Prevention of Chemotherapy-Induced Alopecia in Rats by CDK Inhibitors
Most traditional cytotoxic anticancer agents ablate the rapidly dividing epithelium of the hair follicle and induce alopecia (hair loss). Inhibition of cyclin-dependent kinase 2 (CDK2), a positive regulator of eukaryotic cell cycle progression, may represent a therapeutic strategy for prevention of...
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Veröffentlicht in: | Science (American Association for the Advancement of Science) 2001-01, Vol.291 (5501), p.134-137 |
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creator | Davis, Stephen T. Benson, Bill G. Bramson, H. Neal Chapman, Dennis E. Dickerson, Scott H. Dold, Karen M. Eberwein, Derek J. Edelstein, Mark Frye, Stephen V. Gampe, Robert T. Griffin, Robert J. Harris, Philip A. Hassell, Anne M. Holmes, William D. Hunter, Robert N. Knick, Victoria B. Lackey, Karen Lovejoy, Brett Luzzio, Michael J. Murray, Doris Parker, Patricia Rocque, Warren J. Shewchuk, Lisa Veal, James M. Walker, Duncan H. Kuyper, Lee F. |
description | Most traditional cytotoxic anticancer agents ablate the rapidly dividing epithelium of the hair follicle and induce alopecia (hair loss). Inhibition of cyclin-dependent kinase 2 (CDK2), a positive regulator of eukaryotic cell cycle progression, may represent a therapeutic strategy for prevention of chemotherapy-induced alopecia (CIA) by arresting the cell cycle and reducing the sensitivity of the epithelium to many cell cycle-active antitumor agents. Potent small-molecule inhibitors of CDK2 were developed using structure-based methods. Topical application of these compounds in a neonatal rat model of CIA reduced hair loss at the site of application in 33 to 50% of the animals. Thus, inhibition of CDK2 represents a potentially useful approach for the prevention of CIA in cancer patients. |
doi_str_mv | 10.1126/science.291.5501.134 |
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Neal ; Chapman, Dennis E. ; Dickerson, Scott H. ; Dold, Karen M. ; Eberwein, Derek J. ; Edelstein, Mark ; Frye, Stephen V. ; Gampe, Robert T. ; Griffin, Robert J. ; Harris, Philip A. ; Hassell, Anne M. ; Holmes, William D. ; Hunter, Robert N. ; Knick, Victoria B. ; Lackey, Karen ; Lovejoy, Brett ; Luzzio, Michael J. ; Murray, Doris ; Parker, Patricia ; Rocque, Warren J. ; Shewchuk, Lisa ; Veal, James M. ; Walker, Duncan H. ; Kuyper, Lee F.</creator><creatorcontrib>Davis, Stephen T. ; Benson, Bill G. ; Bramson, H. Neal ; Chapman, Dennis E. ; Dickerson, Scott H. ; Dold, Karen M. ; Eberwein, Derek J. ; Edelstein, Mark ; Frye, Stephen V. ; Gampe, Robert T. ; Griffin, Robert J. ; Harris, Philip A. ; Hassell, Anne M. ; Holmes, William D. ; Hunter, Robert N. ; Knick, Victoria B. ; Lackey, Karen ; Lovejoy, Brett ; Luzzio, Michael J. ; Murray, Doris ; Parker, Patricia ; Rocque, Warren J. ; Shewchuk, Lisa ; Veal, James M. ; Walker, Duncan H. ; Kuyper, Lee F.</creatorcontrib><description>Most traditional cytotoxic anticancer agents ablate the rapidly dividing epithelium of the hair follicle and induce alopecia (hair loss). Inhibition of cyclin-dependent kinase 2 (CDK2), a positive regulator of eukaryotic cell cycle progression, may represent a therapeutic strategy for prevention of chemotherapy-induced alopecia (CIA) by arresting the cell cycle and reducing the sensitivity of the epithelium to many cell cycle-active antitumor agents. Potent small-molecule inhibitors of CDK2 were developed using structure-based methods. Topical application of these compounds in a neonatal rat model of CIA reduced hair loss at the site of application in 33 to 50% of the animals. Thus, inhibition of CDK2 represents a potentially useful approach for the prevention of CIA in cancer patients.