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Journal articles on the topic 'DNA replication – Research – Methodology'

Author: Grafiati

Published: 4 June 2021

Last updated: 11 February 2022

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1

Kristian, Dolly Simon, Adian Fatchur Rochim, and Eko Didik Widianto. "Pengembangan Sistem Replikasi dan Redundansi untuk Meningkatkan Kehandalan Basisdata MySQL." Jurnal Teknologi dan Sistem Komputer 3, no. 4 (October 20, 2015): 523. http://dx.doi.org/10.14710/jtsiskom.3.4.2015.523-529.

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With the development of information technology, humans make it easy to complete every duty. Any information about the work carried out to be very valuable, therefore the information should be stored properly, by organizing a reliable database system when performing data storage on the server information. Build a design application virtualization master slave database servers that are connected with the management node using the virtual application to get the test results replication system performance and redundancy in the design of the cluster system. Methodology of this research include the study of literature, collecting data by interview, observation, literature studies, system design, and testing of the system. In a literature study on the use of research methods to study the literature books, records that can be used as a support in the research. The design of this thesis using MySQL Cluster system with Ndbcluster engine. Last is testing this system on its performance on the server failure or failures occur and reliability in performance. The results obtained are when there is a failure on the primary server, it will be immediately replaced by another server is a slave. And the replication of data between the main server and slave.

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2

Fabrice, Antigny, Ranchoux Benoît, Nadeau Valérie, Edmund Lau, Bonnet Sébastien, and Perros Frédéric. "A Simple Method to AssessIn VivoProliferation in Lung Vasculature with EdU: The Case of MMC-Induced PVOD in Rat." Analytical Cellular Pathology 2015 (2015): 1–6. http://dx.doi.org/10.1155/2015/326385.

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5-Ethynyl-2′-deoxyuridine (EdU) incorporation is becoming the gold standard method forin vitroandin vivovisualization of proliferating cells. The small size of the fluorescent azides used for detection results in a high degree of specimen penetration. It can be used to easily detect DNA replication in large tissue samples or organ explants with low proliferation and turnover of cells formerly believed to be in a “terminal” state of differentiation. Here we describe a protocol for the localization and identification of proliferating cells in quiescent or injured pulmonary vasculature, in a model of pulmonary veno-occlusive disease (PVOD). PVOD is an uncommon form of pulmonary hypertension characterized by progressive obstruction of small pulmonary veins. We previously reported that mitomycin-C (MMC) therapy is associated with PVOD in human. We demonstrated that MMC can induce PVOD in rats, which currently represents the sole animal model that recapitulates human PVOD lesions. Using the EdU assay, we demonstrated that MMC-exposed lungs displayed areas of exuberant microvascular endothelial cell proliferation which mimics pulmonary capillary hemangiomatosis, one of the pathologic hallmarks of human PVOD.In vivopulmonary cell proliferation measurement represents an interesting methodology to investigate the potential efficacy of therapies aimed at normalizing pathologic angioproliferation.

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Dhawan, Andrew, Justin Lathia, David Peereboom, Gene Barnett, Gabrielle Yeaney, and Manmeet Ahluwalia. "COMP-17. LARGE-SCALE TRANSCRIPTOMIC CHARACTERIZATION OF PRIMARY AND RECURRENT GLIOBLASTOMA IDENTIFIES GENE EXPRESSION SIGNATURE OF TUMOR RESPONSE TO STANDARD THERAPY." Neuro-Oncology 21, Supplement_6 (November 2019): vi64—vi65. http://dx.doi.org/10.1093/neuonc/noz175.260.

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Abstract A near-universal phenomenon in glioblastoma is disease recurrence following surgical resection and chemoradiotherapy. Development of biomarkers predictive of therapeutic response to better guide care and inform future targeted therapies is crucial. In this work, a total of 84 glioblastoma surgical specimens involving 44 primary tumors and 40 matched samples at time of re-resection, were characterized utilizing RNA-sequencing. Transcriptomic analysis was carried out with the goal of identifying underlying differences between those patients with prolonged response to standard therapy and delayed time to re-resection. We examined individual gene expression, gene coexpression networks, and well-known gene pathways in this dataset that showed consistent association with time to re-resection in both primary and progressed specimens, independent of tumor molecular subtype. Leveraging this large, well-characterized dataset, and using a novel computational methodology based on a seed-gene approach, we identified a predictive gene signature for therapeutic response. Our analyses revealed a striking degree of heterogeneity among gene expression associated with response to standard therapy and time to re-resection, adding to the complexity of signature derivation. The novel signature we obtained for response showed components involving genes such as those in the IGF pathway (IGF2BP2, IGF2BP3) and PDGF-signalling pathway (MYC, FLI1, ARHGAP4, JAK3) predictive of poor response to therapy. Likewise, predictors of positive response to therapy included genes involved in the apoptosis and RAS pathways (RAB4A, CHUK) and DNA replication pathways (SSBP2). In sum, this is among the largest cohorts of well-characterized clinical tumor samples for which there is transcriptomic information from primary and re-resected samples from matched patients. Our results not only highlight an innovative computational method for gene signature derivation in the setting of significant underlying heterogeneity, but also result in a predictive gene signature, offering the potential to give therapy to those who stand to benefit most.

