Hematopoietic stem cells, leukemic stem cells and chronic myelogenous leukemia
Blood-related cancers, or leukemias, have been shown to arise from a rare subset of cells that escape normal regulation and drive the formation and growth of the tumor. The finding that these so-called cancer stem cells, or leukemic stem cells (LSC), can be purified away from the other cells in the...
Gespeichert in:
Veröffentlicht in: | Cell cycle (Georgetown, Tex.) Tex.), 2005-02, Vol.4 (2), p.266-268 |
---|---|
1. Verfasser: | |
Format: | Artikel |
Sprache: | eng |
Schlagworte: | |
Online-Zugang: | Volltext |
Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
container_end_page | 268 |
---|---|
container_issue | 2 |
container_start_page | 266 |
container_title | Cell cycle (Georgetown, Tex.) |
container_volume | 4 |
creator | Passegué, Emmanuelle |
description | Blood-related cancers, or leukemias, have been shown to arise from a rare subset of cells that escape normal regulation and drive the formation and growth of the tumor. The finding that these so-called cancer stem cells, or leukemic stem cells (LSC), can be purified away from the other cells in the tumor allows their precise analysis to identify candidate molecules and regulatory pathways that play a role in progression, maintenance, and spreading of leukemias. The analyses of the other, numerically dominant, cells in the tumor, while also interesting, do not directly interrogate these key properties of malignancies. Mouse models of human myeloproliferative disorder and acute myelogenous leukemia have highlighted the remarkable conservation of disease mechanisms between both species. They can now be used to identify the LSC for each type of human leukemia and understand how they escape normal regulation and become malignant. Given the clinical importance of LSC identification, the insights gained through these approaches will quickly translate into clinical applications and lead to improved treatments for human leukemias. |
format | Article |
fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_proquest_miscellaneous_67769206</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>67769206</sourcerecordid><originalsourceid>FETCH-LOGICAL-p139t-39da63298aabe973f569b3b2bcd7c8ea3174fd387c057cbe8973a346240bd0763</originalsourceid><addsrcrecordid>eNpVkMFKxDAURYMgzjj6C9KVKwtJX5M0SxnUEQbd6Lq8JK9abZratIv5e2dwZuHqwuFwudwzthRSirzkXC7YZUpfnBeVNuKCLYRUUoIyS_ayoYBTHGJLU-uyNFHIHHVduss6mr8p_IMZ9j5zn2Ps9zjsqIsf1Mc5nVy8YucNdomuj7li748Pb-tNvn19el7fb_NBgJlyMB4VFKZCtGQ0NFIZC7awzmtXEYLQZeOh0o5L7SxVewehVEXJredawYrd_vUOY_yZKU11aNNhIva031MrrZUp-EG8OYqzDeTrYWwDjrv69AD8Am7lV0U</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>67769206</pqid></control><display><type>article</type><title>Hematopoietic stem cells, leukemic stem cells and chronic myelogenous leukemia</title><source>MEDLINE</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><creator>Passegué, Emmanuelle</creator><creatorcontrib>Passegué, Emmanuelle</creatorcontrib><description>Blood-related cancers, or leukemias, have been shown to arise from a rare subset of cells that escape normal regulation and drive the formation and growth of the tumor. The finding that these so-called cancer stem cells, or leukemic stem cells (LSC), can be purified away from the other cells in the tumor allows their precise analysis to identify candidate molecules and regulatory pathways that play a role in progression, maintenance, and spreading of leukemias. The analyses of the other, numerically dominant, cells in the tumor, while also interesting, do not directly interrogate these key properties of malignancies. Mouse models of human myeloproliferative disorder and acute myelogenous leukemia have highlighted the remarkable conservation of disease mechanisms between both species. They can now be used to identify the LSC for each type of human leukemia and understand how they escape normal regulation and become malignant. Given the clinical importance of LSC identification, the insights gained through these approaches will quickly translate into clinical applications and lead to improved treatments for human leukemias.</description><identifier>EISSN: 1551-4005</identifier><identifier>PMID: 15655369</identifier><language>eng</language><publisher>United States</publisher><subject>Animals ; Cell Proliferation ; Disease Models, Animal ; Disease Progression ; Gene Expression Regulation, Leukemic ; Hematopoiesis ; Hematopoietic Stem Cells - pathology ; Hematopoietic Stem Cells - physiology ; Homeodomain Proteins - genetics ; Homeodomain Proteins - physiology ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive - genetics ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive - pathology ; Mice ; Myeloproliferative Disorders - genetics ; Myeloproliferative Disorders - pathology ; Neoplastic Stem Cells - pathology ; Neoplastic Stem Cells - physiology ; Nuclear Proteins - genetics ; Nuclear Proteins - physiology ; Polycomb Repressive Complex 1 ; Proto-Oncogene Proteins - genetics ; Proto-Oncogene Proteins - physiology ; Proto-Oncogene Proteins c-jun - genetics ; Proto-Oncogene Proteins c-jun - physiology ; Repressor Proteins - genetics ; Repressor Proteins - physiology ; Transcription Factor AP-1 - genetics ; Transcription Factor AP-1 - physiology ; Transcription Factors - genetics ; Transcription Factors - physiology ; Wnt Proteins - genetics ; Wnt Proteins - physiology</subject><ispartof>Cell cycle (Georgetown, Tex.), 2005-02, Vol.4 (2), p.266-268</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,781,785</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15655369$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Passegué, Emmanuelle</creatorcontrib><title>Hematopoietic stem cells, leukemic stem cells and chronic myelogenous leukemia</title><title>Cell cycle (Georgetown, Tex.)</title><addtitle>Cell Cycle</addtitle><description>Blood-related cancers, or leukemias, have been shown to arise from a rare subset of cells that escape normal regulation and drive the formation and growth of the tumor. The finding that these so-called cancer stem cells, or leukemic stem cells (LSC), can be purified away from the other cells in the tumor allows their precise analysis to identify candidate molecules and regulatory pathways that play a role in progression, maintenance, and spreading of leukemias. The analyses of the other, numerically dominant, cells in the tumor, while also interesting, do not directly interrogate these key properties of malignancies. Mouse models of human myeloproliferative disorder and acute myelogenous leukemia have highlighted the remarkable conservation of disease mechanisms between both species. They can now be used to identify the LSC for each type of human leukemia and understand how they escape normal regulation and become malignant. Given the clinical importance of LSC identification, the insights gained through these approaches will quickly translate into clinical applications and lead to improved treatments for human leukemias.</description><subject>Animals</subject><subject>Cell Proliferation</subject><subject>Disease Models, Animal</subject><subject>Disease Progression</subject><subject>Gene Expression Regulation, Leukemic</subject><subject>Hematopoiesis</subject><subject>Hematopoietic Stem Cells - pathology</subject><subject>Hematopoietic Stem Cells - physiology</subject><subject>Homeodomain Proteins - genetics</subject><subject>Homeodomain Proteins - physiology</subject><subject>Leukemia, Myelogenous, Chronic, BCR-ABL Positive - genetics</subject><subject>Leukemia, Myelogenous, Chronic, BCR-ABL Positive - pathology</subject><subject>Mice</subject><subject>Myeloproliferative Disorders - genetics</subject><subject>Myeloproliferative Disorders - pathology</subject><subject>Neoplastic Stem Cells - pathology</subject><subject>Neoplastic Stem Cells - physiology</subject><subject>Nuclear Proteins - genetics</subject><subject>Nuclear Proteins - physiology</subject><subject>Polycomb Repressive Complex 1</subject><subject>Proto-Oncogene Proteins - genetics</subject><subject>Proto-Oncogene Proteins - physiology</subject><subject>Proto-Oncogene Proteins c-jun - genetics</subject><subject>Proto-Oncogene Proteins c-jun - physiology</subject><subject>Repressor Proteins - genetics</subject><subject>Repressor Proteins - physiology</subject><subject>Transcription Factor AP-1 - genetics</subject><subject>Transcription Factor AP-1 - physiology</subject><subject>Transcription Factors - genetics</subject><subject>Transcription Factors - physiology</subject><subject>Wnt Proteins - genetics</subject><subject>Wnt Proteins - physiology</subject><issn>1551-4005</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVkMFKxDAURYMgzjj6C9KVKwtJX5M0SxnUEQbd6Lq8JK9abZratIv5e2dwZuHqwuFwudwzthRSirzkXC7YZUpfnBeVNuKCLYRUUoIyS_ayoYBTHGJLU-uyNFHIHHVduss6mr8p_IMZ9j5zn2Ps9zjsqIsf1Mc5nVy8YucNdomuj7li748Pb-tNvn19el7fb_NBgJlyMB4VFKZCtGQ0NFIZC7awzmtXEYLQZeOh0o5L7SxVewehVEXJredawYrd_vUOY_yZKU11aNNhIva031MrrZUp-EG8OYqzDeTrYWwDjrv69AD8Am7lV0U</recordid><startdate>200502</startdate><enddate>200502</enddate><creator>Passegué, Emmanuelle</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope></search><sort><creationdate>200502</creationdate><title>Hematopoietic stem cells, leukemic stem cells and chronic myelogenous leukemia</title><author>Passegué, Emmanuelle</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p139t-39da63298aabe973f569b3b2bcd7c8ea3174fd387c057cbe8973a346240bd0763</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Animals</topic><topic>Cell Proliferation</topic><topic>Disease Models, Animal</topic><topic>Disease Progression</topic><topic>Gene Expression Regulation, Leukemic</topic><topic>Hematopoiesis</topic><topic>Hematopoietic Stem Cells - pathology</topic><topic>Hematopoietic Stem Cells - physiology</topic><topic>Homeodomain Proteins - genetics</topic><topic>Homeodomain