c-Myc and cancer metabolism
The processes of cellular growth regulation and cellular metabolism are closely interrelated. The c-Myc oncogene is a "master regulator" which controls many aspects of both of these processes. The metabolic changes which occur in transformed cells, many of which are driven by c-Myc overexp...
Gespeichert in:
Veröffentlicht in: | Clinical cancer research 2012-10, Vol.18 (20), p.5546-5553 |
---|---|
Hauptverfasser: | , , , , |
Format: | Artikel |
Sprache: | eng |
Schlagworte: | |
Online-Zugang: | Volltext |
Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
container_end_page | 5553 |
---|---|
container_issue | 20 |
container_start_page | 5546 |
container_title | Clinical cancer research |
container_volume | 18 |
creator | Miller, Donald M Thomas, Shelia D Islam, Ashraful Muench, David Sedoris, Kara |
description | The processes of cellular growth regulation and cellular metabolism are closely interrelated. The c-Myc oncogene is a "master regulator" which controls many aspects of both of these processes. The metabolic changes which occur in transformed cells, many of which are driven by c-Myc overexpression, are necessary to support the increased need for nucleic acids, proteins, and lipids necessary for rapid cellular proliferation. At the same time, c-Myc overexpression results in coordinated changes in level of expression of gene families which result in increased cellular proliferation. This interesting duality of c-Myc effects places it in the mainstream of transformational changes and gives it a very important role in regulating the "transformed phenotype." The effects induced by c-Myc can occur either as a "primary oncogene" which is activated by amplification or translocation or as a downstream effect of other activated oncogenes. In either case, it appears that c-Myc plays a central role in sustaining the changes which occur with transformation. Although efforts to use c-Myc as a therapeutic target have been quite frustrating, it appears that this may change in the next few years. |
doi_str_mv | 10.1158/1078-0432.ccr-12-0977 |
format | Article |
fullrecord | <record><control><sourceid>pubmed_cross</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_3505847</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>23071356</sourcerecordid><originalsourceid>FETCH-LOGICAL-c529t-b176c37104f38e7fe7571ab237b4e21c2a8b26e13e8cd8e36c615d95bbff18063</originalsourceid><addsrcrecordid>eNpVkNtKxDAQhoMo7rr6BKL0BbJmkubQG0GKJ1gRRK9DMk210sOSVmHf3pZ1F72agfn_b-Aj5ALYEkCaK2DaUJYKvkSMFDhlmdYHZA5Saiq4kofjvsvMyEnffzIGKbD0mMy4YBqEVHNyjvRpg4lriwRdiyEmTRic7-qqb07JUenqPpz9zgV5u7t9zR_o6vn-Mb9ZUZQ8G6gHrVDokVwKE3QZtNTgPBfap4EDcmc8VwFEMFiYIBQqkEUmvS9LMEyJBbnectdfvgkFhnaIrrbrWDUubmznKvv_0lYf9r37tkIyaVI9AuQWgLHr-xjKfReYnWzZyYSdTNg8f7HA7WRr7F3-fbxv7fSIHzOgZaI</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype></control><display><type>article</type><title>c-Myc and cancer metabolism</title><source>MEDLINE</source><source>American Association for Cancer Research</source><source>EZB-FREE-00999 freely available EZB journals</source><source>Alma/SFX Local Collection</source><creator>Miller, Donald M ; Thomas, Shelia D ; Islam, Ashraful ; Muench, David ; Sedoris, Kara</creator><creatorcontrib>Miller, Donald M ; Thomas, Shelia D ; Islam, Ashraful ; Muench, David ; Sedoris, Kara</creatorcontrib><description>The processes of cellular growth regulation and cellular metabolism are closely interrelated. The c-Myc oncogene is a "master regulator" which controls many aspects of both of these processes. The metabolic changes which occur in transformed cells, many of which are driven by c-Myc overexpression, are necessary to support the increased need for nucleic acids, proteins, and lipids necessary for rapid cellular proliferation. At the same time, c-Myc overexpression results in coordinated changes in level of expression of gene families which result in increased cellular proliferation. This interesting duality of c-Myc effects places it in the mainstream of transformational changes and gives it a very important role in regulating the "transformed phenotype." The effects induced by c-Myc can occur either as a "primary oncogene" which is activated by amplification or translocation or as a downstream effect of other activated oncogenes. In either case, it appears that c-Myc plays a central role in sustaining the changes which occur with transformation. Although efforts to use c-Myc as a therapeutic target have been quite frustrating, it appears that this may change in the next few years.