Relevant bibliographies by topics / DNA Binding Anticancer Drugs

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'DNA Binding Anticancer Drugs'

Author: Grafiati
Published: 4 June 2021
Last updated: 7 September 2023

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Journal articles on the topic "DNA Binding Anticancer Drugs"

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Baguley, Bruce C., Catherine J. Drummond, Ying Yi Chen, and Graeme J. Finlay. "DNA-Binding Anticancer Drugs: One Target, Two Actions." Molecules 26, no. 3 (2021): 552. http://dx.doi.org/10.3390/molecules26030552.

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Amsacrine, an anticancer drug first synthesised in 1970 by Professor Cain and colleagues, showed excellent preclinical activity and underwent clinical trial in 1978 under the auspices of the US National Cancer Institute, showing activity against acute lymphoblastic leukaemia. In 1984, the enzyme DNA topoisomerase II was identified as a molecular target for amsacrine, acting to poison this enzyme and to induce DNA double-strand breaks. One of the main challenges in the 1980s was to determine whether amsacrine analogues could be developed with activity against solid tumours. A multidisciplinary
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Marchini, Sergio, Massimo Broggini, Cristiana Sessa, and Maurizio D’Incalci. "Development of distamycin-related DNA binding anticancer drugs." Expert Opinion on Investigational Drugs 10, no. 9 (2001): 1703–14. http://dx.doi.org/10.1517/13543784.10.9.1703.

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Farmanzadeh, Davood, and Meysam Najafi. "Benzimidazole derivatives as anticancer drugs: A theoretical investigation." Journal of Theoretical and Computational Chemistry 14, no. 03 (2015): 1550018. http://dx.doi.org/10.1142/s0219633615500182.

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In this study the anticancer properties of a series of benzimidazole drugs 1–9 and their interactions with DNA base pairs were investigated. The obtained theoretical results for anticancer activity of synthesized drugs 1–5 were compared to corresponding published experimental results. Based on theoretical and published experimental anticancer scales, drugs 2 and 4 have higher anticancer activity among drugs 1–5. Obtained results reveal that interactions of studied drugs with DNA base pairs are energetically favorable and solvent and electric field (EF) increase the binding energies in comparis
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Wilmańska, Dorota, Malgorzata Czyz, Kazimierz Studzian, Mariola K. Piestrzeniewicz, and Marek Gniazdowski. "Effects of Anticancer Drugs on Transcription in vitro." Zeitschrift für Naturforschung C 56, no. 9-10 (2001): 886–91. http://dx.doi.org/10.1515/znc-2001-9-1034.

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AbstractThe effects of DNA interacting drugs on: (1) total RNA synthesis catalyzed by E.coli and T7 RNA polymerase; (2) synthesis of the initiating dinucleotide (pppApU) by E .coli RNA polymerase (“abortive initiation“); (3) elongation of RNA chains synthesized by T7 RNA polymerase on pT7-7 plasmid DNA bearing T7 RNA polymerase promoter ϕ 10 with human Cu/Zn superoxide dismutase coding sequence, (4) interaction of transcription factor Sp1 and its binding site were studied. Intercalating ligands which form quickly dissociating complexes with DNA (anthracyclines, proflavine, ethidium bromide) ar
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Jia, Shuailong, Runjing Wang, Kui Wu, Hongliang Jiang, and Zhifeng Du. "Elucidation of the Mechanism of Action for Metal Based Anticancer Drugs by Mass Spectrometry-Based Quantitative Proteomics." Molecules 24, no. 3 (2019): 581. http://dx.doi.org/10.3390/molecules24030581.

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The discovery of the anticancer activity of cisplatin and its clinical application has opened a new field for studying metal-coordinated anticancer drugs. Metal-based anticancer drugs, such as cisplatin, can be transported to cells after entering into the human body and form metal–DNA or metal–protein adducts. Then, responding proteins will recognize adducts and form stable complexes. The proteins that were binding with metal-based anticancer drugs were relevant to their mechanism of action. Herein, investigation of the recognition between metal-based anticancer drugs and its binding partners
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Gniazdowski, M., and M. Czyz. "Transcription factors as targets of anticancer drugs." Acta Biochimica Polonica 46, no. 2 (1999): 255–62. http://dx.doi.org/10.18388/abp.1999_4159.

