Next Generation of Cancer-treatment Targeting DNA Repair Pathway
Keywords:
Targeted therapy, DNA repair, PARP inhibitor, Cancer geneticsAbstract
Preservation of genomic information is important for species continuation. DNA repair mechanism is a major pathway responsible for correcting various type of DNA damage from single cellular organisms to complex multicellular organisms. Without DNA repair, mutation starts to accumulate in the genome and leads to genomic instability and cancer. In this article, we will review background of DNA damage repair, DNA repair deficiency in cancer cells and mechanism of targeting DNA repair pathway in cancer cells as a novel target for targeted cancer therapy.
References
Bianconi E, Piovesan A, Facchin F, et al. An estimation of the number of cells in the human body. Ann Hum Biol. 2013;40(6):463-471. doi:10.3109/03014460.2013.807878.
Hanahan D1, Weinberg RA. Hallmarks of cancer: the next generation. Cell. 20114;144(5):646-674. doi:10.1016/j.cell.2011.02.013.
Kennedy RD, D'Andrea AD. DNA repair pathways in clinical practice: lessons from pediatric cancer susceptibility syndromes. J Clin Oncol. 2006;24(23):3799-3808.
Helleday T, Lo J, van Gent DC, Engelward BP. DNA double-strand break repair: from mechanistic understanding to cancer treatment. DNA Repair (Amst). 2007;6(7):923-935.
Swenberg JA, Lu K, Moeller BC, et al. Endogenous versus exogenous DNA adducts: their role in carcinogenesis, epidemiology, and risk assessment. Toxicol Sci. 2011;120 Suppl 1:S130-S145. doi:10.1093/toxsci/kfq371.
Caldecott KW. Single-strand break repair and genetic disease. Nat Rev Genet. 2008;9(8):619-631. doi:10.1038/nrg2380.
Fong PC, Boss DS, Yap TA, et al. Inhibition of poly(ADP-ribose) polymerase in tumors from BRCA mutation carriers. N Engl J Med. 2009;361(2):123-134. doi:10.1056/NEJMoa0900212.
Sertic S, Pizzi S, Lazzaro F, Plevani P, Muzi-Falconi M. NER and DDR: classical music with new instruments. Cell Cycle. 2012;11(4):668-674. doi:10.4161/cc.11.4.19117.
DiGiovanna JJ, Kraemer KH. Shining a light on xeroderma pigmentosum. J Invest Dermatol. 2012;132(3 Pt 2):785-796. doi:10.1038/jid.2011.426.
Guillotin D, Martin SA. Exploiting DNA mismatch repair deficiency as a therapeutic strategy. Exp Cell Res. 2014;329(1):110-115. doi:10.1016/j.yexcr.2014.07.004.
Baumann P, Benson FE, West SC. Human Rad51 protein promotes ATP-dependent homologous pairing and strand transfer reactions in vitro. Cell. 1996;87(4):757-766.
Pierce AJ, Stark JM, Araujo FD, Moynahan ME, Berwick M, Jasin M. Double-strand breaks and tumorigenesis. Trends Cell Biol. 2001;11(11):S52-S59.
Erkko H, Xia B, Nikkilä J, et al. A recurrent mutation in PALB2 in Finnish cancer families. Nature. 2007;446(7133):316-319.
Hartlerode AJ, Scully R. Mechanisms of double-strand break repair in somatic mammalian cells. Biochem J. 2009;423(2):157-168. doi:10.1042/BJ20090942.
Bunting SF, Nussenzweig A. End-joining, translocations and cancer. Nat Rev Cancer. 2013;13(7):443-454. doi:10.1038/nrc3537.
Chambon P, Weill JD, Mandel P. Nicotinamide mononucleotide activation of new DNA-dependent polyadenylic acid synthesizing nuclear enzyme. Biochem Biophys Res Commun. 1963;11:39-43.
Jagtap P, Szabó C. Poly(ADP-ribose) polymerase and the therapeutic effects of its inhibitors. Nat Rev Drug Discov. 2005;4(5):421-440.
Rouleau M, Patel A, Hendzel MJ, Kaufmann SH, Poirier GG. PARP inhibition: PARP1 and beyond. Nat Rev Cancer. 2010;10(4):293-301. doi:10.1038/nrc2812.
Khan OA, Gore M, Lorigan P, et al. A phase I study of the safety and tolerability of olaparib (AZD2281, KU0059436) and dacarbazine in patients with advanced solid tumours. Br J Cancer. 2011;104(5):750-755. doi:10.1038/bjc.2011.8.
Kummar S, Chen A, Ji J, et al. Phase I study of PARP inhibitor ABT-888 in combination with topotecan in adults with refractory solid tumors and lymphomas. Cancer Res. 2011;71(17):5626-5634. doi:10.1158/0008-5472.CAN-11-1227.
Banasik M, Komura H, Shimoyama M, Ueda K. Specific inhibitors of poly(ADP-ribose) synthetase and mono(ADP-ribosyl)transferase. J Biol Chem. 1992;267(3):1569-1575.
Minesh P. Mehta WJC, Ding Wang, et al. Phase I safety and pharmacokinetic (PK) study of veliparib in combination with whole brain radiation therapy (WBRT) in patients (pts) with brin metastases. J Clin Oncol, 2012;(suppl; abstr 2013).
Tutt A, Robson M, Garber JE, et al. Oral poly(ADP-ribose) polymerase inhibitor olaparib in patients with BRCA1 or BRCA2 mutations and advanced breast cancer: a proof-of-concept trial. Lancet. 2010;376(9737):235-244. doi:10.1016/S0140-6736(10)60892-6.
Audeh MW, Carmichael J, Penson RT, et al. Oral poly(ADP-ribose) polymerase inhibitor olaparib in patients with BRCA1 or BRCA2 mutations and recurrent ovarian cancer: a proof-of-concept trial. Lancet. 2010;376(9737):245-251. doi:10.1016/S0140-6736(10)60893-8.
Bajrami I, Frankum JR, Konde A, et al. Genome-wide profiling of genetic synthetic lethality identifies CDK12 as a novel determinant of PARP1/2 inhibitor sensitivity. Cancer Res. 2014;74(1):287-297. doi:10.1158/0008-5472.CAN-13-2541.
Cao L, Xu X, Bunting SF, et al. A selective requirement for 53BP1 in the biological response to genomic instability induced by Brca1 deficiency. Mol Cell. 2009;35(4):534-541. doi:10.1016/j.molcel.2009.06.037.
Grotsky DA, Gonzalez-Suarez I, Novell A, et al. BRCA1 loss activates cathepsin L-mediated degradation of 53BP1 in breast cancer cells. J Cell Biol. 2013;200(2):187-202. doi:10.1083/jcb.201204053.
Downloads
Published
How to Cite
Issue
Section
License
Copyright (c) 2015 By the authors. Licensee RMJ, Faculty of Medicine Ramathibodi Hospital, Mahidol University, Bangkok, Thailand
This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.