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Tumor growth fueled by spurious senescence phenotypes
Cancer treatments can induce a form of senescence that halts cellular division while allowing continued secretion of tumor-promoting proteins. We recently found that antiangiogenic treatment resistance can lead to a transient hijacking of the senescence-controlled secretory machinery that, when ther...
| Autores principales: | , |
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| Formato: | Online Artículo Texto |
| Lenguaje: | English |
| Publicado: |
Taylor & Francis
2019
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| Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6512925/ https://www.ncbi.nlm.nih.gov/pubmed/31131302 http://dx.doi.org/10.1080/23723556.2019.1575707 |
| Sumario: | Cancer treatments can induce a form of senescence that halts cellular division while allowing continued secretion of tumor-promoting proteins. We recently found that antiangiogenic treatment resistance can lead to a transient hijacking of the senescence-controlled secretory machinery that, when therapeutically targeted during treatment cessation, can blunt rebound tumor growth. |
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