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Several general and gene- and cell-selective transcription factors are required for specific transcription to occur. Many of them exert their functions through specific contacts either in the promoter region or at distant sequences regulating the initiation. These contacts may be altered by anticancer drugs which form non-covalent complexes with DNA. Covalent modifications of DNA by alkylating agents may prevent transcription factors from recognizing their specific sequences or may constitute multiple "unnatural" binding sites in DNA which attract the factors thus decreasing their availability
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Ali, Imran, Waseem A. Wani, Kishwar Saleem, and Ming-Fa Hsieh. "Anticancer metallodrugs of glutamic acid sulphonamides: in silico, DNA binding, hemolysis and anticancer studies." RSC Adv. 4, no. 56 (2014): 29629–41. http://dx.doi.org/10.1039/c4ra02570a.

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In response to an increased demand for effective anticancer drugs, a series of disodium sulphonamides ofl-glutamic acid (L1–L3) was synthesized. Sulphonamides were complexed with copper(ii), nickel(ii) and ruthenium(iii) ions, separately and respectively.
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Kulkarni, Preeti, Suraksha Kadam, Disha Sharma, Manisha Mishra, and Vaidhun Bhaskar. "DNA Topoisomerases: As target for anti-cancer drugs." Indian Journal of Pharmacy and Pharmacology 9, no. 1 (2022): 13–17. http://dx.doi.org/10.18231/j.ijpp.2022.003.

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Topoisomerase inhibitors are agents designed to interfere with the action of topoisomerase enzymes I and II. Topoisomerases are enzymes that control the changes in DNA tridimensional structure by catalyzing the breaking and rejoining of the phosphodiester backbone of DNA strands during the normal cell cycle. DNA Topoisomerases control the conformational changes in DNA topology by breaking and resealing DNA strands during normal cellular growth, that’s why these are essential enzymes. A major class of anticancer drugs acts as inhibitors of DNA Topoisomerases. This paper gives a brief review on
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ERDEM, A., H. KARADENIZ, A. CALISKAN, and A. VASEASHTA. "ELECTROCHEMICAL DNA SENSOR TECHNOLOGY FOR MONITORING OF DRUG–DNA INTERACTIONS." Nano 03, no. 04 (2008): 229–32. http://dx.doi.org/10.1142/s1793292008001064.

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The objective of this investigation is to understand the nature and dynamics of binding small molecules to bio-macromolecules using electrochemical methods. The investigation pertaining to the design of site- and conformation-specific reagents provides a rationale for new studies of drug delivery design. Some anticancer drugs and DNA interactions have been undertaken by using a variety of techniques. Determination of interaction between DNA and DNA-targeted molecules would be valuable in the design of molecule-specific electrochemical biosensors for applications in diagnostics, development of
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Delgado, Justine L., Chao-Ming Hsieh, Nei-Li Chan, and Hiroshi Hiasa. "Topoisomerases as anticancer targets." Biochemical Journal 475, no. 2 (2018): 373–98. http://dx.doi.org/10.1042/bcj20160583.

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Many cancer type-specific anticancer agents have been developed and significant advances have been made toward precision medicine in cancer treatment. However, traditional or nonspecific anticancer drugs are still important for the treatment of many cancer patients whose cancers either do not respond to or have developed resistance to cancer-specific anticancer agents. DNA topoisomerases, especially type IIA topoisomerases, are proved therapeutic targets of anticancer and antibacterial drugs. Clinically successful topoisomerase-targeting anticancer drugs act through topoisomerase poisoning, wh
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Dissertations / Theses on the topic "DNA Binding Anticancer Drugs"

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Leczkowska, Anna. "Non-covalent DNA-binding ruthenium anticancer drugs." Thesis, University of Birmingham, 2011. http://etheses.bham.ac.uk//id/eprint/1695/.

