF-I, IGF-II, and insulin) activation
of IGF-IR homodimers and IGF-IR/INSR hybrids (but not INSR homodimers) leading to reduced cellular viability in serum-deprived
cultures. AMG 479 inhibited >80% of basal IGF-IR activity in BxPC-3 and MiaPaCa2 xenografts and prevented IGF-IR and IGF-IR/INSR
hybrid activation following challenge with supraphysiologic concentrations of IGF-I. As a single agent, AMG 479 inhibited
(∼80%) the growth of pancreatic carcinoma xenografts, and long-term treatment was associated with reduced IGF-IR signaling
activity and expression. Efficacy seemed to be the result of two distinct biological effects: proapoptotic in BxPC-3 and antimitogenic
in MiaPaCa2. The combination of AMG 479 with gemcitabine resulted in additive inhibitory activity both in vitro and in vivo . These results indicate that AMG 479 is a clinical candidate, both as a single agent and in combination with gemcitabine,
for the treatment of patients with pancreatic carcinoma.[Mol Cancer Ther 2009;8(5):1095–105]</abstract><cop>United States</cop><pub>American Association for Cancer Research</pub><pmid>19366899</pmid><doi>10.1158/1535-7163.MCT-08-1171</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | AMG 479 Animals Antibodies, Monoclonal - pharmacology Antimetabolites, Antineoplastic - pharmacology Caspase 3 - metabolism Cell Line, Tumor Cell Proliferation - drug effects Cell Survival - drug effects Deoxycytidine - analogs & derivatives Deoxycytidine - pharmacology Drug Synergism Female Humans hybrid receptors IGF-IR insulin receptor Insulin-Like Growth Factor I - metabolism Insulin-Like Growth Factor II - metabolism Mice Mice, Nude pancreatic carcinoma Pancreatic Neoplasms - pathology Protein Binding - drug effects Receptor, IGF Type 1 - antagonists & inhibitors Receptor, IGF Type 1 - metabolism Receptor, Insulin - metabolism Signal Transduction - drug effects Xenograft Model Antitumor Assays |
| title | AMG 479, a fully human anti–insulin-like growth factor receptor type I monoclonal antibody, inhibits the growth and survival of pancreatic carcinoma cells |
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