A Randomized Phase II Trial of Thalidomide, an Angiogenesis Inhibitor, in Patients with Androgen-independent Prostate Cancer
Purpose: Thalidomide is a potent teratogen that causes dysmelia in humans. Recently, in vitro data suggested that it inhibits angiogenesis. Prostate cancer is dependent on the recruitment of new blood vessels to grow and metastasize. Based on those data, we initiated a Phase II trial of thalidomide...
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| Veröffentlicht in: | Clinical cancer research 2001-07, Vol.7 (7), p.1888-1893 |
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| creator | FIGG, William D DAHUT, William CHEN, Clara C DIXON, Shannon KOHLER, David R KRÜGER, Erwin A GUBISH, Ed PLUDA, James M REED, Eddie DURAY, Paul HAMILTON, Michael TOMPKINS, Anne STEINBERG, Seth M JONES, Elizabeth PREMKUMAR, Ahalya LINEHAN, W. Marston FLOETER, Mary Kay |
| description | Purpose: Thalidomide is a potent teratogen that causes dysmelia in humans. Recently, in vitro data suggested that it inhibits angiogenesis. Prostate cancer is dependent on the recruitment of new blood vessels to grow
and metastasize. Based on those data, we initiated a Phase II trial of thalidomide in patients with metastatic androgen-independent
prostate cancer.
Experimental Design: This was an open-label, randomized Phase II study. Thalidomide was administered either at a dose of 200 mg/day (low-dose
arm) or at an initial dose of 200 mg/day that escalated to 1200 mg/day (high-dose arm).
Results: A total of 63 patients were enrolled onto the study (50 patients on the low-dose arm and 13 patients on the high-dose arm).
Serum prostate-specific antigen (PSA) decline of ≥50% was noted in 18% of patients on the low-dose arm and in none of the
patients on the high-dose arm. Four patients were maintained for >150 days. The most prevalent complications were constipation,
fatigue, neurocortical, and neurosensory.
Conclusion: Thalidomide, an antiangiogenesis agent, has some activity in patients with metastatic prostate cancer who have failed multiple
therapies. A total of 27% of all patients had a decline in PSA of ≥40%, often associated with an improvement of clinical symptoms.
Because our preclinical studies had shown that thalidomide increases PSA secretion, we believe that the magnitude of PSA decline
seen in our trial justifies further study. |
| format | Article |
| fullrecord | <record><control><sourceid>pubmed_pasca</sourceid><recordid>TN_cdi_pubmed_primary_11448901</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>11448901</sourcerecordid><originalsourceid>FETCH-LOGICAL-g293t-72a443dc5e8dd00f0b64c55599ea31133ca17fb8d910f4b99f5e16e2655cd1ce3</originalsourceid><addsrcrecordid>eNpF0F9LwzAQAPAiipvTryB5EHxZIWmSNXkcwz-DgUPmc7km1zbSpSOpDMUPb-cmcnAXyI_j7s6SMZMyT3k2k-fDm-YqpYJno-QqxndKmWBUXCYjxoRQmrJx8j0nr-Btt3VfaMm6gYhkuSSb4KAlXUU2DbTu8G1xSsCTua9dV6PH6CJZ-saVru_ClDhP1tA79H0ke9c3A7ThAFPnLe5wSL4n69DFHnokC_AGw3VyUUEb8eZUJ8nb48Nm8ZyuXp6Wi_kqrTPN-zTPQAhujURlLaUVLWfCSCm1RuCMcW6A5VWprGa0EqXWlUQ2w-EG0lhmkE-S22Pf3Ue5RVvsgttC-Cz-zjCAuxOAaKCtwjCei_-OqkzoA7s_ssbVzd4FLMzvHgEjQjBNkQ_BlFL8BzW8dYw</addsrcrecordid><sourcetype>Index Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype></control><display><type>article</type><title>A Randomized Phase II Trial of Thalidomide, an Angiogenesis Inhibitor, in Patients with Androgen-independent Prostate Cancer</title><source>MEDLINE</source><source>American Association for Cancer Research</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>Alma/SFX Local Collection</source><creator>FIGG, William D ; DAHUT, William ; CHEN, Clara C ; DIXON, Shannon ; KOHLER, David R ; KRÜGER, Erwin A ; GUBISH, Ed ; PLUDA, James M ; REED, Eddie ; DURAY, Paul ; HAMILTON, Michael ; TOMPKINS, Anne ; STEINBERG, Seth M ; JONES, Elizabeth ; PREMKUMAR, Ahalya ; LINEHAN, W. Marston ; FLOETER, Mary Kay</creator><creatorcontrib>FIGG, William D ; DAHUT, William ; CHEN, Clara C ; DIXON, Shannon ; KOHLER, David R ; KRÜGER, Erwin A ; GUBISH, Ed ; PLUDA, James M ; REED, Eddie ; DURAY, Paul ; HAMILTON, Michael ; TOMPKINS, Anne ; STEINBERG, Seth M ; JONES, Elizabeth ; PREMKUMAR, Ahalya ; LINEHAN, W. Marston ; FLOETER, Mary Kay</creatorcontrib><description>Purpose: Thalidomide is a potent teratogen that causes dysmelia in humans. Recently, in vitro data suggested that it inhibits angiogenesis. Prostate cancer is dependent on the recruitment of new blood vessels to grow
and metastasize. Based on those data, we initiated a Phase II trial of thalidomide in patients with metastatic androgen-independent
prostate cancer.
Experimental Design: This was an open-label, randomized Phase II study. Thalidomide was administered either at a dose of 200 mg/day (low-dose
arm) or at an initial dose of 200 mg/day that escalated to 1200 mg/day (high-dose arm).
Results: A total of 63 patients were enrolled onto the study (50 patients on the low-dose arm and 13 patients on the high-dose arm).
Serum prostate-specific antigen (PSA) decline of ≥50% was noted in 18% of patients on the low-dose arm and in none of the
patients on the high-dose arm. Four patients were maintained for >150 days. The most prevalent complications were constipation,
fatigue, neurocortical, and neurosensory.
Conclusion: Thalidomide, an antiangiogenesis agent, has some activity in patients with metastatic prostate cancer who have failed multiple
therapies. A total of 27% of all patients had a decline in PSA of ≥40%, often associated with an improvement of clinical symptoms.
Because our preclinical studies had shown that thalidomide increases PSA secretion, we believe that the magnitude of PSA decline
seen in our trial justifies further study.</description><identifier>ISSN: 1078-0432</identifier><identifier>EISSN: 1557-3265</identifier><identifier>PMID: 11448901</identifier><language>eng</language><publisher>Philadelphia, PA: American Association for Cancer Research</publisher><subject>Aged ; Aged, 80 and over ; Androgens - physiology ; Angiogenesis Inhibitors - therapeutic use ; Antineoplastic agents ; Biological and medical sciences ; Chemotherapy ; Dose-Response Relationship, Drug ; Endothelial Growth Factors - blood ; Fibroblast Growth Factor 2 - blood ; Fibroblast Growth Factor 2 - drug effects ; Follow-Up Studies ; Humans ; Lymphokines - blood ; Lymphokines - drug effects ; Lymphotoxin-alpha - blood ; Male ; Medical sciences ; Middle Aged ; Mood Disorders - chemically induced ; Neovascularization, Pathologic - pathology ; Neutropenia - chemically induced ; Pharmacology. Drug treatments ; Prostate-Specific Antigen - blood ; Prostate-Specific Antigen - drug effects ; Prostatic Neoplasms - blood supply ; Prostatic Neoplasms - drug therapy ; Prostatic Neoplasms - pathology ; Survival Analysis ; Thalidomide - therapeutic use ; Time Factors ; Treatment Outcome ; Tumor Necrosis Factor-alpha - drug effects ; Tumor Necrosis Factor-alpha - metabolism ; Vascular Endothelial Growth Factor A ; Vascular Endothelial Growth Factors</subject><ispartof>Clinical cancer research, 2001-07, Vol.7 (7), p.1888-1893</ispartof><rights>2001 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1082491$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11448901$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>FIGG, William D</creatorcontrib><creatorcontrib>DAHUT, William</creatorcontrib><creatorcontrib>CHEN, Clara C</creatorcontrib><creatorcontrib>DIXON, Shannon</creatorcontrib><creatorcontrib>KOHLER, David R</creatorcontrib><creatorcontrib>KRÜGER, Erwin