![[ Back to EurekAlert! ]](https://lh3.googleusercontent.com/blogger_img_proxy/AEn0k_vPcNBx5ij6PVISPh-ZDGJ6WON8Dgu2W6yy5Ur3HJm6E4TvEd90ByasxJNjUGQiC7eE55_qg3xLMdzZ_SwopGX0FnKVYRbGglY9SZnsYqI=s0-d){kind=small}
Public release date: 19-Jan-2012[ | E-mail |
Share ] Contact: Dr. Stefano Zapperi
stefano.zapperi@cnr.it
39-026-617-3385
Public Library of Science
A collaboration between a cancer biologist from the University of Milano and 2 physicists has shown that cell senescence occurs spontaneously in melanoma cells, but does not stop their growth
Since cancer cells grow indefinitely, it is commonly believed that senescence could act as a barrier against tumor growth and potentially be used as a way to treat cancer. A collaboration between a cancer biologist from the University of Milano, Italy, and two physicists, from the National Research Council of Italy and from Cornell University, has shown that cell senescence occurs spontaneously in melanoma cells, but does not stop their growth, which is sustained by a small population of cancer stem cells. The results, published in the open-access journal PLoS Computational Biology on January 19 explain why it is difficult to treat cancer cells by inducing senescence alone.
The work explores the relationship between melanoma and senescence, the normal process where cells decline and eventually stop duplicating after reaching maturity. The investigators followed the long-term evolution of melanoma cell populations, monitoring the number of senescent cells. After three months, growth slowed and most of the cells turned senescent, however growth did not stop and eventually resumed its initial rate until the senescent cells had almost disappeared.
The authors mathematically modeled the experimental data using the cancer stem cell hypothesis, where a sub-group of cancer cells replicate indefinitely, and are thus unaffected by senescence. These cancer stem cells give rise to a larger population of cancer cells that can duplicate only a finite number of times. The model yielded an indirect confirmation of the presence of cancer stem cells in melanoma, an issue that is still controversial in the cancer research community.
Although a large fraction of cancer cells are susceptible to senescence, the researchers conclude that inducing senescence is unlikely to provide a successful therapeutic strategy because these cells are irrelevant for tumor growth. However, the indirect evidence of cancer stem cells in melanoma may enable the development of new methods to treat specific kinds of cancer. The challenge will be in the strong resistance to drug induced senescence that would be found in the cancer stem cells. Along this line of research, treatment of tumors would focus on targeting only these cancer stem cells, rather than every single cancerous cell.
###
FINANCIAL DISCLOSURE: JPS acknowledges NCI-U54CA143876 for support. CAMLP is supported by PRIN 2008BP25KN004. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
COMPETING INTERESTS: The authors have declared that no competing interests exist.
CITATION: La Porta CAM, Zapperi S, Sethna JP (2012) Senescent Cells in Growing Tumors: Population Dynamics and Cancer Stem Cells. PLoS Comput Biol 8(1): e1002316. doi:10.1371/journal.pcbi.1002316
CONTACT:
Dr. Stefano Zapperi, CNR-IENI, Milano, Italy, phone: +39-02 66173 385, phone: stefano.zapperi@cnr.it
Dr. Caterina La Porta, Department of Biomolecular Science and Biotechnology, University of Milan, phone: +390250314927, email: caterina.laporta@unimi.it
Disclaimer
This press release refers to an upcoming article in PLoS Computational Biology. The release is provided by journal staff, or by the article authors and/or their institutions. Any opinions expressed in this release or article are the personal views of the journal staff and/or article contributors, and do not necessarily represent the views or policies of PLoS. PLoS expressly disclaims any and all warranties and liability in connection with the information found in the releases and articles and your use of such information.
Media Permissions
PLoS Journals publish under a Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.5/), which permits free reuse of all materials published with the article, so long as the work is cited (e.g., Kaltenbach LS et al. (2007) Huntingtin Interacting Proteins Are Genetic Modifiers of Neurodegeneration. PLoS Genet 3(5): e82. doi:10.1371/journal.pgen.0030082). No prior permission is required from the authors or publisher. For queries about the license, please contact the relative journal contact indicated here: http://www.plos.org/journals/embargopolicy.php
About PLoS Computational Biology
PLoS Computational Biology (www.ploscompbiol.org) features works of exceptional significance that further our understanding of living systems at all scales through the application of computational methods. All works published in PLoS Computational Biology are open access. Everything is immediately available subject only to the condition that the original authorship and source are properly attributed. Copyright is retained.
About the Public Library of Science
The Public Library of Science (PLoS) is a non-profit organization of scientists and physicians committed to making the world's scientific and medical literature a freely available public resource. For more information, visit http://www.plos.org.
