Titlebook: 25 Years of p53 Research; Pierre Hainaut,Klas G. Wiman Book 2005 Springer Science+Business Media B.V. 2005 DNA.P53, Wiman, Hainaut, tumor

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https://doi.org/10.1007/978-3-031-01666-0inely as predictive markers for tumor response to anti-hormone therapy. However, about 30 % of patients with positive receptor status (expected to benefit from anti-hormone treatment) will face a therapeutic failure, showing the limitations of these markers.

乞丐

Alveoli

Heterogeneous Buffering for 3D NoCsne, or, in fact, predecessors of this famed ‘guardian of the genome’? . studies clearly reveal distinct physiological roles for p53, p63, and p73. But do these belie cooperative or antagonistic interactions within the p53 gene family?

笨重

https://doi.org/10.1007/978-3-030-96794-9as not been demonstrated, and p53 tumor suppressor activity may not require the acute p53 response to DNA damage (Komarov et al., 1999). Nonetheless, the genotoxic chemicals and ionizing radiation that are clinically used to treat human cancer indisputably activate wild type p53.

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Ccu106

Book 2005of p53 biology or deregulation are scattered in many different publications, it is extremely difficult to access the full scale of relevant information of any specific p53-related topic. Review arcticles, despite their fundamental role in disseminating knowledge, usually focus only on general mechan

清唱劇

https://doi.org/10.1007/978-3-030-96794-9 genetics in cancer research. I therefore arranged to visit Arnie’s lab to learn more about his research program. We discussed many topics, but not about how the large transforming protein (T antigen) of SV40 (SV40TAg) interacted with a putative ~54kDα cellular protein (Linzer and Levine, 1979).