A</creatorcontrib><creatorcontrib>GUBISH, Ed</creatorcontrib><creatorcontrib>PLUDA, James M</creatorcontrib><creatorcontrib>REED, Eddie</creatorcontrib><creatorcontrib>DURAY, Paul</creatorcontrib><creatorcontrib>HAMILTON, Michael</creatorcontrib><creatorcontrib>TOMPKINS, Anne</creatorcontrib><creatorcontrib>STEINBERG, Seth M</creatorcontrib><creatorcontrib>JONES, Elizabeth</creatorcontrib><creatorcontrib>PREMKUMAR, Ahalya</creatorcontrib><creatorcontrib>LINEHAN, W. Marston</creatorcontrib><creatorcontrib>FLOETER, Mary Kay</creatorcontrib><title>A Randomized Phase II Trial of Thalidomide, an Angiogenesis Inhibitor, in Patients with Androgen-independent Prostate Cancer</title><title>Clinical cancer research</title><addtitle>Clin Cancer Res</addtitle><description>Purpose: Thalidomide is a potent teratogen that causes dysmelia in humans. Recently, in vitro data suggested that it inhibits angiogenesis. Prostate cancer is dependent on the recruitment of new blood vessels to grow
and metastasize. Based on those data, we initiated a Phase II trial of thalidomide in patients with metastatic androgen-independent
prostate cancer.
Experimental Design: This was an open-label, randomized Phase II study. Thalidomide was administered either at a dose of 200 mg/day (low-dose
arm) or at an initial dose of 200 mg/day that escalated to 1200 mg/day (high-dose arm).
Results: A total of 63 patients were enrolled onto the study (50 patients on the low-dose arm and 13 patients on the high-dose arm).
Serum prostate-specific antigen (PSA) decline of ≥50% was noted in 18% of patients on the low-dose arm and in none of the
patients on the high-dose arm. Four patients were maintained for >150 days. The most prevalent complications were constipation,
fatigue, neurocortical, and neurosensory.
Conclusion: Thalidomide, an antiangiogenesis agent, has some activity in patients with metastatic prostate cancer who have failed multiple
therapies. A total of 27% of all patients had a decline in PSA of ≥40%, often associated with an improvement of clinical symptoms.
Because our preclinical studies had shown that thalidomide increases PSA secretion, we believe that the magnitude of PSA decline
seen in our trial justifies further study.</description><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Androgens - physiology</subject><subject>Angiogenesis Inhibitors - therapeutic use</subject><subject>Antineoplastic agents</subject><subject>Biological and medical sciences</subject><subject>Chemotherapy</subject><subject>Dose-Response Relationship, Drug</subject><subject>Endothelial Growth Factors - blood</subject><subject>Fibroblast Growth Factor 2 - blood</subject><subject>Fibroblast Growth Factor 2 - drug effects</subject><subject>Follow-Up Studies</subject><subject>Humans</subject><subject>Lymphokines - blood</subject><subject>Lymphokines - drug effects</subject><subject>Lymphotoxin-alpha - blood</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Mood Disorders - chemically induced</subject><subject>Neovascularization, Pathologic - pathology</subject><subject>Neutropenia - chemically induced</subject><subject>Pharmacology. Drug treatments</subject><subject>Prostate-Specific Antigen - blood</subject><subject>Prostate-Specific Antigen - drug effects</subject><subject>Prostatic Neoplasms - blood supply</subject><subject>Prostatic Neoplasms - drug therapy</subject><subject>Prostatic Neoplasms - pathology</subject><subject>Survival Analysis</subject><subject>Thalidomide - therapeutic use</subject><subject>Time Factors</subject><subject>Treatment Outcome</subject><subject>Tumor Necrosis Factor-alpha - drug effects</subject><subject>Tumor Necrosis Factor-alpha - metabolism</subject><subject>Vascular