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4

Preston, Bradley D., Tina M. Albertson, and Alan J. Herr. "DNA replication fidelity and cancer." Seminars in Cancer Biology 20, no. 5 (October 2010): 281–93. http://dx.doi.org/10.1016/j.semcancer.2010.10.009.

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5

Li, Zhuo, Lori M. Kelman, and Zvi Kelman. "Thermococcus kodakarensis DNA replication." Biochemical Society Transactions 41, no. 1 (January 29, 2013): 332–38. http://dx.doi.org/10.1042/bst20120303.

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DNA replication plays an essential role in all life forms. Research on archaeal DNA replication began approximately 20 years ago. Progress was hindered, however, by the lack of genetic tools to supplement the biochemical and structural studies. This has changed, however, and genetic approaches are now available for several archaeal species. One of these organisms is the thermophilic euryarchaeon Thermococcus kodakarensis. In the present paper, the recent developments in the biochemical, structural and genetic studies on the replication machinery of T. kodakarensis are summarized.

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6

Ekundayo, Babatunde, and Franziska Bleichert. "Origins of DNA replication." PLOS Genetics 15, no. 9 (September 12, 2019): e1008320. http://dx.doi.org/10.1371/journal.pgen.1008320.

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7

Zhukovskaya, N., P. Branch, G. Aquilina, and P. Karran. "DNA replication arrest and tolerance to DNA methylation damage." Carcinogenesis 15, no. 10 (1994): 2189–94. http://dx.doi.org/10.1093/carcin/15.10.2189.

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8

Henricksen, Leigh A., and Robert A. Bambara. "Multiprotein reactions in mammalian DNA replication." Leukemia Research 22, no. 1 (January 1998): 1–5. http://dx.doi.org/10.1016/s0145-2126(97)00113-6.

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9

Arana, Mercedes E., and Thomas A. Kunkel. "Mutator phenotypes due to DNA replication infidelity." Seminars in Cancer Biology 20, no. 5 (October 2010): 304–11. http://dx.doi.org/10.1016/j.semcancer.2010.10.003.

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10

Desaintes, Christian, and Caroline Demeret. "Control of papillomavirus DNA replication and transcription." Seminars in Cancer Biology 7, no. 6 (December 1996): 339–47. http://dx.doi.org/10.1006/scbi.1996.0043.

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11

Cheung, Andrew K. "Porcine circovirus: Transcription and DNA replication." Virus Research 164, no. 1-2 (March 2012): 46–53. http://dx.doi.org/10.1016/j.virusres.2011.10.012.

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12

Lo Piano, Ambra, María I. Martínez-Jiménez, Lisa Zecchi, and Silvia Ayora. "Recombination-dependent concatemeric viral DNA replication." Virus Research 160, no. 1-2 (September 2011): 1–14. http://dx.doi.org/10.1016/j.virusres.2011.06.009.

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13

Puccetti, Matthew V., Clare M. Adams, Saul Kushinsky, and Christine M. Eischen. "Smarcal1 and Zranb3 Protect Replication Forks from Myc-Induced DNA Replication Stress." Cancer Research 79, no. 7 (January 4, 2019): 1612–23. http://dx.doi.org/10.1158/0008-5472.can-18-2705.

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14

Ubhi, Tajinder, and Grant W. Brown. "Exploiting DNA Replication Stress for Cancer Treatment." Cancer Research 79, no. 8 (April 9, 2019): 1730–39. http://dx.doi.org/10.1158/0008-5472.can-18-3631.

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15

Kara, Neesha, Felix Krueger, Peter Rugg-Gunn, and Jonathan Houseley. "Genome-wide analysis of DNA replication and DNA double-strand breaks using TrAEL-seq." PLOS Biology 19, no. 3 (March 24, 2021): e3000886. http://dx.doi.org/10.1371/journal.pbio.3000886.

