By Anderson T. Wang, Peter J. McHugh (auth.), Lawrence Panasci, Raquel Aloyz, Moulay Alaoui-Jamali (eds.)
A entire evaluate of the hot advancements in DNA fix examine that experience power for translational functions. The e-book explains intimately a few of the organic mechanisms through which melanoma cells can sidestep anticancer treatment and boundaries its usefulness in sufferers. in addition they evaluation the influence of such novel inhibitors of DNA fix mechanisms as methylguanine-DNA-methyltransferase. additionally tested are inhibitors of different DNA fix enzymes equivalent to PARP and DNA-PK. The publication captures-for either melanoma researchers and oncologists facing hallmark "relapse" or "drug resistance" phenomena on a regular basis-the many fascinating new makes use of of DNA fix inhibitors, both on my own or together with anticancer therapies.
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Additional resources for Advances in DNA Repair in Cancer Therapy
Crit Rev Biochem Mol Biol 45(5):424–439 120. Garcia-Higuera I, Taniguchi T et al (2001) Interaction of the Fanconi anemia proteins and BRCA1 in a common pathway. Mol Cell 7(2):249–262 121. Smogorzewska A, Matsuoka S et al (2007) Identification of the FANCI protein, a monoubiquitinated FANCD2 paralog required for DNA repair. Cell 129(2):289–301 122. Meetei AR, Yan Z et al (2004) FANCL replaces BRCA1 as the likely ubiquitin ligase responsible for FANCD2 monoubiquitination. Cell Cycle 3(2):179–181 123.
Salles et al. The Non Homologous End-Joining Pathway In mammalian cells, NHEJ is the predominant repair pathway for DSB repair which, throughout the cell cycle, ligates the two DNA ends together with minimal end processing [45, 46]. NHEJ consists of at least two genetically and biochemically distinct sub-pathways (Fig. 1): (1) a main canonical end-joining pathway (C-NHEJ) and (2) an alternative NHEJ (A-NHEJ) or backup NHEJ (B-NHEJ) (hereafter referred to as A-NHEJ) [47–49]. Since C-NHEJ is essential both for cell survival after IR treatment and V(D)J recombination, which generates the antibody and T cell receptor diversity required for lymphocyte maturation, cells from RS-SCID (radiosensitive-severe combined immunodeficiency) patients have helped to genetically define the NHEJ components .
Nat Rev Genet 7(1):45–54 7. Begg AC, Stewart FA, Vens C (2011) Strategies to improve radiotherapy with targeted drugs. Nat Rev Cancer 11(4):239–253 8. Helleday T, Petermann E, Lundin C et al (2008) DNA repair pathways as targets for cancer therapy. Nat Rev Cancer 8(3):193–204 9. Guzi TJ, Paruch K, Dwyer MP et al (2011) Targeting the replication checkpoint using SCH 900776, a potent and functionally selective CHK1 inhibitor identified via high content screening. Mol Cancer Ther 10(4):591–602 10.
Advances in DNA Repair in Cancer Therapy by Anderson T. Wang, Peter J. McHugh (auth.), Lawrence Panasci, Raquel Aloyz, Moulay Alaoui-Jamali (eds.)