The Cyclin-like Protein Spy1 Regulates Growth and Division Characteristics of the CD133+ Population in Human Glioma
The heterogeneity of brain cancers, as most solid tumors, complicates diagnosis and treatment. Identifying and targeting populations of cells driving tumorigenesis is a top priority for the cancer biology field. This is not a trivial task; considerable variance exists in the driving mutations, ident...
Gespeichert in:
| Veröffentlicht in: | Cancer cell 2014-01, Vol.25 (1), p.64-76 |
|---|---|
| Hauptverfasser: | , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 76 |
|---|---|
| container_issue | 1 |
| container_start_page | 64 |
| container_title | Cancer cell |
| container_volume | 25 |
| creator | Lubanska, Dorota Market-Velker, Brenna A. deCarvalho, Ana C. Mikkelsen, Tom Fidalgo da Silva, Elizabeth Porter, Lisa A. |
| description | The heterogeneity of brain cancers, as most solid tumors, complicates diagnosis and treatment. Identifying and targeting populations of cells driving tumorigenesis is a top priority for the cancer biology field. This is not a trivial task; considerable variance exists in the driving mutations, identifying markers, and evolutionary pressures influencing initiating cells in different individual tumors. Despite this, the ability to self-renew and differentiate must be conserved to reseed a heterogeneous tumor mass. Focusing on one example of a tumor-initiating cell population, we demonstrate that the atypical cyclin-like protein Spy1 plays a role in balancing the division properties of glioma cells with stemness properties. This mechanistic insight may provide new opportunities for therapeutic intervention of brain cancer.
[Display omitted]
•Spy1 levels are prognostic for poor survival in human glioma•Spy1 drives proliferation and stemness properties in human glioma•Spy1 levels are critical for fate of neural cells with stem/progenitor properties•Spy1 plays an important role in symmetric division of glioma stem cells |
| doi_str_mv | 10.1016/j.ccr.2013.12.006 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_1490709810</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S1535610813005357</els_id><sourcerecordid>1490709810</sourcerecordid><originalsourceid>FETCH-LOGICAL-c396t-77a8129cfde96ad81e368a828063c5ce46841cf664f1ce98dd779f7e290004e13</originalsourceid><addsrcrecordid>eNp9kM1O3DAURq2qqPz1AdhUXlaqEnzjjGOrq2ooAxISCOjaMs5Nx9MkntoOaN4eR0O7ZGUvznekewg5A1YCA3G-Ka0NZcWAl1CVjIkP5AhkIwsupPiY_wu-KAQweUiOY9ywvIFGfSKHVV3zugJ2ROLjGulyZ3s3Fr37g_Qu-IRupA_bHdB7_D31JmGkq-Bf0pqasaUX7tlF50e6XJtgbMLgYnI2Ut_RNNsugPNv9M5v5-0MZt3VNJiRrnrnB3NKDjrTR_z89p6QX5c_H5dXxc3t6nr546awXIlUNI2RUCnbtaiEaSVgPsvISjLB7cJiLWQNthOi7sCikm3bNKprsFKMsRqBn5Cve-82-L8TxqQHFy32vRnRT1FDrVjDlASWUdijNvgYA3Z6G9xgwk4D03NrvdG5tZ5ba6h0bp03X97009OA7f_Fv7gZ-L4HMB_57DDoaB2OFlsX0CbdeveO_hXSgo4f</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1490709810</pqid></control><display><type>article</type><title>The Cyclin-like Protein Spy1 Regulates Growth and Division Characteristics of the CD133+ Population in Human Glioma</title><source>MEDLINE</source><source>Cell Press Free Archives</source><source>ScienceDirect Journals (5 years ago - present)</source><source>EZB-FREE-00999 freely available EZB journals</source><creator>Lubanska, Dorota ; Market-Velker, Brenna A. ; deCarvalho, Ana C. ; Mikkelsen, Tom ; Fidalgo da Silva, Elizabeth ; Porter, Lisa A.</creator><creatorcontrib>Lubanska, Dorota ; Market-Velker, Brenna A. ; deCarvalho, Ana C. ; Mikkelsen, Tom ; Fidalgo da Silva, Elizabeth ; Porter, Lisa A.</creatorcontrib><description>The heterogeneity of brain cancers, as most solid tumors, complicates diagnosis and treatment. Identifying and targeting populations of cells driving tumorigenesis is a top priority for the cancer biology field. This is not a trivial task; considerable variance exists in the driving mutations, identifying markers, and evolutionary pressures influencing initiating cells in different individual tumors. Despite this, the ability to self-renew and differentiate must be conserved to reseed a heterogeneous tumor mass. Focusing on one example of a tumor-initiating cell population, we demonstrate that the atypical cyclin-like protein Spy1 plays a role in balancing the division properties of glioma cells with stemness properties. This mechanistic insight may provide new opportunities for therapeutic intervention of brain cancer.