Proteins - physiology</topic><topic>Leukemia, Myelogenous, Chronic, BCR-ABL Positive - genetics</topic><topic>Leukemia, Myelogenous, Chronic, BCR-ABL Positive - pathology</topic><topic>Mice</topic><topic>Myeloproliferative Disorders - genetics</topic><topic>Myeloproliferative Disorders - pathology</topic><topic>Neoplastic Stem Cells - pathology</topic><topic>Neoplastic Stem Cells - physiology</topic><topic>Nuclear Proteins - genetics</topic><topic>Nuclear Proteins - physiology</topic><topic>Polycomb Repressive Complex 1</topic><topic>Proto-Oncogene Proteins - genetics</topic><topic>Proto-Oncogene Proteins - physiology</topic><topic>Proto-Oncogene Proteins c-jun - genetics</topic><topic>Proto-Oncogene Proteins c-jun - physiology</topic><topic>Repressor Proteins - genetics</topic><topic>Repressor Proteins - physiology</topic><topic>Transcription Factor AP-1 - genetics</topic><topic>Transcription Factor AP-1 - physiology</topic><topic>Transcription Factors - genetics</topic><topic>Transcription Factors - physiology</topic><topic>Wnt Proteins - genetics</topic><topic>Wnt Proteins - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Passegué, Emmanuelle</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><jtitle>Cell cycle (Georgetown, Tex.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Passegué, Emmanuelle</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Hematopoietic stem cells, leukemic stem cells and chronic myelogenous leukemia</atitle><jtitle>Cell cycle (Georgetown, Tex.)</jtitle><addtitle>Cell Cycle</addtitle><date>2005-02</date><risdate>2005</risdate><volume>4</volume><issue>2</issue><spage>266</spage><epage>268</epage><pages>266-268</pages><eissn>1551-4005</eissn><abstract>Blood-related cancers, or leukemias, have been shown to arise from a rare subset of cells that escape normal regulation and drive the formation and growth of the tumor. The finding that these so-called cancer stem cells, or leukemic stem cells (LSC), can be purified away from the other cells in the tumor allows their precise analysis to identify candidate molecules and regulatory pathways that play a role in progression, maintenance, and spreading of leukemias. The analyses of the other, numerically dominant, cells in the tumor, while also interesting, do not directly interrogate these key properties of malignancies. Mouse models of human myeloproliferative disorder and acute myelogenous leukemia have highlighted the remarkable conservation of disease mechanisms between both species. They can now be used to identify the LSC for each type of human leukemia and understand how they escape normal regulation and become malignant. Given the clinical importance of LSC identification, the insights gained through these approaches will quickly translate into clinical applications and lead to improved treatments for human leukemias.</abstract><cop>United States</cop><pmid>15655369</pmid><tpages>3</tpages></addata></record> |
fulltext | fulltext |
identifier | EISSN: 1551-4005 |
ispartof | Cell cycle (Georgetown, Tex.), 2005-02, Vol.4 (2), p.266-268 |
issn | 1551-4005 |
language | eng |
recordid | cdi_proquest_miscellaneous_67769206 |
source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals |
subjects | Animals Cell Proliferation Disease Models, Animal Disease Progression Gene Expression Regulation, Leukemic Hematopoiesis Hematopoietic Stem Cells - pathology Hematopoietic Stem Cells - physiology Homeodomain Proteins - genetics Homeodomain Proteins - physiology Leukemia, Myelogenous, Chronic, BCR-ABL Positive - genetics Leukemia, Myelogenous, Chronic, BCR-ABL Positive - pathology Mice Myeloproliferative Disorders - genetics Myeloproliferative Disorders - pathology Neoplastic Stem Cells - pathology Neoplastic Stem Cells - physiology Nuclear Proteins - genetics Nuclear Proteins - physiology Polycomb Repressive Complex 1 Proto-Oncogene Proteins - genetics Proto-Oncogene Proteins - physiology Proto-Oncogene Proteins c-jun - genetics Proto-Oncogene Proteins c-jun - physiology Repressor Proteins - genetics Repressor Proteins - physiology Transcription Factor AP-1 - genetics Transcription Factor AP-1 - physiology Transcription Factors - genetics Transcription Factors - physiology Wnt Proteins - genetics Wnt Proteins - physiology |
title | Hematopoietic stem cells, leukemic stem cells and chronic myelogenous leukemia |
url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-11T17%3A12%3A34IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Hematopoietic%20stem%20cells,%20leukemic%20stem%20cells%20and%20chronic%20myelogenous%20leukemia&rft.jtitle=Cell%20cycle%20(Georgetown,%20Tex.)&rft.au=Passegu%C3%A9,%20Emmanuelle&rft.date=2005-02&rft.volume=4&rft.issue=2&rft.spage=266&rft.epage=268&rft.pages=266-268&rft.eissn=1551-4005&rft_id=info:doi/&rft_dat=%3Cproquest_pubme%3E67769206%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=67769206&rft_id=info:pmid/15655369&rfr_iscdi=true |