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The research work described in this thesis concerns metal-based anticancer drugs with an emphasis on non-covalent DNA-binding supramolecular assemblies. The project involves the preparation of a series of mono- and bi-metallic ruthenium complexes with a primary focus on fluorescent dinuclear triple-stranded helicates with different structural topographies. Emphasis is then directed towards an investigation of the DNA binding characteristics of these molecules and an evaluation of their anticancer properties in human cancer cell lines. Attention is brought to the significance that the cylinder-
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Todd, Ryan Christopher 1981. "Structural and functional consequences of platinum anticancer drug binding to free and nucleosomal DNA." Thesis, Massachusetts Institute of Technology, 2010. http://hdl.handle.net/1721.1/57802.

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Thesis (Ph. D.)--Massachusetts Institute of Technology, Dept. of Chemistry, 2010.<br>Vita. Cataloged from PDF version of thesis.<br>Includes bibliographical references.<br>Cisplatin, carboplatin, and oxaliplatin are three FDA-approved members of the platinum anticancer drug family. These compounds induce apoptosis in tumor cells by binding to nuclear DNA, forming a variety of adducts, and triggering cellular responses, one of which is the inhibition of transcription. The focus of this thesis is on studying the structure of these adducts, and correlating these effects with inhibition of transcr
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Farhad, Mohammad. "Studies on new trinuclear palladium compounds." Connect to full text, 2007. http://hdl.handle.net/2123/2477.

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Doctor of Philosophy(PhD)<br>The present study deals with the synthesis and characterization of six tri-palladium complexes code named MH3, MH4, MH5, MH6, MH7 and MH8 that contained two planaramine ligands bound to the central or each of the terminal metal ions. The activity of the compounds against human cancer cell lines: A2780, A2780cisR and A2780ZD0473R, cell uptake, levels of DNA-binding and nature of interaction with salmon sperm and pBR322 plasmid DNA have also been determined. Whereas cisplatin binds with DNA forming mainly intrastrand GG adduct that causes local bending of a DNA stran
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Majmudar, Pooja M. "Investigating Molecular Targets of Phosphaplatins: A Class of Novel Non-DNA-Binding Platinum Anticancer Agents in the Treatment of Ovarian Cancer." Ohio University / OhioLINK, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=ohiou1300373466.

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Trimmer, Elizabeth Eloise 1966. "Specific binding of human SRY (Sex-Determining Region Y) to DNA adducts of the anticancer drug cisplatin." Thesis, Massachusetts Institute of Technology, 1997. http://hdl.handle.net/1721.1/46076.

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Hotze, Anna Catharina Genovefa. "Design of ruthenium anticancer drugs : study of the structure-activity relationships and binding to DNA model bases of ruthenium complexes with 2-phenylazopyridine ligands /." Rotterdam : Optima Grafische Communicatie, 2003. http://catalogue.bnf.fr/ark:/12148/cb399315937.

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Bezoski, Brittany A. "Metal Binding Characteristics of Heterocyclic and Carbocyclic Anticancer Drugs." University of Toledo Health Science Campus / OhioLINK, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=mco1481287656969232.

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Punchihewa, Chandanamalie. "DNA and DNA-Interacting Proteins as Anticancer Drug Targets." Diss., The University of Arizona, 2006. http://hdl.handle.net/10150/194379.

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DNA is both the oldest and newest of targets for cancer therapy. While it is already being targeted by many anticancer drugs in the clinic, the development of sequence-specific DNA binders has brought it back to the limelight as a valuable anticancer drug target.My studies on DNA interacting agents was initiated with the DNA intercalator campotothecin, and also included topoisomerase I enzyme. I have evaluated the structure of topoisomerase I C-terminal domain that consists of the active site tyrosine. My data indicate that this domain exists in a molten globule conformation with a fluctuating
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Jung, Yongwon 1977. "Cellular responses against DNA damaged by platinum anticancer drugs." Thesis, Massachusetts Institute of Technology, 2005. http://hdl.handle.net/1721.1/33746.

