By Anderson T. Wang, Peter J. McHugh (auth.), Lawrence Panasci, Raquel Aloyz, Moulay Alaoui-Jamali (eds.)
A entire assessment of the new advancements in DNA fix study that experience strength for translational purposes. The ebook explains intimately a few of the organic mechanisms through which melanoma cells can avert anticancer remedy and boundaries its usefulness in sufferers. in addition they overview the effect of such novel inhibitors of DNA fix mechanisms as methylguanine-DNA-methyltransferase. additionally tested are inhibitors of alternative DNA fix enzymes similar to PARP and DNA-PK. The ebook captures-for either melanoma researchers and oncologists facing hallmark "relapse" or "drug resistance" phenomena on a regular basis-the many interesting new makes use of of DNA fix inhibitors, both by myself or together with anticancer therapies.
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Extra info for Advances in DNA Repair in Cancer Therapy
Reinhardt HC, Aslanian AS et al (2007) p53-deficient cells rely on ATM- and ATR-mediated checkpoint signaling through the p38MAPK/MK2 pathway for survival after DNA damage. Cancer Cell 11(2):175–189 149. Koniaras K, Cuddihy AR et al (2001) Inhibition of Chk1-dependent G2 DNA damage checkpoint radiosensitizes p53 mutant human cells. Oncogene 20(51):7453–7463 150. Bergman AM, Ruiz van Haperen VW et al (1996) Synergistic interaction between cisplatin and gemcitabine in vitro. Clin Cancer Res 2(3):521–530 151.
Asaithamby A, Hu B, Chen DJ (2011) Unrepaired clustered DNA lesions induce chromosome breakage in human cells. Proc Natl Acad Sci U S A 108(20):8293–8298 20. Sedelnikova OA, Redon CE, Dickey JS et al (2010) Role of oxidatively induced DNA lesions in human pathogenesis. Mutat Res 704(1–3):152–159 21. Singleton BK, Griffin CS, Thacker J (2002) Clustered DNA damage leads to complex genetic changes in irradiated human cells. Cancer Res 62(21):6263–6269 22. Pommier Y, Leo E, Zhang H et al (2010) DNA topoisomerases and their poisoning by anticancer and antibacterial drugs.
The DNA-PK holoenzyme (Ku/DNA-PKcs) recognizes, protects and bridges the DNA-ends in addition to having a serine/threonine protein kinase activity . DNAPK conformational change mediated by autophosphorylation is necessary for activation of end-processing enzymes, such as the Artemis nuclease . Ligation requires the concerted action of LIG4, XRCC4, and Cer-XLF, the latter promoting readenylation of LIG4 . The ligation complex also has a role upstream of the ligation reaction, since it stimulates processing of DNA ends [62, 63].
Advances in DNA Repair in Cancer Therapy by Anderson T. Wang, Peter J. McHugh (auth.), Lawrence Panasci, Raquel Aloyz, Moulay Alaoui-Jamali (eds.)