</description><identifier>ISSN: 0036-8075</identifier><identifier>EISSN: 1095-9203</identifier><identifier>DOI: 10.1126/science.291.5501.134</identifier><identifier>PMID: 11141566</identifier><identifier>CODEN: SCIEAS</identifier><language>eng</language><publisher>Washington, DC: American Society for the Advancement of Science</publisher><subject>Alopecia ; Alopecia - chemically induced ; Alopecia - prevention & control ; Animals ; Animals, Newborn ; Antineoplastic Agents - toxicity ; Antineoplastic Combined Chemotherapy Protocols - toxicity ; Antineoplastics ; Apoptosis - drug effects ; Atoms ; Baldness ; Biological and medical sciences ; Cancer ; CDC2-CDC28 Kinases ; Cdk2 kinase ; Cell cycle ; Cell Cycle - drug effects ; Cell Line ; Chemotherapy ; Complications and side effects ; Cyclin-Dependent Kinase 2 ; cyclin-dependent kinase inhibitors ; Cyclin-Dependent Kinases - antagonists & inhibitors ; Cyclin-Dependent Kinases - metabolism ; Cyclins ; Cyclophosphamide - toxicity ; Cytoprotection - drug effects ; DNA - biosynthesis ; Doxorubicin - toxicity ; Drug Design ; Drug therapy ; Drug toxicity and drugs side effects treatment ; Enzyme Inhibitors - chemical synthesis ; Enzyme Inhibitors - chemistry ; Enzyme Inhibitors - pharmacology ; Epithelial cells ; Epithelium - drug effects ; Etoposide - toxicity ; Hair ; Hair Follicle - cytology ; Hair Follicle - drug effects ; Hair follicles ; Humans ; Indoles - chemical synthesis ; Indoles - chemistry ; Indoles - pharmacology ; Inhibition ; Medical sciences ; Mice ; Mice, SCID ; Narcotics ; Pharmacology. Drug treatments ; Phosphorylation ; Prevention ; Protein-Serine-Threonine Kinases - antagonists & inhibitors ; Protein-Serine-Threonine Kinases - metabolism ; Rats ; Retinoblastoma Protein - metabolism ; Rodents ; Scalp ; Scalp - transplantation ; Sulfonamides - chemical synthesis ; Sulfonamides - chemistry ; Sulfonamides - pharmacology ; Toxicity: skin, dermoskeleton ; Transplantation, Heterologous</subject><ispartof>Science (American Association for the Advancement of Science), 2001-01, Vol.291 (5501), p.134-137</ispartof><rights>Copyright 2001 American Association for the Advancement of Science</rights><rights>2001 INIST-CNRS</rights><rights>COPYRIGHT 2001 American Association for the Advancement of Science</rights><rights>Copyright American Association for the Advancement of Science Jan 5, 2001</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c809t-76650c4aeebed33f8045cdd08397ca3272fad69d741cf16aa10d899bd3d4c8de3</citedby><cites>FETCH-LOGICAL-c809t-76650c4aeebed33f8045cdd08397ca3272fad69d741cf16aa10d899bd3d4c8de3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.jstor.org/stable/pdf/3082192$$EPDF$$P50$$Gjstor$$H</linktopdf><linktohtml>$$Uhttps://www.jstor.org/stable/3082192$$EHTML$$P50$$Gjstor$$H</linktohtml><link.rule.ids>314,777,781,800,2871,2872,27905,27906,57998,58231</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=853631$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11141566$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Davis, Stephen T.</creatorcontrib><creatorcontrib>Benson, Bill G.</creatorcontrib><creatorcontrib>Bramson, H. Neal</creatorcontrib><creatorcontrib>Chapman, Dennis E.</creatorcontrib><creatorcontrib>Dickerson, Scott H.</creatorcontrib><creatorcontrib>Dold, Karen M.</creatorcontrib><creatorcontrib>Eberwein, Derek J.</creatorcontrib><creatorcontrib>Edelstein, Mark</creatorcontrib><creatorcontrib>Frye, Stephen V.</creatorcontrib><creatorcontrib>Gampe, Robert T.</creatorcontrib><creatorcontrib>Griffin, Robert J.</creatorcontrib><creatorcontrib>Harris, Philip A.</creatorcontrib><creatorcontrib>Hassell, Anne M.</creatorcontrib><creatorcontrib>Holmes, William D.</creatorcontrib><creatorcontrib>Hunter, Robert N.</creatorcontrib><creatorcontrib>Knick, Victoria B.</creatorcontrib><creatorcontrib>Lackey, Karen</creatorcontrib><creatorcontrib>Lovejoy, Brett</creatorcontrib><creatorcontrib>Luzzio, Michael J.</creatorcontrib><creatorcontrib>Murray, Doris</creatorcontrib><creatorcontrib>Parker, Patricia</creatorcontrib><creatorcontrib>Rocque, Warren J.</creatorcontrib><creatorcontrib>Shewchuk, Lisa</creatorcontrib><creatorcontrib>Veal, James M.</creatorcontrib><creatorcontrib>Walker, Duncan H.