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Faithful replication of the entire genome requires replication forks to copy large contiguous tracts of DNA, and sites of persistent replication fork stalling present a major threat to genome stability. Understanding the distribution of sites at which replication forks stall, and the ensuing fork processing events, requires genome-wide methods that profile replication fork position and the formation of recombinogenic DNA ends. Here, we describe Transferase-Activated End Ligation sequencing (TrAEL-seq), a method that captures single-stranded DNA 3′ ends genome-wide and with base pair resolution. TrAEL-seq labels both DNA breaks and replication forks, providing genome-wide maps of replication fork progression and fork stalling sites in yeast and mammalian cells. Replication maps are similar to those obtained by Okazaki fragment sequencing; however, TrAEL-seq is performed on asynchronous populations of wild-type cells without incorporation of labels, cell sorting, or biochemical purification of replication intermediates, rendering TrAEL-seq far simpler and more widely applicable than existing replication fork direction profiling methods. The specificity of TrAEL-seq for DNA 3′ ends also allows accurate detection of double-strand break sites after the initiation of DNA end resection, which we demonstrate by genome-wide mapping of meiotic double-strand break hotspots in a dmc1Δ mutant that is competent for end resection but not strand invasion. Overall, TrAEL-seq provides a flexible and robust methodology with high sensitivity and resolution for studying DNA replication and repair, which will be of significant use in determining mechanisms of genome instability.

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16

Kuo, H. Kenny, Jack D. Griffith, and Kenneth N. Kreuzer. "5-Azacytidine–Induced Methyltransferase-DNA Adducts Block DNA Replication In vivo." Cancer Research 67, no. 17 (September 1, 2007): 8248–54. http://dx.doi.org/10.1158/0008-5472.can-07-1038.

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17

Takeda, David Y., and Anindya Dutta. "DNA replication and progression through S phase." Oncogene 24, no. 17 (April 2005): 2827–43. http://dx.doi.org/10.1038/sj.onc.1208616.

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18

Bian, Xing, and Wenchu Lin. "Targeting DNA Replication Stress and DNA Double-Strand Break Repair for Optimizing SCLC Treatment." Cancers 11, no. 9 (September 2, 2019): 1289. http://dx.doi.org/10.3390/cancers11091289.

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Small cell lung cancer (SCLC), accounting for about 15% of all cases of lung cancer worldwide, is the most lethal form of lung cancer. Despite an initially high response rate of SCLC to standard treatment, almost all patients are invariably relapsed within one year. Effective therapeutic strategies are urgently needed to improve clinical outcomes. Replication stress is a hallmark of SCLC due to several intrinsic factors. As a consequence, constitutive activation of the replication stress response (RSR) pathway and DNA damage repair system is involved in counteracting this genotoxic stress. Therefore, therapeutic targeting of such RSR and DNA damage repair pathways will be likely to kill SCLC cells preferentially and may be exploited in improving chemotherapeutic efficiency through interfering with DNA replication to exert their functions. Here, we summarize potentially valuable targets involved in the RSR and DNA damage repair pathways, rationales for targeting them in SCLC treatment and ongoing clinical trials, as well as possible predictive biomarkers for patient selection in the management of SCLC.

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19

Sotiriou, Sotirios K., and Thanos D. Halazonetis. "Remodeling Collapsed DNA Replication Forks for Cancer Development." Cancer Research 79, no. 7 (April 1, 2019): 1297–98. http://dx.doi.org/10.1158/0008-5472.can-19-0216.

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20

Bauermeister, Anelize, Munira Muhammad Abdel Baqui, and Luiz Alberto Beraldo Moraes. "DNA–EB in agarose gel assay: a simple methodology in the search for DNA-binders in crude extracts from actinomycetes." Analytical Methods 8, no. 12 (2016): 2653–59. http://dx.doi.org/10.1039/c5ay02603b.

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21

Stratmann, S. A., and A. M. van Oijen. "DNA replication at the single-molecule level." Chem. Soc. Rev. 43, no. 4 (2014): 1201–20. http://dx.doi.org/10.1039/c3cs60391a.

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22

Branzei, Dana, and Michele Giannattasio. "SIRFing the replication fork: Assessing protein interactions with nascent DNA." Journal of Cell Biology 217, no. 4 (March 1, 2018): 1177–79. http://dx.doi.org/10.1083/jcb.201802083.