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Thesis (Ph. D.)--Massachusetts Institute of Technology, Dept. of Chemistry, 2005.<br>Vita.<br>Includes bibliographical references.<br>The anticancer activity of platinum-based drugs such as cisplatin, carboplatin, and oxaliplatin is mediated by their ability to attack DNA such that generated adducts trigger numerous cellular responses. A better understanding of these processes is critical for developing more effective therapeutic approaches, which can increase the anti-cancer activity of the drugs while minimizing side effects and extending successful treatment to a wider range of human cancer
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Sobhanian, Ali. "Synthetic and spectral studies of potential anticancer drugs." Thesis, University of Hertfordshire, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.361263.

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Books on the topic "DNA Binding Anticancer Drugs"

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Snapka, Robert M. The SV40 replicon model for analysis of anticancer drugs. R.G. Landes, 1996.

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The SV40 replicon model for analysis of anticancer drugs. Academic Press, 1996.

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NATO ASI/FEBS Course on DNA-Ligand Interactions: From Drugs to Proteins (1986 Abbey of Fontevraud). DNA-ligand interactions: From drugs to proteins. Plenum Press, 1987.

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Drug-DNA interaction protocols. 2nd ed. Humana Press, Springer Science+Business Media, 2010.

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DNA-Ligand Interactions:From Drugs to Proteins. Springer, 1987.

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DNA-ligand interactions. Plenum published in cooperation with NATO Scientific Affairs Division, 1987.

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Storr, Tim. Ligand Design in Medicinal Inorganic Chemistry. Wiley & Sons, Limited, John, 2014.

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Storr, Tim. Ligand Design in Medicinal Inorganic Chemistry. Wiley & Sons, Incorporated, John, 2014.

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Storr, Tim. Ligand Design in Medicinal Inorganic Chemistry. Wiley & Sons, Incorporated, John, 2014.

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Storr, Tim. Ligand Design in Medicinal Inorganic Chemistry. Wiley & Sons, Incorporated, John, 2014.

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Book chapters on the topic "DNA Binding Anticancer Drugs"

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Wierenga, Wendell. "DNA-Minor Groove Binding Anticancer Agents." In Cytotoxic Anticancer Drugs: Models and Concepts for Drug Discovery and Development. Springer US, 1992. http://dx.doi.org/10.1007/978-1-4615-3492-1_5.

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Majumder, Parijat, Suman K. Pradhan, Pukhrambam Grihanjali Devi, Sudipta Pal, and Dipak Dasgupta. "Chromatin as a Target for the DNA-Binding Anticancer Drugs." In Subcellular Biochemistry. Springer Netherlands, 2007. http://dx.doi.org/10.1007/1-4020-5466-1_8.

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Marzilli, Luigi G., Tammy Page Kline, David Live, and Gerald Zon. "Platinum Anticancer Drug Binding to Oligonucleotide Models of DNA." In ACS Symposium Series. American Chemical Society, 1989. http://dx.doi.org/10.1021/bk-1989-0402.ch009.

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Wilson, W. David, and Farial A. Tanious. "Kinetic Analysis of Drug-Nucleic Acid Binding Modes: Absolute Rates and Effects of Salt Concentration." In Molecular Aspects of Anticancer Drug-DNA Interactions. Macmillan Education UK, 1994. http://dx.doi.org/10.1007/978-1-349-13330-7_6.

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Dhar, Shanta, and Stephen J. Lippard. "Structural and Mechanistic Studies of Anticancer Platinum Drugs: Uptake, Activation, and the Cellular Response to DNA Binding." In Platinum and Other Heavy Metal Compounds in Cancer Chemotherapy. Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-459-3_18.

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Sparreboom, Alex, and Walter J. Loos. "Protein Binding of Anticancer Drugs." In Handbook of Anticancer Pharmacokinetics and Pharmacodynamics. Humana Press, 2004. http://dx.doi.org/10.1007/978-1-59259-734-5_12.

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Denny, William A., and Bruce C. Baguley. "Acridine-based Anticancer Drugs." In Molecular Aspects of Anticancer Drug-DNA Interactions. Macmillan Education UK, 1994. http://dx.doi.org/10.1007/978-1-349-13330-7_7.

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Lambert, Bernard, and Jean-Bernard Le Pecq. "Pharmacology of DNA Binding Drugs." In DNA—Ligand Interactions. Springer US, 1987. http://dx.doi.org/10.1007/978-1-4684-5383-6_9.