</creatorcontrib><creatorcontrib>Kuyper, Lee F.</creatorcontrib><title>Prevention of Chemotherapy-Induced Alopecia in Rats by CDK Inhibitors</title><title>Science (American Association for the Advancement of Science)</title><addtitle>Science</addtitle><description>Most traditional cytotoxic anticancer agents ablate the rapidly dividing epithelium of the hair follicle and induce alopecia (hair loss). Inhibition of cyclin-dependent kinase 2 (CDK2), a positive regulator of eukaryotic cell cycle progression, may represent a therapeutic strategy for prevention of chemotherapy-induced alopecia (CIA) by arresting the cell cycle and reducing the sensitivity of the epithelium to many cell cycle-active antitumor agents. Potent small-molecule inhibitors of CDK2 were developed using structure-based methods. Topical application of these compounds in a neonatal rat model of CIA reduced hair loss at the site of application in 33 to 50% of the animals. Thus, inhibition of CDK2 represents a potentially useful approach for the prevention of CIA in cancer patients.</description><subject>Alopecia</subject><subject>Alopecia - chemically induced</subject><subject>Alopecia - prevention & control</subject><subject>Animals</subject><subject>Animals, Newborn</subject><subject>Antineoplastic Agents - toxicity</subject><subject>Antineoplastic Combined Chemotherapy Protocols - toxicity</subject><subject>Antineoplastics</subject><subject>Apoptosis - drug effects</subject><subject>Atoms</subject><subject>Baldness</subject><subject>Biological and medical sciences</subject><subject>Cancer</subject><subject>CDC2-CDC28 Kinases</subject><subject>Cdk2 kinase</subject><subject>Cell cycle</subject><subject>Cell Cycle - drug effects</subject><subject>Cell Line</subject><subject>Chemotherapy</subject><subject>Complications and side effects</subject><subject>Cyclin-Dependent Kinase 2</subject><subject>cyclin-dependent kinase inhibitors</subject><subject>Cyclin-Dependent Kinases - antagonists & inhibitors</subject><subject>Cyclin-Dependent Kinases - metabolism</subject><subject>Cyclins</subject><subject>Cyclophosphamide - toxicity</subject><subject>Cytoprotection - drug effects</subject><subject>DNA - biosynthesis</subject><subject>Doxorubicin - toxicity</subject><subject>Drug Design</subject><subject>Drug therapy</subject><subject>Drug toxicity and drugs side effects treatment</subject><subject>Enzyme Inhibitors - chemical synthesis</subject><subject>Enzyme Inhibitors - chemistry</subject><subject>Enzyme Inhibitors - pharmacology</subject><subject>Epithelial cells</subject><subject>Epithelium - drug effects</subject><subject>Etoposide - toxicity</subject><subject>Hair</subject><subject>Hair Follicle - cytology</subject><subject>Hair Follicle - drug effects</subject><subject>Hair follicles</subject><subject>Humans</subject><subject>Indoles - chemical synthesis</subject><subject>Indoles - chemistry</subject><subject>Indoles - pharmacology</subject><subject>Inhibition</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, SCID</subject><subject>Narcotics</subject><subject>Pharmacology. Drug treatments</subject><subject>Phosphorylation</subject><subject>Prevention</subject><subject>Protein-Serine-Threonine Kinases - antagonists & inhibitors</subject><subject>Protein-Serine-Threonine Kinases - metabolism</subject><subject>Rats</subject><subject>Retinoblastoma Protein - metabolism</subject><subject>Rodents</subject><subject>Scalp</subject><subject>Scalp - transplantation</subject><subject>Sulfonamides - chemical synthesis</subject><subject>Sulfonamides - chemistry</subject><subject>Sulfonamides - pharmacology</subject><subject>Toxicity: skin, dermoskeleton</subject><subject>Transplantation, Heterologous</subject><issn>0036-8075</issn><issn>1095-9203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2001</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqN0u-L0zAYwPEiijdP_4NDigeeL-xMmjZpXs7dOYfDib_ehix5umV0yUxacf-9GSt3noxj9EWh-SSQp98kucBoiHFO3wVlwCoY5hwPyxLhISbFo2SAES8zniPyOBkgRGhWIVaeJc9CWCMU1zh5mpxhjAtcUjpIbr54-A22Nc6mrk7HK9i4dgVebnfZ1OpOgU5HjduCMjI1Nv0q25Audun4-lM6tSuzMK3z4XnypJZNgBf9-zz58eHm-_hjNptPpuPRLFMV4m3GKC2RKiTAAjQhdYWKUmmNKsKZkiRneS015ZoVWNWYSomRrjhfaKILVWkg58nV4dytd786CK3YmKCgaaQF1wXBCkJ4HAaL8vWDEjNGGGU4wlf_wbXrvI23EDkmJWM5L-7QUjYgjK1d66XanyhGlOcMEcYjensELcHGaTbOQm3i5395doTHR8PGqGP-zT0fSQt_2qXsQhDTb59PpvOfJ9P3k1NpNZk9MIqeKtc0sAQRmxjP7_HiwJV3IXioxdabjfQ7gZHYxy762EWMXexjFzH2uO1l_-u6xQb03aa-7ggueyCDkk3tpVUm3LqqJJTsC7g4qHWILd-uElTlmOfkL9krCuY</recordid><startdate>20010105</startdate><enddate>20010105</enddate><creator>Davis, Stephen T.