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Roy et al. (2018. J. Cell. Biol. https://doi.org/10.1083/jcb.201709121) describe an ingenious single-cell assay system, in situ analysis of protein interactions at DNA replication forks (SIRF), for the quantitative analysis of protein interactions with nascent DNA at active and stalled replication forks. The sensitive and accurate SIRF methodology is suitable for multiparameter measurements in cell populations.

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23

Mughal, Muhammad Jameel, Ravikiran Mahadevappa, and Hang Fai Kwok. "DNA replication licensing proteins: Saints and sinners in cancer." Seminars in Cancer Biology 58 (October 2019): 11–21. http://dx.doi.org/10.1016/j.semcancer.2018.11.009.

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24

Permana, Paskasari A., and Robert M. Snapka. "Aldehyde-induced protein—DNA crosslinks disrupt specific stages of SV4I) DNA replication." Carcinogenesis 15, no. 5 (1994): 1031–36. http://dx.doi.org/10.1093/carcin/15.5.1031.

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25

Turnell, Andrew S., and Roger J. Grand. "DNA viruses and the cellular DNA-damage response." Journal of General Virology 93, no. 10 (October 1, 2012): 2076–97. http://dx.doi.org/10.1099/vir.0.044412-0.

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It is clear that a number of host-cell factors facilitate virus replication and, conversely, a number of other factors possess inherent antiviral activity. Research, particularly over the last decade or so, has revealed that there is a complex inter-relationship between viral infection and the host-cell DNA-damage response and repair pathways. There is now a realization that viruses can selectively activate and/or repress specific components of these host-cell pathways in a temporally coordinated manner, in order to promote virus replication. Thus, some viruses, such as simian virus 40, require active DNA-repair pathways for optimal virus replication, whereas others, such as adenovirus, go to considerable lengths to inactivate some pathways. Although there is ever-increasing molecular insight into how viruses interact with host-cell damage pathways, the precise molecular roles of these pathways in virus life cycles is not well understood. The object of this review is to consider how DNA viruses have evolved to manage the function of three principal DNA damage-response pathways controlled by the three phosphoinositide 3-kinase (PI3K)-related protein kinases ATM, ATR and DNA-PK and to explore further how virus interactions with these pathways promote virus replication.

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26

Malacaria, Eva, Masayoshi Honda, Annapaola Franchitto, Maria Spies, and Pietro Pichierri. "Physiological and Pathological Roles of RAD52 at DNA Replication Forks." Cancers 12, no. 2 (February 10, 2020): 402. http://dx.doi.org/10.3390/cancers12020402.

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Understanding basic molecular mechanisms underlying the biology of cancer cells is of outmost importance for identification of novel therapeutic targets and biomarkers for patient stratification and better therapy selection. One of these mechanisms, the response to replication stress, fuels cancer genomic instability. It is also an Achille’s heel of cancer. Thus, identification of pathways used by the cancer cells to respond to replication-stress may assist in the identification of new biomarkers and discovery of new therapeutic targets. Alternative mechanisms that act at perturbed DNA replication forks and involve fork degradation by nucleases emerged as crucial for sensitivity of cancer cells to chemotherapeutics agents inducing replication stress. Despite its important role in homologous recombination and recombinational repair of DNA double strand breaks in lower eukaryotes, RAD52 protein has been considered dispensable in human cells and the full range of its cellular functions remained unclear. Very recently, however, human RAD52 emerged as an important player in multiple aspects of replication fork metabolism under physiological and pathological conditions. In this review, we describe recent advances on RAD52’s key functions at stalled or collapsed DNA replication forks, in particular, the unexpected role of RAD52 as a gatekeeper, which prevents unscheduled processing of DNA. Last, we will discuss how these functions can be exploited using specific inhibitors in targeted therapy or for an informed therapy selection.

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27

Bambara, Robert A., James J. Crute, and Alan F. Wahl. "Is Ap4A an Activator of Eukaryotic DNA Replication?" Cancer Investigation 3, no. 5 (January 1985): 473–79. http://dx.doi.org/10.3109/07357908509039809.

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28

Zhang, Jingwen, Austin M. Dulak, Maureen M. Hattersley, Brandon S. Willis, Jenni Nikkilä, Anderson Wang, Alan Lau, et al. "BRD4 facilitates replication stress-induced DNA damage response." Oncogene 37, no. 28 (April 11, 2018): 3763–77. http://dx.doi.org/10.1038/s41388-018-0194-3.