[Display omitted]
•Spy1 levels are prognostic for poor survival in human glioma•Spy1 drives proliferation and stemness properties in human glioma•Spy1 levels are critical for fate of neural cells with stem/progenitor properties•Spy1 plays an important role in symmetric division of glioma stem cells</description><identifier>ISSN: 1535-6108</identifier><identifier>EISSN: 1878-3686</identifier><identifier>DOI: 10.1016/j.ccr.2013.12.006</identifier><identifier>PMID: 24434210</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>AC133 Antigen ; Animals ; Antigens, CD - metabolism ; Biomarkers, Tumor - analysis ; Brain Neoplasms - genetics ; Brain Neoplasms - metabolism ; Brain Neoplasms - pathology ; Cell Cycle Proteins - genetics ; Cell Cycle Proteins - metabolism ; Cell Division ; Glioma - genetics ; Glioma - metabolism ; Glioma - pathology ; Glycoproteins - metabolism ; Humans ; Mice ; Mice, Inbred BALB C ; Microdissection ; Neoplastic Stem Cells - metabolism ; Neural Stem Cells - metabolism ; Peptides - metabolism ; Prognosis ; Tissue Array Analysis</subject><ispartof>Cancer cell, 2014-01, Vol.25 (1), p.64-76</ispartof><rights>2014 Elsevier Inc.</rights><rights>Copyright © 2014 Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c396t-77a8129cfde96ad81e368a828063c5ce46841cf664f1ce98dd779f7e290004e13</citedby><cites>FETCH-LOGICAL-c396t-77a8129cfde96ad81e368a828063c5ce46841cf664f1ce98dd779f7e290004e13</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.ccr.2013.12.006$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>314,780,784,3548,27922,27923,45993</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24434210$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lubanska, Dorota</creatorcontrib><creatorcontrib>Market-Velker, Brenna A.</creatorcontrib><creatorcontrib>deCarvalho, Ana C.</creatorcontrib><creatorcontrib>Mikkelsen, Tom</creatorcontrib><creatorcontrib>Fidalgo da Silva, Elizabeth</creatorcontrib><creatorcontrib>Porter, Lisa A.</creatorcontrib><title>The Cyclin-like Protein Spy1 Regulates Growth and Division Characteristics of the CD133+ Population in Human Glioma</title><title>Cancer cell</title><addtitle>Cancer Cell</addtitle><description>The heterogeneity of brain cancers, as most solid tumors, complicates diagnosis and treatment. Identifying and targeting populations of cells driving tumorigenesis is a top priority for the cancer biology field. This is not a trivial task; considerable variance exists in the driving mutations, identifying markers, and evolutionary pressures influencing initiating cells in different individual tumors. Despite this, the ability to self-renew and differentiate must be conserved to reseed a heterogeneous tumor mass. Focusing on one example of a tumor-initiating cell population, we demonstrate that the atypical cyclin-like protein Spy1 plays a role in balancing the division properties of glioma cells with stemness properties. This mechanistic insight may provide new opportunities for therapeutic intervention of brain cancer.