Endothelial Growth Factor A</subject><subject>Vascular Endothelial Growth Factors</subject><issn>1078-0432</issn><issn>1557-3265</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2001</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpF0F9LwzAQAPAiipvTryB5EHxZIWmSNXkcwz-DgUPmc7km1zbSpSOpDMUPb-cmcnAXyI_j7s6SMZMyT3k2k-fDm-YqpYJno-QqxndKmWBUXCYjxoRQmrJx8j0nr-Btt3VfaMm6gYhkuSSb4KAlXUU2DbTu8G1xSsCTua9dV6PH6CJZ-saVru_ClDhP1tA79H0ke9c3A7ThAFPnLe5wSL4n69DFHnokC_AGw3VyUUEb8eZUJ8nb48Nm8ZyuXp6Wi_kqrTPN-zTPQAhujURlLaUVLWfCSCm1RuCMcW6A5VWprGa0EqXWlUQ2w-EG0lhmkE-S22Pf3Ue5RVvsgttC-Cz-zjCAuxOAaKCtwjCei_-OqkzoA7s_ssbVzd4FLMzvHgEjQjBNkQ_BlFL8BzW8dYw</recordid><startdate>20010701</startdate><enddate>20010701</enddate><creator>FIGG, William D</creator><creator>DAHUT, William</creator><creator>CHEN, Clara C</creator><creator>DIXON, Shannon</creator><creator>KOHLER, David R</creator><creator>KRÜGER, Erwin A</creator><creator>GUBISH, Ed</creator><creator>PLUDA, James M</creator><creator>REED, Eddie</creator><creator>DURAY, Paul</creator><creator>HAMILTON, Michael</creator><creator>TOMPKINS, Anne</creator><creator>STEINBERG, Seth M</creator><creator>JONES, Elizabeth</creator><creator>PREMKUMAR, Ahalya</creator><creator>LINEHAN, W. Marston</creator><creator>FLOETER, Mary Kay</creator><general>American Association for Cancer Research</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope></search><sort><creationdate>20010701</creationdate><title>A Randomized Phase II Trial of Thalidomide, an Angiogenesis Inhibitor, in Patients with Androgen-independent Prostate Cancer</title><author>FIGG, William D ; DAHUT, William ; CHEN, Clara C ; DIXON, Shannon ; KOHLER, David R ; KRÜGER, Erwin A ; GUBISH, Ed ; PLUDA, James M ; REED, Eddie ; DURAY, Paul ; HAMILTON, Michael ; TOMPKINS, Anne ; STEINBERG, Seth M ; JONES, Elizabeth ; PREMKUMAR, Ahalya ; LINEHAN, W. 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Drug treatments</topic><topic>Prostate-Specific Antigen - blood</topic><topic>Prostate-Specific Antigen - drug effects</topic><topic>Prostatic Neoplasms - blood supply</topic><topic>Prostatic Neoplasms - drug therapy</topic><topic>Prostatic Neoplasms - pathology</topic><topic>Survival Analysis</topic><topic>Thalidomide - therapeutic use</topic><topic>Time Factors</topic><topic>Treatment Outcome</topic><topic>Tumor Necrosis Factor-alpha - drug effects</topic><topic>Tumor Necrosis Factor-alpha - metabolism</topic><topic>Vascular Endothelial Growth Factor A</topic><topic>Vascular Endothelial Growth Factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>FIGG, William D</creatorcontrib><creatorcontrib>DAHUT, William</creatorcontrib><creatorcontrib>CHEN, Clara C</creatorcontrib><creatorcontrib>DIXON, Shannon</creatorcontrib><creatorcontrib>KOHLER, David R</creatorcontrib><creatorcontrib>KRÜGER, Erwin A</creatorcontrib><creatorcontrib>GUBISH, Ed</creatorcontrib><creatorcontrib>PLUDA, James M</creatorcontrib><creatorcontrib>REED, Eddie</creatorcontrib><creatorcontrib>DURAY, Paul</creatorcontrib><creatorcontrib>HAMILTON, Michael</creatorcontrib><creatorcontrib>TOMPKINS, Anne</creatorcontrib><creatorcontrib>STEINBERG, Seth M</creatorcontrib><creatorcontrib>JONES, Elizabeth</creatorcontrib><creatorcontrib>PREMKUMAR, Ahalya</creatorcontrib><creatorcontrib>LINEHAN, W. Marston</creatorcontrib><creatorcontrib>FLOETER, Mary Kay</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><jtitle>Clinical cancer research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>FIGG, William D</au><au>DAHUT, William</au><au>CHEN, Clara C</au><au>DIXON, Shannon</au><au>KOHLER, David R</au><au>KRÜGER, Erwin A</au><au>GUBISH, Ed</au><au>PLUDA, James M</au><au>REED, Eddie</au><au>DURAY, Paul</au><au>HAMILTON, Michael</au><au>TOMPKINS, Anne</au><au>STEINBERG, Seth