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29

Lebofsky, Ronald, and Johannes C. Walter. "New Myc-anisms for DNA Replication and Tumorigenesis?" Cancer Cell 12, no. 2 (August 2007): 102–3. http://dx.doi.org/10.1016/j.ccr.2007.07.013.

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30

Xie, Maohua, Yun Yen, Taofeek K. Owonikoko, Suresh S. Ramalingam, Fadlo R. Khuri, Walter J. Curran, Paul W. Doetsch, and Xingming Deng. "Bcl2 Induces DNA Replication Stress by Inhibiting Ribonucleotide Reductase." Cancer Research 74, no. 1 (November 6, 2013): 212–23. http://dx.doi.org/10.1158/0008-5472.can-13-1536-t.

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31

Kalma, Yael, Lea Marash, Yocheved Lamed, and Doron Ginsberg. "Expression analysis using DNA microarrays demonstrates that E2F-1 up-regulates expression of DNA replication genes including replication protein A2." Oncogene 20, no. 11 (March 2001): 1379–87. http://dx.doi.org/10.1038/sj.onc.1204230.

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32

Dreyer, Stephan, Viola Paulus-Hock, Rosie Upstill-Goddard, Eirini Lampraki, Nigel Jamieson, Susie Cooke, Peter Bailey, Andrew Biankin, and David Kuang-Fu Chang. "Defining DNA damage repair deficiency and replication stress in pancreatic cancer." Journal of Clinical Oncology 37, no. 4_suppl (February 1, 2019): 285. http://dx.doi.org/10.1200/jco.2019.37.4_suppl.285.

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285 Background: Integrated multi-omic analyses revealed 24% of pancreatic cancer (PC) harbor defects in DNA damage response (DDR) and a subgroup demonstrate upregulation in replication stress pathways. DDR defective tumors preferentially respond to DNA damaging agents, and clinical responses to cell cycle inhibitors are seen in undefined subgroups, representing novel therapeutic strategies for PC. The aim of this study is to define and refine therapeutic segments for agents targeting DDR and replication stress in PC. Methods: We performed whole genome and RNA sequencing (RNAseq) on 48 patient-derived cell lines (PDCL) generated and characterized as part of the International Cancer Genome Initiative (ICGC). This identified increased replication stress in a sub-group of tumours, correlating with previously defined molecular subtypes of PC, irrespective of DDR status. Cytotoxic viability assays were performed using agents targeting the DDR pathway and cell cycle checkpoints, including Cisplatin, and inhibitors of PARP, ATR, WEE1, CHK1, CDK4/6 and PLK4. Subcutaneous patient derived xenografts (PDX) were generated to test therapeutic regimens in vivo. Results: DDR defective models, as defined by signatures of homologous recombination deficiency (HRD) were highly sensitive to Cisplatin and PARP inhibitors. Replication stress predicted differential responses to cell cycle inhibitors of WEE1, CHK1, CDK4/6 and PLK4. A novel mRNA signature of ATR inhibitor sensitivity was generated and correlated with response. Response to cell cycle checkpoint inhibitors were independent of DDR status, but strongly associated with replication stress. Conclusions: This proof of concept data demonstrates DDR deficiency and increased Replication Stress to be attractive targets in PC. Therapeutic vulnerabilities extend beyond platinum chemotherapy and can be targeted with novel small molecule inhibitors, with independent biomarkers predicting response to agents targeting either DDR or cell cycle checkpoints. This has led to the design and development of several personalized medicine trials via the Precision Panc platform targeting DDR and Replication stress, and will allow clinical testing of signatures of HRD and replication stress.

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33

Chen, Xi, Shijun Zhong, Xiao Zhu, Barbara Dziegielewska, Tom Ellenberger, Gerald M. Wilson, Alexander D. MacKerell, and Alan E. Tomkinson. "Rational Design of Human DNA Ligase Inhibitors that Target Cellular DNA Replication and Repair." Cancer Research 68, no. 9 (May 1, 2008): 3169–77. http://dx.doi.org/10.1158/0008-5472.can-07-6636.

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34

Franchet, Camille, and Jean-Sébastien Hoffmann. "When RAD52 Allows Mitosis to Accept Unscheduled DNA Synthesis." Cancers 12, no. 1 (December 19, 2019): 26. http://dx.doi.org/10.3390/cancers12010026.