</description><identifier>ISSN: 1078-0432</identifier><identifier>EISSN: 1557-3265</identifier><identifier>DOI: 10.1158/1078-0432.ccr-12-0977</identifier><identifier>PMID: 23071356</identifier><language>eng</language><publisher>United States</publisher><subject>Cell Proliferation ; Cell Transformation, Neoplastic - genetics ; Cell Transformation, Neoplastic - metabolism ; Gene Expression Regulation, Neoplastic ; Glutamine - metabolism ; Glycolysis ; Humans ; Mitochondria - metabolism ; Molecular Targeted Therapy ; Neoplasms - genetics ; Neoplasms - metabolism ; Proto-Oncogene Proteins c-myc - genetics ; Proto-Oncogene Proteins c-myc - metabolism</subject><ispartof>Clinical cancer research, 2012-10, Vol.18 (20), p.5546-5553</ispartof><rights>2012 AACR</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c529t-b176c37104f38e7fe7571ab237b4e21c2a8b26e13e8cd8e36c615d95bbff18063</citedby><cites>FETCH-LOGICAL-c529t-b176c37104f38e7fe7571ab237b4e21c2a8b26e13e8cd8e36c615d95bbff18063</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,3356,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23071356$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Miller, Donald M</creatorcontrib><creatorcontrib>Thomas, Shelia D</creatorcontrib><creatorcontrib>Islam, Ashraful</creatorcontrib><creatorcontrib>Muench, David</creatorcontrib><creatorcontrib>Sedoris, Kara</creatorcontrib><title>c-Myc and cancer metabolism</title><title>Clinical cancer research</title><addtitle>Clin Cancer Res</addtitle><description>The processes of cellular growth regulation and cellular metabolism are closely interrelated. The c-Myc oncogene is a "master regulator" which controls many aspects of both of these processes. The metabolic changes which occur in transformed cells, many of which are driven by c-Myc overexpression, are necessary to support the increased need for nucleic acids, proteins, and lipids necessary for rapid cellular proliferation. At the same time, c-Myc overexpression results in coordinated changes in level of expression of gene families which result in increased cellular proliferation. This interesting duality of c-Myc effects places it in the mainstream of transformational changes and gives it a very important role in regulating the "transformed phenotype." The effects induced by c-Myc can occur either as a "primary oncogene" which is activated by amplification or translocation or as a downstream effect of other activated oncogenes. In either case, it appears that c-Myc plays a central role in sustaining the changes which occur with transformation. Although efforts to use c-Myc as a therapeutic target have been quite frustrating, it appears that this may change in the next few years.</description><subject>Cell Proliferation</subject><subject>Cell Transformation, Neoplastic - genetics</subject><subject>Cell Transformation, Neoplastic - metabolism</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Glutamine - metabolism</subject><subject>Glycolysis</subject><subject>Humans</subject><subject>Mitochondria - metabolism</subject><subject>Molecular Targeted Therapy</subject><subject>Neoplasms - genetics</subject><subject>Neoplasms - metabolism</subject><subject>Proto-Oncogene Proteins c-myc - genetics</subject><subject>Proto-Oncogene Proteins c-myc - metabolism</subject><issn>1078-0432</issn><issn>1557-3265</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVkNtKxDAQhoMo7rr6BKL0BbJmkubQG0GKJ1gRRK9DMk210sOSVmHf3pZ1F72agfn_b-Aj5ALYEkCaK2DaUJYKvkSMFDhlmdYHZA5Saiq4kofjvsvMyEnffzIGKbD0mMy4YBqEVHNyjvRpg4lriwRdiyEmTRic7-qqb07JUenqPpz9zgV5u7t9zR_o6vn-Mb9ZUZQ8G6gHrVDokVwKE3QZtNTgPBfap4EDcmc8VwFEMFiYIBQqkEUmvS9LMEyJBbnectdfvgkFhnaIrrbrWDUubmznKvv_0lYf9r37tkIyaVI9AuQWgLHr-xjKfReYnWzZyYSdTNg8f7HA7WRr7F3-fbxv7fSIHzOgZaI</recordid><startdate>20121015</startdate><enddate>20121015</enddate><creator>Miller, Donald M</creator><creator>Thomas, Shelia D</creator><creator>Islam, Ashraful</creator><creator>Muench, David</creator><creator>Sedoris, Kara</creator><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>5PM</scope></search><sort><creationdate>20121015</creationdate><title>c-Myc and cancer metabolism</title><author>Miller, Donald