</creator><creator>Benson, Bill G.</creator><creator>Bramson, H. 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Neal ; Chapman, Dennis E. ; Dickerson, Scott H. ; Dold, Karen M. ; Eberwein, Derek J. ; Edelstein, Mark ; Frye, Stephen V. ; Gampe, Robert T. ; Griffin, Robert J. ; Harris, Philip A. ; Hassell, Anne M. ; Holmes, William D. ; Hunter, Robert N. ; Knick, Victoria B. ; Lackey, Karen ; Lovejoy, Brett ; Luzzio, Michael J. ; Murray, Doris ; Parker, Patricia ; Rocque, Warren J. ; Shewchuk, Lisa ; Veal, James M. ; Walker, Duncan H. ; Kuyper, Lee F.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c809t-76650c4aeebed33f8045cdd08397ca3272fad69d741cf16aa10d899bd3d4c8de3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2001</creationdate><topic>Alopecia</topic><topic>Alopecia - chemically induced</topic><topic>Alopecia - prevention & control</topic><topic>Animals</topic><topic>Animals, Newborn</topic><topic>Antineoplastic Agents - toxicity</topic><topic>Antineoplastic Combined Chemotherapy Protocols - toxicity</topic><topic>Antineoplastics</topic><topic>Apoptosis - drug effects</topic><topic>Atoms</topic><topic>Baldness</topic><topic>Biological and medical sciences</topic><topic>Cancer</topic><topic>CDC2-CDC28 Kinases</topic><topic>Cdk2 kinase</topic><topic>Cell cycle</topic><topic>Cell Cycle - drug effects</topic><topic>Cell Line</topic><topic>Chemotherapy</topic><topic>Complications and side effects</topic><topic>Cyclin-Dependent Kinase 2</topic><topic>cyclin-dependent kinase inhibitors</topic><topic>Cyclin-Dependent Kinases - antagonists & inhibitors</topic><topic>Cyclin-Dependent Kinases - metabolism</topic><topic>Cyclins</topic><topic>Cyclophosphamide - toxicity</topic><topic>Cytoprotection - drug effects</topic><topic>DNA - biosynthesis</topic><topic>Doxorubicin - toxicity</topic><topic>Drug Design</topic><topic>Drug therapy</topic><topic>Drug toxicity and drugs side effects treatment</topic><topic>Enzyme Inhibitors - chemical synthesis</topic><topic>Enzyme Inhibitors - chemistry</topic><topic>Enzyme Inhibitors - pharmacology</topic><topic>Epithelial cells</topic><topic>Epithelium - drug effects</topic><topic>Etoposide - toxicity</topic><topic>Hair</topic><topic>Hair Follicle - cytology</topic><topic>Hair Follicle - drug effects</topic><topic>Hair follicles</topic><topic>Humans</topic><topic>Indoles - chemical synthesis</topic><topic>Indoles - chemistry</topic><topic>Indoles - pharmacology</topic><topic>Inhibition</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, SCID</topic><topic>Narcotics</topic><topic>Pharmacology. 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BioEngineering Abstracts</collection><collection>Environmental Science Database</collection><collection>Earth, Atmospheric & Aquatic Science Database</collection><collection>Materials Science Collection</collection><collection>ProQuest One Education</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>Engineering Collection</collection><collection>Environmental Science Collection</collection><collection>ProQuest Central Basic</collection><collection>University of Michigan</collection><collection>Genetics Abstracts</collection><collection>Biotechnology Research Abstracts</collection><jtitle>Science (American Association for the Advancement of Science)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Davis, Stephen T.</au><au>Benson, Bill G.</au><au>Bramson, H. Neal</au><au>Chapman, Dennis E.