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Faithful duplication of the human genome during the S phase of cell cycle and accurate segregation of sister chromatids in mitosis are essential for the maintenance of chromosome stability from one generation of cells to the next. Cells that are copying their DNA in preparation for division can suffer from ‘replication stress’ (RS) due to various external or endogenous impediments that slow or stall replication forks. RS is a major cause of pathologies including cancer, premature ageing and other disorders associated with genomic instability. It particularly affects genomic loci where progression of replication forks is intrinsically slow or problematic, such as common fragile site (CFS), telomeres, and repetitive sequences. Although the eukaryotic cell cycle is conventionally thought of as several separate steps, each of which must be completed before the next one is initiated, it is now accepted that incompletely replicated chromosomal domains generated in S phase upon RS at these genomic loci can result in late DNA synthesis in G2/M. In 2013, during investigations into the mechanism by which the specialized DNA polymerase eta (Pol η) contributes to the replication and stability of CFS, we unveiled that indeed some DNA synthesis was still occurring in early mitosis at these loci. This surprising observation of mitotic DNA synthesis that differs fundamentally from canonical semi-conservative DNA replication in S-phase has been then confirmed, called “MiDAS”and believed to counteract potentially lethal chromosome mis-segregation and non-disjunction. While other contributions in this Special Issue of Cancers focus on the role of RAS52RAD52 during MiDAS, this review emphases on the discovery of MiDAS and its molecular effectors.

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35

Ligasová, Anna, and Karel Koberna. "DNA Replication: From Radioisotopes to Click Chemistry." Molecules 23, no. 11 (November 17, 2018): 3007. http://dx.doi.org/10.3390/molecules23113007.

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The replication of nuclear and mitochondrial DNA are basic processes assuring the doubling of the genetic information of eukaryotic cells. In research of the basic principles of DNA replication, and also in the studies focused on the cell cycle, an important role is played by artificially-prepared nucleoside and nucleotide analogues that serve as markers of newly synthesized DNA. These analogues are incorporated into the DNA during DNA replication, and are subsequently visualized. Several methods are used for their detection, including the highly popular click chemistry. This review aims to provide the readers with basic information about the various possibilities of the detection of replication activity using nucleoside and nucleotide analogues, and to show the strengths and weaknesses of those different detection systems, including click chemistry for microscopic studies.

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36

Rassool, Feyruz V., Philip S. North, Ghulam J. Mufti, and Ian D. Hickson. "Constitutive DNA damage is linked to DNA replication abnormalities in Bloom's syndrome cells." Oncogene 22, no. 54 (November 2003): 8749–57. http://dx.doi.org/10.1038/sj.onc.1206970.

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37

Kumar Karanam, Narasimha, Lianghao Ding, Asaithamby Aroumougame, and Michael Story. "EXTH-05. THERAPEUTIC IMPLICATIONS OF TTFIELDS INDUCED DNA DAMAGE AND REPLICATION STRESS IN NOVEL COMBINATIONS FOR CANCER TREATMENT." Neuro-Oncology 21, Supplement_6 (November 2019): vi83. http://dx.doi.org/10.1093/neuonc/noz175.339.

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Abstract TTFields are low-intensity, intermediate frequency, alternating electric fields which are applied to tumor regions using non-invasive arrays. TTFields is approved for the treatment of glioblastoma and mesothelioma with clinical trials ongoing in other cancer types. The mechanism of action for TTFields includes interference with mitosis, reduced DNA double strand break (DSB) repair capacity and the frank induction of DNA DSBs. The mechanism by which TTFields induces DNA DSBs appears to be through the enhancement of DNA replication stress with continued TTFields exposure. The induction of DNA DSBs appears to be as a result of significantly reduced expression of the DNA replication complex genes MCM6 and MCM10 as well as the Fanconi’s Anemia (FA) pathway genes. TTFields treatment increases the number of RPA foci, decreases nascent DNA length and increases R-loop formation which are markers of DNA replication stress. These results suggest that TTFields-induced replication stress is the underlying mechanism and cellular endogenous source of DNA DSB generation via replication fork collapse. The current study suggests that TTFields exposure causes a conditional vulnerability environment that renders cells more susceptible to chemotherapeutic agents that induce DNA damage and/or cause replication stress. Supporting this is the synergistic cell killing seen with TTFields exposure concomitant with cisplatin, TTFields plus concomitant PARP inhibition with or without subsequent radiation, or radiation given at the completion of a TTFields exposure. Finally, TTFields-induced mitotic aberrations and DNA damage/replication stress events, although intimately linked to one another as one can expose the other, are likely initiated independently of one another as suggested by the gene expression analysis of 47 key mitosis regulator genes. These results establish that enhanced replication stress and reduced DNA repair capacity are also major mechanisms of TTFields effects, effects for which there are therapeutic implications.