M</au><au>JONES, Elizabeth</au><au>PREMKUMAR, Ahalya</au><au>LINEHAN, W. Marston</au><au>FLOETER, Mary Kay</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>A Randomized Phase II Trial of Thalidomide, an Angiogenesis Inhibitor, in Patients with Androgen-independent Prostate Cancer</atitle><jtitle>Clinical cancer research</jtitle><addtitle>Clin Cancer Res</addtitle><date>2001-07-01</date><risdate>2001</risdate><volume>7</volume><issue>7</issue><spage>1888</spage><epage>1893</epage><pages>1888-1893</pages><issn>1078-0432</issn><eissn>1557-3265</eissn><abstract>Purpose: Thalidomide is a potent teratogen that causes dysmelia in humans. Recently, in vitro data suggested that it inhibits angiogenesis. Prostate cancer is dependent on the recruitment of new blood vessels to grow
and metastasize. Based on those data, we initiated a Phase II trial of thalidomide in patients with metastatic androgen-independent
prostate cancer.
Experimental Design: This was an open-label, randomized Phase II study. Thalidomide was administered either at a dose of 200 mg/day (low-dose
arm) or at an initial dose of 200 mg/day that escalated to 1200 mg/day (high-dose arm).
Results: A total of 63 patients were enrolled onto the study (50 patients on the low-dose arm and 13 patients on the high-dose arm).
Serum prostate-specific antigen (PSA) decline of ≥50% was noted in 18% of patients on the low-dose arm and in none of the
patients on the high-dose arm. Four patients were maintained for >150 days. The most prevalent complications were constipation,
fatigue, neurocortical, and neurosensory.
Conclusion: Thalidomide, an antiangiogenesis agent, has some activity in patients with metastatic prostate cancer who have failed multiple
therapies. A total of 27% of all patients had a decline in PSA of ≥40%, often associated with an improvement of clinical symptoms.
Because our preclinical studies had shown that thalidomide increases PSA secretion, we believe that the magnitude of PSA decline
seen in our trial justifies further study.</abstract><cop>Philadelphia, PA</cop><pub>American Association for Cancer Research</pub><pmid>11448901</pmid><tpages>6</tpages></addata></record> |
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| ispartof | Clinical cancer research, 2001-07, Vol.7 (7), p.1888-1893 |
| issn | 1078-0432 1557-3265 |
| language | eng |
| recordid | cdi_pubmed_primary_11448901 |
| source | MEDLINE; American Association for Cancer Research; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection |
| subjects | Aged Aged, 80 and over Androgens - physiology Angiogenesis Inhibitors - therapeutic use Antineoplastic agents Biological and medical sciences Chemotherapy Dose-Response Relationship, Drug Endothelial Growth Factors - blood Fibroblast Growth Factor 2 - blood Fibroblast Growth Factor 2 - drug effects Follow-Up Studies Humans Lymphokines - blood Lymphokines - drug effects Lymphotoxin-alpha - blood Male Medical sciences Middle Aged Mood Disorders - chemically induced Neovascularization, Pathologic - pathology Neutropenia - chemically induced Pharmacology. Drug treatments Prostate-Specific Antigen - blood Prostate-Specific Antigen - drug effects Prostatic Neoplasms - blood supply Prostatic Neoplasms - drug therapy Prostatic Neoplasms - pathology Survival Analysis Thalidomide - therapeutic use Time Factors Treatment Outcome Tumor Necrosis Factor-alpha - drug effects Tumor Necrosis Factor-alpha - metabolism Vascular Endothelial Growth Factor A Vascular Endothelial Growth Factors |
| title | A Randomized Phase II Trial of Thalidomide, an Angiogenesis Inhibitor, in Patients with Androgen-independent Prostate Cancer |
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