</au><au>Dickerson, Scott H.</au><au>Dold, Karen M.</au><au>Eberwein, Derek J.</au><au>Edelstein, Mark</au><au>Frye, Stephen V.</au><au>Gampe, Robert T.</au><au>Griffin, Robert J.</au><au>Harris, Philip A.</au><au>Hassell, Anne M.</au><au>Holmes, William D.</au><au>Hunter, Robert N.</au><au>Knick, Victoria B.</au><au>Lackey, Karen</au><au>Lovejoy, Brett</au><au>Luzzio, Michael J.</au><au>Murray, Doris</au><au>Parker, Patricia</au><au>Rocque, Warren J.</au><au>Shewchuk, Lisa</au><au>Veal, James M.</au><au>Walker, Duncan H.</au><au>Kuyper, Lee F.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Prevention of Chemotherapy-Induced Alopecia in Rats by CDK Inhibitors</atitle><jtitle>Science (American Association for the Advancement of Science)</jtitle><addtitle>Science</addtitle><date>2001-01-05</date><risdate>2001</risdate><volume>291</volume><issue>5501</issue><spage>134</spage><epage>137</epage><pages>134-137</pages><issn>0036-8075</issn><eissn>1095-9203</eissn><coden>SCIEAS</coden><abstract>Most traditional cytotoxic anticancer agents ablate the rapidly dividing epithelium of the hair follicle and induce alopecia (hair loss). Inhibition of cyclin-dependent kinase 2 (CDK2), a positive regulator of eukaryotic cell cycle progression, may represent a therapeutic strategy for prevention of chemotherapy-induced alopecia (CIA) by arresting the cell cycle and reducing the sensitivity of the epithelium to many cell cycle-active antitumor agents. Potent small-molecule inhibitors of CDK2 were developed using structure-based methods. Topical application of these compounds in a neonatal rat model of CIA reduced hair loss at the site of application in 33 to 50% of the animals. Thus, inhibition of CDK2 represents a potentially useful approach for the prevention of CIA in cancer patients.</abstract><cop>Washington, DC</cop><pub>American Society for the Advancement of Science</pub><pmid>11141566</pmid><doi>10.1126/science.291.5501.134</doi><tpages>4</tpages></addata></record> |
fulltext | fulltext |
identifier | ISSN: 0036-8075 |
ispartof | Science (American Association for the Advancement of Science), 2001-01, Vol.291 (5501), p.134-137 |
issn | 0036-8075 1095-9203 |
language | eng |
recordid | cdi_proquest_miscellaneous_743395507 |
source | MEDLINE; American Association for the Advancement of Science; Jstor Complete Legacy |
subjects | Alopecia Alopecia - chemically induced Alopecia - prevention & control Animals Animals, Newborn Antineoplastic Agents - toxicity Antineoplastic Combined Chemotherapy Protocols - toxicity Antineoplastics Apoptosis - drug effects Atoms Baldness Biological and medical sciences Cancer CDC2-CDC28 Kinases Cdk2 kinase Cell cycle Cell Cycle - drug effects Cell Line Chemotherapy Complications and side effects Cyclin-Dependent Kinase 2 cyclin-dependent kinase inhibitors Cyclin-Dependent Kinases - antagonists & inhibitors Cyclin-Dependent Kinases - metabolism Cyclins Cyclophosphamide - toxicity Cytoprotection - drug effects DNA - biosynthesis Doxorubicin - toxicity Drug Design Drug therapy Drug toxicity and drugs side effects treatment Enzyme Inhibitors - chemical synthesis Enzyme Inhibitors - chemistry Enzyme Inhibitors - pharmacology Epithelial cells Epithelium - drug effects Etoposide - toxicity Hair Hair Follicle - cytology Hair Follicle - drug effects Hair follicles Humans Indoles - chemical synthesis Indoles - chemistry Indoles - pharmacology Inhibition Medical sciences Mice Mice, SCID Narcotics Pharmacology. Drug treatments Phosphorylation Prevention Protein-Serine-Threonine Kinases - antagonists & inhibitors Protein-Serine-Threonine Kinases - metabolism Rats Retinoblastoma Protein - metabolism Rodents Scalp Scalp - transplantation Sulfonamides - chemical synthesis Sulfonamides - chemistry Sulfonamides - pharmacology Toxicity: skin, dermoskeleton Transplantation, Heterologous |
title | Prevention of Chemotherapy-Induced Alopecia in Rats by CDK Inhibitors |
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