M ; Thomas, Shelia D ; Islam, Ashraful ; Muench, David ; Sedoris, Kara</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c529t-b176c37104f38e7fe7571ab237b4e21c2a8b26e13e8cd8e36c615d95bbff18063</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Cell Proliferation</topic><topic>Cell Transformation, Neoplastic - genetics</topic><topic>Cell Transformation, Neoplastic - metabolism</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Glutamine - metabolism</topic><topic>Glycolysis</topic><topic>Humans</topic><topic>Mitochondria - metabolism</topic><topic>Molecular Targeted Therapy</topic><topic>Neoplasms - genetics</topic><topic>Neoplasms - metabolism</topic><topic>Proto-Oncogene Proteins c-myc - genetics</topic><topic>Proto-Oncogene Proteins c-myc - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Miller, Donald M</creatorcontrib><creatorcontrib>Thomas, Shelia D</creatorcontrib><creatorcontrib>Islam, Ashraful</creatorcontrib><creatorcontrib>Muench, David</creatorcontrib><creatorcontrib>Sedoris, Kara</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Clinical cancer research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Miller, Donald M</au><au>Thomas, Shelia D</au><au>Islam, Ashraful</au><au>Muench, David</au><au>Sedoris, Kara</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>c-Myc and cancer metabolism</atitle><jtitle>Clinical cancer research</jtitle><addtitle>Clin Cancer Res</addtitle><date>2012-10-15</date><risdate>2012</risdate><volume>18</volume><issue>20</issue><spage>5546</spage><epage>5553</epage><pages>5546-5553</pages><issn>1078-0432</issn><eissn>1557-3265</eissn><abstract>The processes of cellular growth regulation and cellular metabolism are closely interrelated. The c-Myc oncogene is a "master regulator" which controls many aspects of both of these processes. The metabolic changes which occur in transformed cells, many of which are driven by c-Myc overexpression, are necessary to support the increased need for nucleic acids, proteins, and lipids necessary for rapid cellular proliferation. At the same time, c-Myc overexpression results in coordinated changes in level of expression of gene families which result in increased cellular proliferation. This interesting duality of c-Myc effects places it in the mainstream of transformational changes and gives it a very important role in regulating the "transformed phenotype." The effects induced by c-Myc can occur either as a "primary oncogene" which is activated by amplification or translocation or as a downstream effect of other activated oncogenes. In either case, it appears that c-Myc plays a central role in sustaining the changes which occur with transformation. Although efforts to use c-Myc as a therapeutic target have been quite frustrating, it appears that this may change in the next few years.</abstract><cop>United States</cop><pmid>23071356</pmid><doi>10.1158/1078-0432.ccr-12-0977</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
fulltext | fulltext |
identifier | ISSN: 1078-0432 |
ispartof | Clinical cancer research, 2012-10, Vol.18 (20), p.5546-5553 |
issn | 1078-0432 1557-3265 |
language | eng |
recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_3505847 |
source | MEDLINE; American Association for Cancer Research; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
subjects | Cell Proliferation Cell Transformation, Neoplastic - genetics Cell Transformation, Neoplastic - metabolism Gene Expression Regulation, Neoplastic Glutamine - metabolism Glycolysis Humans Mitochondria - metabolism Molecular Targeted Therapy Neoplasms - genetics Neoplasms - metabolism Proto-Oncogene Proteins c-myc - genetics Proto-Oncogene Proteins c-myc - metabolism |
title | c-Myc and cancer metabolism |
url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-24T06%3A14%3A40IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-pubmed_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=c-Myc%20and%20cancer%20metabolism&rft.jtitle=Clinical%20cancer%20research&rft.au=Miller,%20Donald%20M&rft.date=2012-10-15&rft.volume=18&rft.issue=20&rft.spage=5546&rft.epage=5553&rft.pages=5546-5553&rft.issn=1078-0432&rft.eissn=1557-3265&rft_id=info:doi/10.1158/1078-0432.ccr-12-0977&rft_dat=%3Cpubmed_cross%3E23071356%3C/pubmed_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_id=info:pmid/23071356&rfr_iscdi=true |