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McKeage, Mark J., and Lloyd R. Kelland. "New Platinum Drugs." In Molecular Aspects of Anticancer Drug-DNA Interactions. Macmillan Education UK, 1993. http://dx.doi.org/10.1007/978-1-349-12356-8_6.

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Pommier, Yves, Juana Barceló, Takahisa Furuta, Haruyuki Takemura, and Olivier Sordet. "Mechanisms of topoisomerase I inhibition by anticancer drugs." In DNA Topoisomerases in Cancer Therapy. Springer US, 2003. http://dx.doi.org/10.1007/978-1-4615-0141-1_2.

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Conference papers on the topic "DNA Binding Anticancer Drugs"

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Nesher, Elimelech, Alfiya Safina, Ieman Aljahdali, et al. "Abstract 1755: Chromatin trapping is a key factor for anticancer cytotoxicity of DNA-binding small molecule drugs." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-1755.

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Nesher, Elimelech, Alfiya Safina, Ieman Aljahdali, et al. "Abstract 1755: Chromatin trapping is a key factor for anticancer cytotoxicity of DNA-binding small molecule drugs." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-1755.

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Milović, Emilija, Nenad Janković, Jelena Petronijević, and Nenad Joksimović. "CHEMICO-BIOLOGICAL INTERACTION OF SELECTED TETRAHYDROPYRIMIDINES." In 1st INTERNATIONAL Conference on Chemo and BioInformatics. Institute for Information Technologies, University of Kragujevac, 2021. http://dx.doi.org/10.46793/iccbi21.347m.

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Tetrahydropyrimidines (THPMs) attracted attention as a very important class of aza heterocycles with broad pharmacological activities during the past years. In many studies have been proven that THPMs have anticancer, anti-inflammatory, antimicrobial, antioxidant, antifungal, anti-HIV activity. Bearing in mind our interest in medicinal and Biginelli chemistry, we investigated interaction with important biomacromolecules (DNA, BSA) and our earlier synthetized THPMs derivatives with proven very good cytotoxic activity.[1] Investigation of affinity of compounds A and B (Figure 1) to bind to bovin
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Trnkova, Libuse, Dalibor Huska, Vojtech Adam, et al. "Electrochemical biosensor for investigation of anticancer drugs interactions (doxorubicin and ellipticine) with DNA." In 2009 IEEE Sensors. IEEE, 2009. http://dx.doi.org/10.1109/icsens.2009.5398361.

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Muguruma, Kazuya, Masakazu Yashiro, Hiroaki Tanaka, et al. "Abstract 100: The effect of synergic anti-proliferation of DNA methyltransferase inhibitor binding to anti-cancer drugs in gastric cancer." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-100.

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Teo, Ka Yaw, and Bumsoo Han. "Freezing-Assisted Intracellular Drug Delivery to Multi-Drug Resistant Cancer Cells." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-192373.

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The efficacy of chemotherapy is significantly impaired by multi-drug resistance (MDR) of cancer cells. The mechanism of MDR is associated with the overexpression of certain ATP-binding cassette protein transporters in plasma membranes. These transporters actively keep intracellular drug concentration below the cell-killing threshold by extruding cytotoxic drugs. Various strategies to overcome MDR have been proposed and have shown promising results at the laboratory level. However, pharmacokinetic alteration of co-administered anticancer agents reduces their clinical effectiveness. This leads t
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Sauvaigo, Sylvie, Anne Forestier, Fanny Sarrazy, Sylvain Caillat, and Yves Vandenbrouck. "Abstract 3419: A multiplexed enzymatic repair assay on biochip reveals a functional DNA repair signature in cancer cell lines exposed to cytotoxic anticancer drugs." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-3419.

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Adnan, Ashfaq, and Wing Kam Liu. "Electrostatic Self-Assembly of Functionalized Nanodiamonds and Their Binding Capacity With Doxorubicin Drugs." In ASME 2010 First Global Congress on NanoEngineering for Medicine and Biology. ASMEDC, 2010. http://dx.doi.org/10.1115/nemb2010-13164.