[Display omitted]
•Spy1 levels are prognostic for poor survival in human glioma•Spy1 drives proliferation and stemness properties in human glioma•Spy1 levels are critical for fate of neural cells with stem/progenitor properties•Spy1 plays an important role in symmetric division of glioma stem cells</description><subject>AC133 Antigen</subject><subject>Animals</subject><subject>Antigens, CD - metabolism</subject><subject>Biomarkers, Tumor - analysis</subject><subject>Brain Neoplasms - genetics</subject><subject>Brain Neoplasms - metabolism</subject><subject>Brain Neoplasms - pathology</subject><subject>Cell Cycle Proteins - genetics</subject><subject>Cell Cycle Proteins - metabolism</subject><subject>Cell Division</subject><subject>Glioma - genetics</subject><subject>Glioma - metabolism</subject><subject>Glioma - pathology</subject><subject>Glycoproteins - metabolism</subject><subject>Humans</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Microdissection</subject><subject>Neoplastic Stem Cells - metabolism</subject><subject>Neural Stem Cells - metabolism</subject><subject>Peptides - metabolism</subject><subject>Prognosis</subject><subject>Tissue Array Analysis</subject><issn>1535-6108</issn><issn>1878-3686</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kM1O3DAURq2qqPz1AdhUXlaqEnzjjGOrq2ooAxISCOjaMs5Nx9MkntoOaN4eR0O7ZGUvznekewg5A1YCA3G-Ka0NZcWAl1CVjIkP5AhkIwsupPiY_wu-KAQweUiOY9ywvIFGfSKHVV3zugJ2ROLjGulyZ3s3Fr37g_Qu-IRupA_bHdB7_D31JmGkq-Bf0pqasaUX7tlF50e6XJtgbMLgYnI2Ut_RNNsugPNv9M5v5-0MZt3VNJiRrnrnB3NKDjrTR_z89p6QX5c_H5dXxc3t6nr546awXIlUNI2RUCnbtaiEaSVgPsvISjLB7cJiLWQNthOi7sCikm3bNKprsFKMsRqBn5Cve-82-L8TxqQHFy32vRnRT1FDrVjDlASWUdijNvgYA3Z6G9xgwk4D03NrvdG5tZ5ba6h0bp03X97009OA7f_Fv7gZ-L4HMB_57DDoaB2OFlsX0CbdeveO_hXSgo4f</recordid><startdate>20140113</startdate><enddate>20140113</enddate><creator>Lubanska, Dorota</creator><creator>Market-Velker, Brenna A.</creator><creator>deCarvalho, Ana C.</creator><creator>Mikkelsen, Tom</creator><creator>Fidalgo da Silva, Elizabeth</creator><creator>Porter, Lisa A.</creator><general>Elsevier Inc</general><scope>6I.</scope><scope>AAFTH</scope><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>20140113</creationdate><title>The Cyclin-like Protein Spy1 Regulates Growth and Division Characteristics of the CD133+ Population in Human Glioma</title><author>Lubanska, Dorota ; Market-Velker, Brenna A. ; deCarvalho, Ana C. ; Mikkelsen, Tom ; Fidalgo da Silva, Elizabeth ; Porter, Lisa A.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c396t-77a8129cfde96ad81e368a828063c5ce46841cf664f1ce98dd779f7e290004e13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>AC133 Antigen</topic><topic>Animals</topic><topic>Antigens, CD - metabolism</topic><topic>Biomarkers, Tumor - analysis</topic><topic>Brain Neoplasms - genetics</topic><topic>Brain Neoplasms - metabolism</topic><topic>Brain Neoplasms - pathology</topic><topic>Cell Cycle Proteins - genetics</topic><topic>Cell Cycle Proteins - metabolism</topic><topic>Cell Division</topic><topic>Glioma - genetics</topic><topic>Glioma - metabolism</topic><topic>Glioma - pathology</topic><topic>Glycoproteins - metabolism</topic><topic>Humans</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Microdissection</topic><topic>Neoplastic Stem Cells - metabolism</topic><topic>Neural Stem Cells - metabolism</topic><topic>Peptides - metabolism</topic><topic>Prognosis</topic><topic>Tissue Array Analysis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lubanska, Dorota</creatorcontrib><creatorcontrib>Market-Velker, Brenna A.</creatorcontrib><creatorcontrib>deCarvalho, Ana C.</creatorcontrib><creatorcontrib>Mikkelsen, Tom</creatorcontrib><creatorcontrib>Fidalgo da Silva, Elizabeth</creatorcontrib><creatorcontrib>Porter, Lisa A.