[ | E-mail | Share ] ?
AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.
Public release date: 19-Jan-2012[ | E-mail |
Share ] Contact: Dr. Stefano Zapperi
stefano.zapperi@cnr.it
39-026-617-3385
Public Library of Science
A collaboration between a cancer biologist from the University of Milano and 2 physicists has shown that cell senescence occurs spontaneously in melanoma cells, but does not stop their growth
Since cancer cells grow indefinitely, it is commonly believed that senescence could act as a barrier against tumor growth and potentially be used as a way to treat cancer. A collaboration between a cancer biologist from the University of Milano, Italy, and two physicists, from the National Research Council of Italy and from Cornell University, has shown that cell senescence occurs spontaneously in melanoma cells, but does not stop their growth, which is sustained by a small population of cancer stem cells. The results, published in the open-access journal PLoS Computational Biology on January 19 explain why it is difficult to treat cancer cells by inducing senescence alone.
The work explores the relationship between melanoma and senescence, the normal process where cells decline and eventually stop duplicating after reaching maturity. The investigators followed the long-term evolution of melanoma cell populations, monitoring the number of senescent cells. After three months, growth slowed and most of the cells turned senescent, however growth did not stop and eventually resumed its initial rate until the senescent cells had almost disappeared.
The authors mathematically modeled the experimental data using the cancer stem cell hypothesis, where a sub-group of cancer cells replicate indefinitely, and are thus unaffected by senescence. These cancer stem cells give rise to a larger population of cancer cells that can duplicate only a finite number of times. The model yielded an indirect confirmation of the presence of cancer stem cells in melanoma, an issue that is still controversial in the cancer research community.
Although a large fraction of cancer cells are susceptible to senescence, the researchers conclude that inducing senescence is unlikely to provide a successful therapeutic strategy because these cells are irrelevant for tumor growth. However, the indirect evidence of cancer stem cells in melanoma may enable the development of new methods to treat specific kinds of cancer. The challenge will be in the strong resistance to drug induced senescence that would be found in the cancer stem cells. Along this line of research, treatment of tumors would focus on targeting only these cancer stem cells, rather than every single cancerous cell.
###
FINANCIAL DISCLOSURE: JPS acknowledges NCI-U54CA143876 for support. CAMLP is supported by PRIN 2008BP25KN004. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
COMPETING INTERESTS: The authors have declared that no competing interests exist.
CITATION: La Porta CAM, Zapperi S, Sethna JP (2012) Senescent Cells in Growing Tumors: Population Dynamics and Cancer Stem Cells. PLoS Comput Biol 8(1): e1002316. doi:10.1371/journal.pcbi.1002316
CONTACT:
Dr. Stefano Zapperi, CNR-IENI, Milano, Italy, phone: +39-02 66173 385, phone: stefano.zapperi@cnr.it
Dr. Caterina La Porta, Department of Biomolecular Science and Biotechnology, University of Milan, phone: +390250314927, email: caterina.laporta@unimi.it
Disclaimer
This press release refers to an upcoming article in PLoS Computational Biology. The release is provided by journal staff, or by the article authors and/or their institutions. Any opinions expressed in this release or article are the personal views of the journal staff and/or article contributors, and do not necessarily represent the views or policies of PLoS. PLoS expressly disclaims any and all warranties and liability in connection with the information found in the releases and articles and your use of such information.
Media Permissions
PLoS Journals publish under a Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.5/), which permits free reuse of all materials published with the article, so long as the work is cited (e.g., Kaltenbach LS et al. (2007) Huntingtin Interacting Proteins Are Genetic Modifiers of Neurodegeneration. PLoS Genet 3(5): e82. doi:10.1371/journal.pgen.0030082). No prior permission is required from the authors or publisher. For queries about the license, please contact the relative journal contact indicated here: http://www.plos.org/journals/embargopolicy.php
About PLoS Computational Biology
PLoS Computational Biology (www.ploscompbiol.org) features works of exceptional significance that further our understanding of living systems at all scales through the application of computational methods. All works published in PLoS Computational Biology are open access. Everything is immediately available subject only to the condition that the original authorship and source are properly attributed. Copyright is retained.
About the Public Library of Science
The Public Library of Science (PLoS) is a non-profit organization of scientists and physicians committed to making the world's scientific and medical literature a freely available public resource. For more information, visit http://www.plos.org.
[ | E-mail | Share ] ?
AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.
Source: http://www.eurekalert.org/pub_releases/2012-01/plos-csd011712.php
power rangers jungle fury ufc 139 fight card houston nutt houston nutt peter marshall peter marshall zombie boy
No comments:
Post a Comment
Note: Only a member of this blog may post a comment.