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Present new cancer therapies based on cellular aging

 
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Manuel Serrano, Head of the Tumor Suppression of National Cancer Research Center (CNIO), comments in an article published in the journal Nature the latest research on the relationship between cell senescence and cancer. Part of the results was published last month in Nature Cell Biology and another part is published today in Nature. The works are very useful for developing future therapies.

Two recent studies have attempted to sensitize the mechanisms leading to senescence. One such research is published today in the journal Nature and comes from the group led by Pier Paolo Pandolfi (Harvard University, USA). The first investigation, led by Bruno Amati (European Institute of Oncology, Milan) was published last month in Nature Cell Biology and attended also investiogadores Mariano Barbacid and Oscar Fernandez-Capetillo.

Both groups have managed to genetically engineer mice to make them more susceptible to stress and therefore tumor to senescence. Thus they have failed to protect mice without causing cancer, in addition, no adverse side effects. Both research groups also used chemotherapeutic compounds under development to demonstrate the same principle of “sensitization to senescence.

What is that cell aging?

Manuel Serrano, Head of the Tumor Suppression of National Cancer Research Center (CNIO), told SINC how can induce cellular senescence or aging in tumor cells to prevent cancer: “A tumor passes through three stages in its formation. The pre-tumor stage, the pre-malignant and malignant phase, the latter being the corresponding to the cancer. The transition from one phase to another is characterized by a sharp increase in what is known as intrinsically associated cell stress the tumor process.

According to the investigator at the National Center for Cancer Research (CNIO), “this cellular stress, which consists of breaks in DNA, increased oxidation of cellular components and other similar changes, leading to a collapse of the proliferation called cellular senescence. Most tumors are aborted training in pre-malignant stage because the high rate of senescence, which prevents the cells continue to multiply.

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References:

Hui-Kuan Lin; Zhenbang Chen; Guocan Wang, Caterina Nardella, Szu-Wei Lee3; Chan-Hsin Chan, Wei-Lei Yang, Jing Wang; Ainara Egia, Keiichi I. Nakayama, Carlos Cordon-Cardo, Julie Teruya-Feldstein and Pier Paolo Pandolfi, “suppresses tumorigenesis by targeting SKP2 Arf-p53-independent cellular senescence, Nature18 March 2010.

Stefano Campaner, Mirko Doni, Per Hydbring, Alessandro Verrecchia, Lucia Bianchi, Domenico Sardella, Thomas Schlecker, Daniele Perna, Susanna Tronnersjo, Matilde Murga, Oscar Fernandez-Capetillo, Mariano Barbacid, Lars-Gunnar Larsson, and Bruno Amati, “senescence Cdk2 induced by c-myc oncogene, Nature Cell Biology February 12, 2010.

Source: SINC

Category: Life ScienceTags: cancer, cell aging, cell senescence

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