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Oncogene-Induced Senescence: Putting the Brakes on Tumor Development
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| Zeitschriftentitel: | Cancer Research |
|---|---|
| Personen und Körperschaften: | , |
| In: | Cancer Research, 66, 2006, 6, S. 2881-2884 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
American Association for Cancer Research (AACR)
|
| Schlagwörter: |
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Braig, Melanie Schmitt, Clemens A. Braig, Melanie Schmitt, Clemens A. |
|---|---|
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Braig, Melanie Schmitt, Clemens A. |
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Braig, Melanie Schmitt, Clemens A. Cancer Research Oncogene-Induced Senescence: Putting the Brakes on Tumor Development Cancer Research Oncology |
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braig, melanie |
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Braig, Melanie Schmitt, Clemens A. 0008-5472 1538-7445 American Association for Cancer Research (AACR) Cancer Research Oncology http://dx.doi.org/10.1158/0008-5472.can-05-4006 <jats:title>Abstract</jats:title> <jats:p>Cellular senescence, a permanent cell cycle arrest, is considered a safeguard mechanism that may prevent aged or abnormal cells from further expansion. Although the term “replicative senescence” stands for the widely accepted model of a terminal growth arrest due to telomere attrition, the significance of “oncogene-inducible senescence” remained an issue of debate over the years. A number of recent studies now show the effect of this acute and telomere-independent form of senescence as a tumor-protective, fail-safe mechanism in vivo that shares conceptual and possibly therapeutic similarities with the genetically encoded apoptosis machinery. (Cancer Res 2006; 66(6): 2881-4)</jats:p> Oncogene-Induced Senescence: Putting the Brakes on Tumor Development Cancer Research |
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| title |
Oncogene-Induced Senescence: Putting the Brakes on Tumor Development |
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Oncogene-Induced Senescence: Putting the Brakes on Tumor Development |
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Oncogene-Induced Senescence: Putting the Brakes on Tumor Development |
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Oncogene-Induced Senescence: Putting the Brakes on Tumor Development |
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Oncogene-Induced Senescence: Putting the Brakes on Tumor Development |
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Oncogene-Induced Senescence: Putting the Brakes on Tumor Development |
| title_sort |
oncogene-induced senescence: putting the brakes on tumor development |
| topic |
Cancer Research Oncology |
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http://dx.doi.org/10.1158/0008-5472.can-05-4006 |
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2006 |
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2881-2884 |
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<jats:title>Abstract</jats:title>
<jats:p>Cellular senescence, a permanent cell cycle arrest, is considered a safeguard mechanism that may prevent aged or abnormal cells from further expansion. Although the term “replicative senescence” stands for the widely accepted model of a terminal growth arrest due to telomere attrition, the significance of “oncogene-inducible senescence” remained an issue of debate over the years. A number of recent studies now show the effect of this acute and telomere-independent form of senescence as a tumor-protective, fail-safe mechanism in vivo that shares conceptual and possibly therapeutic similarities with the genetically encoded apoptosis machinery. (Cancer Res 2006; 66(6): 2881-4)</jats:p> |
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| description | <jats:title>Abstract</jats:title> <jats:p>Cellular senescence, a permanent cell cycle arrest, is considered a safeguard mechanism that may prevent aged or abnormal cells from further expansion. Although the term “replicative senescence” stands for the widely accepted model of a terminal growth arrest due to telomere attrition, the significance of “oncogene-inducible senescence” remained an issue of debate over the years. A number of recent studies now show the effect of this acute and telomere-independent form of senescence as a tumor-protective, fail-safe mechanism in vivo that shares conceptual and possibly therapeutic similarities with the genetically encoded apoptosis machinery. (Cancer Res 2006; 66(6): 2881-4)</jats:p> |
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| spelling | Braig, Melanie Schmitt, Clemens A. 0008-5472 1538-7445 American Association for Cancer Research (AACR) Cancer Research Oncology http://dx.doi.org/10.1158/0008-5472.can-05-4006 <jats:title>Abstract</jats:title> <jats:p>Cellular senescence, a permanent cell cycle arrest, is considered a safeguard mechanism that may prevent aged or abnormal cells from further expansion. Although the term “replicative senescence” stands for the widely accepted model of a terminal growth arrest due to telomere attrition, the significance of “oncogene-inducible senescence” remained an issue of debate over the years. A number of recent studies now show the effect of this acute and telomere-independent form of senescence as a tumor-protective, fail-safe mechanism in vivo that shares conceptual and possibly therapeutic similarities with the genetically encoded apoptosis machinery. (Cancer Res 2006; 66(6): 2881-4)</jats:p> Oncogene-Induced Senescence: Putting the Brakes on Tumor Development Cancer Research |
| spellingShingle | Braig, Melanie, Schmitt, Clemens A., Cancer Research, Oncogene-Induced Senescence: Putting the Brakes on Tumor Development, Cancer Research, Oncology |
| title | Oncogene-Induced Senescence: Putting the Brakes on Tumor Development |
| title_full | Oncogene-Induced Senescence: Putting the Brakes on Tumor Development |
| title_fullStr | Oncogene-Induced Senescence: Putting the Brakes on Tumor Development |
| title_full_unstemmed | Oncogene-Induced Senescence: Putting the Brakes on Tumor Development |
| title_short | Oncogene-Induced Senescence: Putting the Brakes on Tumor Development |
| title_sort | oncogene-induced senescence: putting the brakes on tumor development |
| title_unstemmed | Oncogene-Induced Senescence: Putting the Brakes on Tumor Development |
| topic | Cancer Research, Oncology |
| url | http://dx.doi.org/10.1158/0008-5472.can-05-4006 |