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While cancers have no known cure, some of them can be successfully treated with the combination of surgery and systematic therapy. In general, systemic/widespread chemotherapy is usually injected into the bloodstream to attempt to target cancer cells. Such procedure often imparts devastating side effects because cancer drugs are nonspecific in activity, and transporting them throughout the bloodstream further reduces their ability to target the right region. This means that they kill both healthy and unhealthy cells. It has been observed that the physiological conditions of the fluids around l
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Matić, Sanja, Snežana Stanić, Nevena Tomašević, Rino Ragno, and Milan Mladenović. "DISCLOSING THE TRUE NATURE OF HESPERETIN’S ANTIGENOTOXICITY „IN VIVO“ WITHIN THE „DROSOPHILA MELANOGASTER“ SOMATIC CELLS THROUGH THE EXTENSIVE GENOTOXICAL AND STRUCTURE-BASED STUDIES." In 1st INTERNATIONAL Conference on Chemo and BioInformatics. Institute for Information Technologies, University of Kragujevac, 2021. http://dx.doi.org/10.46793/iccbi21.427m.

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Previously unreported genotoxic and antigenotoxic potentials of hesperetin (Hes) were revealed by treating the Drosophila melanogaster (dm) whose DNA has been altered by means of O6-ethylguanine (dmGO6-Et) and O4-ethylthymine (dmTO4-Et) lesions appearance, caused by ethyl methanesulfonate (EMS), a proven alkylating agent and mutagen. Therefore, Hes potencies were determined by means of the comet assay on somatic cells level, where compound exerted no genotoxic effects but acted genotoxically as a Topoisomerase IIα (dmTopIIα) catalytic inhibitor by invading the Binding and Cleavage Domain and s
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Reports on the topic "DNA Binding Anticancer Drugs"

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Beerman, Terry A. Discovery of DNA Binding Anticancer Drugs That Target Oncogenic Transcription Factors Associated With Human Breast Cancer. Defense Technical Information Center, 2001. http://dx.doi.org/10.21236/ada403322.

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Chiang, Shu-Yuan. DNA Binding Drugs Targeting the Regulatory DNA Binding Site of the ETS Domain Family Transcription Factor. Defense Technical Information Center, 1998. http://dx.doi.org/10.21236/ada352305.

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Chen, Fu-Ming. Sequence-Specific and Synergistic Binding of Drugs to DNA. Defense Technical Information Center, 1995. http://dx.doi.org/10.21236/ada306436.

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Chen, Fu-Ming. Sequence-Specific and Synergistic Binding of Drugs to DNA. Defense Technical Information Center, 1999. http://dx.doi.org/10.21236/ada392011.

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Wang, Yong-Dong. DNA Binding Drugs Targeting the Regulatory DNA Binding Site of the ETS Domain Family Transcription Factor Associated With Human Breast Cancer. Defense Technical Information Center, 2000. http://dx.doi.org/10.21236/ada392560.

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Wang, Yong-Dong. DNA Binding Drugs Targeting the Regulatory DNA Binding Site of the ETS Domain Family Transcription Factor Associated With Human Breast Cancer. Defense Technical Information Center, 1999. http://dx.doi.org/10.21236/ada381309.

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Leslie, Stephanie J. Evaluation of DNA Binding Drugs as Inhibitors of ESX, an ETS Domain Transcription Factor Associated with Breast Cancer: Effects of ESX/DNA Complex Disruption. Defense Technical Information Center, 2001. http://dx.doi.org/10.21236/ada401300.

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Macedo, Luciana, and Linda Malkas. The Human Breast Cancer DNA Synthesome Can Serve as a Novel In Vitro Model System for Studying the Mechanism of Action of Anticancer Drugs. Defense Technical Information Center, 2000. http://dx.doi.org/10.21236/ada393926.

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Jiang, Haiyan. The Human Breast Cancer Cell DNA Synthesome Can Serve as a Novel in Vitro Model System for Studying the Mechanism of Action of Anticancer Drugs. Defense Technical Information Center, 1999. http://dx.doi.org/10.21236/ada384124.

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