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Wharton, S. B., S. Hibberd, K. L. Eward, D. Crimmins, D. A. Jellinek, D. Levy, K. Stoeber, and G. H. Williams. "DNA replication licensing and cell cycle kinetics of oligodendroglial tumours." British Journal of Cancer 91, no. 2 (June 15, 2004): 262–69. http://dx.doi.org/10.1038/sj.bjc.6601949.

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39

Schneikert, Jean, and Jürgen Behrens. "Truncated APC is required for cell proliferation and DNA replication." International Journal of Cancer 119, no. 1 (July 1, 2006): 74–79. http://dx.doi.org/10.1002/ijc.21826.

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40

Watson, Nicholas B., Suparna Mukhopadhyay, and W. Glenn McGregor. "Translesion DNA replication proteins as molecular targets for cancer prevention." Cancer Letters 241, no. 1 (September 2006): 13–22. http://dx.doi.org/10.1016/j.canlet.2005.10.013.

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41

Wohlberedt, Kai, Ina Klusmann, Polina K. Derevyanko, Kester Henningsen, Josephine Ann Mun Yee Choo, Valentina Manzini, Anna Magerhans, et al. "Mdm4 supports DNA replication in a p53-independent fashion." Oncogene 39, no. 25 (May 19, 2020): 4828–43. http://dx.doi.org/10.1038/s41388-020-1325-1.

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42

Arentson, Elizabeth, Patrick Faloon, Junghee Seo, Eunpyo Moon, Joey M. Studts, Daved H. Fremont, and Kyunghee Choi. "Oncogenic potential of the DNA replication licensing protein CDT1." Oncogene 21, no. 8 (February 2002): 1150–58. http://dx.doi.org/10.1038/sj.onc.1205175.

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Vig, Baldev K., Dieter Schroeter, and Neidhard Paweletz. "Early replication of repetitive DNA associated with inactive centromeres." Cancer Genetics and Cytogenetics 50, no. 1 (November 1990): 57–65. http://dx.doi.org/10.1016/0165-4608(90)90238-6.

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Mocanu, Camelia, and Kok-Lung Chan. "Mind the replication gap." Royal Society Open Science 8, no. 6 (June 2021): 201932. http://dx.doi.org/10.1098/rsos.201932.

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Unlike bacteria, mammalian cells need to complete DNA replication before segregating their chromosomes for the maintenance of genome integrity. Thus, cells have evolved efficient pathways to restore stalled and/or collapsed replication forks during S-phase, and when necessary, also to delay cell cycle progression to ensure replication completion. However, strong evidence shows that cells can proceed to mitosis with incompletely replicated DNA when under mild replication stress (RS) conditions. Consequently, the incompletely replicated genomic gaps form, predominantly at common fragile site regions, where the converging fork-like DNA structures accumulate. These branched structures pose a severe threat to the faithful disjunction of chromosomes as they physically interlink the partially duplicated sister chromatids. In this review, we provide an overview discussing how cells respond and deal with the under-replicated DNA structures that escape from the S/G2 surveillance system. We also focus on recent research of a mitotic break-induced replication pathway (also known as mitotic DNA repair synthesis), which has been proposed to operate during prophase in an attempt to finish DNA synthesis at the under-replicated genomic regions. Finally, we discuss recent data on how mild RS may cause chromosome instability and mutations that accelerate cancer genome evolution.

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Blank, Heidi M., Chonghua Li, John E. Mueller, Lydia M. Bogomolnaya, Mary Bryk, and Michael Polymenis. "An Increase in Mitochondrial DNA Promotes Nuclear DNA Replication in Yeast." PLoS Genetics 4, no. 4 (April 25, 2008): e1000047. http://dx.doi.org/10.1371/journal.pgen.1000047.

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Kumar, Asmita, David T. Brown, and Gregory H. Leno. "DNA intercalators differentially affect chromatin structure and DNA replication in Xenopus egg extract." Anti-Cancer Drugs 15, no. 6 (July 2004): 633–39. http://dx.doi.org/10.1097/01.cad.0000131686.14013.4f.

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Koussa, Natasha C., and Duncan J. Smith. "Limiting DNA polymerase delta alters replication dynamics and leads to a dependence on checkpoint activation and recombination-mediated DNA repair." PLOS Genetics 17, no. 1 (January 25, 2021): e1009322. http://dx.doi.org/10.1371/journal.pgen.1009322.