</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><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>Cancer cell</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lubanska, Dorota</au><au>Market-Velker, Brenna A.</au><au>deCarvalho, Ana C.</au><au>Mikkelsen, Tom</au><au>Fidalgo da Silva, Elizabeth</au><au>Porter, Lisa A.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The Cyclin-like Protein Spy1 Regulates Growth and Division Characteristics of the CD133+ Population in Human Glioma</atitle><jtitle>Cancer cell</jtitle><addtitle>Cancer Cell</addtitle><date>2014-01-13</date><risdate>2014</risdate><volume>25</volume><issue>1</issue><spage>64</spage><epage>76</epage><pages>64-76</pages><issn>1535-6108</issn><eissn>1878-3686</eissn><abstract>The heterogeneity of brain cancers, as most solid tumors, complicates diagnosis and treatment. Identifying and targeting populations of cells driving tumorigenesis is a top priority for the cancer biology field. This is not a trivial task; considerable variance exists in the driving mutations, identifying markers, and evolutionary pressures influencing initiating cells in different individual tumors. Despite this, the ability to self-renew and differentiate must be conserved to reseed a heterogeneous tumor mass. Focusing on one example of a tumor-initiating cell population, we demonstrate that the atypical cyclin-like protein Spy1 plays a role in balancing the division properties of glioma cells with stemness properties. This mechanistic insight may provide new opportunities for therapeutic intervention of brain cancer.
[Display omitted]
•Spy1 levels are prognostic for poor survival in human glioma•Spy1 drives proliferation and stemness properties in human glioma•Spy1 levels are critical for fate of neural cells with stem/progenitor properties•Spy1 plays an important role in symmetric division of glioma stem cells</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>24434210</pmid><doi>10.1016/j.ccr.2013.12.006</doi><tpages>13</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1535-6108 |
| ispartof | Cancer cell, 2014-01, Vol.25 (1), p.64-76 |
| issn | 1535-6108 1878-3686 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_1490709810 |
| source | MEDLINE; Cell Press Free Archives; ScienceDirect Journals (5 years ago - present); EZB-FREE-00999 freely available EZB journals |
| subjects | AC133 Antigen Animals Antigens, CD - metabolism Biomarkers, Tumor - analysis Brain Neoplasms - genetics Brain Neoplasms - metabolism Brain Neoplasms - pathology Cell Cycle Proteins - genetics Cell Cycle Proteins - metabolism Cell Division Glioma - genetics Glioma - metabolism Glioma - pathology Glycoproteins - metabolism Humans Mice Mice, Inbred BALB C Microdissection Neoplastic Stem Cells - metabolism Neural Stem Cells - metabolism Peptides - metabolism Prognosis Tissue Array Analysis |
| title | The Cyclin-like Protein Spy1 Regulates Growth and Division Characteristics of the CD133+ Population in Human Glioma |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-09T21%3A20%3A10IST&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=The%20Cyclin-like%20Protein%20Spy1%20Regulates%20Growth%20and%20Division%20Characteristics%20of%20the%20CD133+%20Population%20in%20Human%20Glioma&rft.jtitle=Cancer%20cell&rft.au=Lubanska,%20Dorota&rft.date=2014-01-13&rft.volume=25&rft.issue=1&rft.spage=64&rft.epage=76&rft.pages=64-76&rft.issn=1535-6108&rft.eissn=1878-3686&rft_id=info:doi/10.1016/j.ccr.2013.12.006&rft_dat=%3Cproquest_cross%3E1490709810%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=1490709810&rft_id=info:pmid/24434210&rft_els_id=S1535610813005357&rfr_iscdi=true |