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DNA polymerase delta (Pol δ) plays several essential roles in eukaryotic DNA replication and repair. At the replication fork, Pol δ is responsible for the synthesis and processing of the lagging-strand. At replication origins, Pol δ has been proposed to initiate leading-strand synthesis by extending the first Okazaki fragment. Destabilizing mutations in human Pol δ subunits cause replication stress and syndromic immunodeficiency. Analogously, reduced levels of Pol δ in Saccharomyces cerevisiae lead to pervasive genome instability. Here, we analyze how the depletion of Pol δ impacts replication origin firing and lagging-strand synthesis during replication elongation in vivo in S. cerevisiae. By analyzing nascent lagging-strand products, we observe a genome-wide change in both the establishment and progression of replication. S-phase progression is slowed in Pol δ depletion, with both globally reduced origin firing and slower replication progression. We find that no polymerase other than Pol δ is capable of synthesizing a substantial amount of lagging-strand DNA, even when Pol δ is severely limiting. We also characterize the impact of impaired lagging-strand synthesis on genome integrity and find increased ssDNA and DNA damage when Pol δ is limiting; these defects lead to a strict dependence on checkpoint signaling and resection-mediated repair pathways for cellular viability.

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Wu, Xiaohua. "Replication Stress Response Links RAD52 to Protecting Common Fragile Sites." Cancers 11, no. 10 (September 29, 2019): 1467. http://dx.doi.org/10.3390/cancers11101467.

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Rad52 in yeast is a key player in homologous recombination (HR), but mammalian RAD52 is dispensable for HR as shown by the lack of a strong HR phenotype in RAD52-deficient cells and in RAD52 knockout mice. RAD52 function in mammalian cells first emerged with the discovery of its important backup role to BRCA (breast cancer genes) in HR. Recent new evidence further demonstrates that RAD52 possesses multiple activities to cope with replication stress. For example, replication stress-induced DNA repair synthesis in mitosis (MiDAS) and oncogene overexpression-induced DNA replication are dependent on RAD52. RAD52 becomes essential in HR to repair DSBs containing secondary structures, which often arise at collapsed replication forks. RAD52 is also implicated in break-induced replication (BIR) and is found to inhibit excessive fork reversal at stalled replication forks. These various functions of RAD52 to deal with replication stress have been linked to the protection of genome stability at common fragile sites, which are often associated with the DNA breakpoints in cancer. Therefore, RAD52 has important recombination roles under special stress conditions in mammalian cells, and presents as a promising anti-cancer therapy target.

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Bertolin, Agustina P., Jean-Sébastien Hoffmann, and Vanesa Gottifredi. "Under-Replicated DNA: The Byproduct of Large Genomes?" Cancers 12, no. 10 (September 25, 2020): 2764. http://dx.doi.org/10.3390/cancers12102764.

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In this review, we provide an overview of how proliferating eukaryotic cells overcome one of the main threats to genome stability: incomplete genomic DNA replication during S phase. We discuss why it is currently accepted that double fork stalling (DFS) events are unavoidable events in higher eukaryotes with large genomes and which responses have evolved to cope with its main consequence: the presence of under-replicated DNA (UR-DNA) outside S phase. Particular emphasis is placed on the processes that constrain the detrimental effects of UR-DNA. We discuss how mitotic DNA synthesis (MiDAS), mitotic end joining events and 53BP1 nuclear bodies (53BP1-NBs) deal with such specific S phase DNA replication remnants during the subsequent phases of the cell cycle.

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Pavlov, Youri I., Anna S. Zhuk, and Elena I. Stepchenkova. "DNA Polymerases at the Eukaryotic Replication Fork Thirty Years after: Connection to Cancer." Cancers 12, no. 12 (November 24, 2020): 3489. http://dx.doi.org/10.3390/cancers12123489.

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Recent studies on tumor genomes revealed that mutations in genes of replicative DNA polymerases cause a predisposition for cancer by increasing genome instability. The past 10 years have uncovered exciting details about the structure and function of replicative DNA polymerases and the replication fork organization. The principal idea of participation of different polymerases in specific transactions at the fork proposed by Morrison and coauthors 30 years ago and later named “division of labor,” remains standing, with an amendment of the broader role of polymerase δ in the replication of both the lagging and leading DNA strands. However, cancer-associated mutations predominantly affect the catalytic subunit of polymerase ε that participates in leading strand DNA synthesis. We analyze how new findings in the DNA replication field help elucidate the polymerase variants’ effects on cancer.

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