Relevant bibliographies by topics / Anticancer treatment

Contents

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

Academic literature on the topic 'Anticancer treatment'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2025

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Journal articles on the topic "Anticancer treatment"

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Frączek, Paulina, Aneta Kilian-Kita, Mirosława Püsküllüoglu, and Krzysztof Krzemieniecki. "Acupuncture as anticancer treatment?" Współczesna Onkologia 6 (2016): 453–57. http://dx.doi.org/10.5114/wo.2016.65604.

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de Bree, Eelco, John Romanos, and Dimitris D. Tsiftsis. "Hyperthermia in anticancer treatment." European Journal of Surgical Oncology (EJSO) 28, no. 1 (February 2002): 95. http://dx.doi.org/10.1053/ejso.2001.1220.

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Falanga, Anna, and Marina Marchetti. "Anticancer treatment and thrombosis." Thrombosis Research 129, no. 3 (March 2012): 353–59. http://dx.doi.org/10.1016/j.thromres.2011.10.025.

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Attina, Giorgio, Stefano Mastrangelo, and Antonio Ruggiero. "Telomerase and Anticancer Treatment." Biomedical and Pharmacology Journal 15, no. 4 (December 20, 2022): 1881–88. http://dx.doi.org/10.13005/bpj/2526.

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Current chemotherapy uses compounds of organometallic nature that act with different mechanisms of action. Many pharmacological studies are directed toward the creation of compounds with more specific and selective activity toward tumor targets, including telomerase. The design and synthesis of such compounds with specific antitelomerase activity must consider the mechanism of action of the enzyme and its structure. The discovery of a close correlation between telomerase activation, cell immortalization and oncogenesis has suggested that telomerase inhibitors could be potent therapeutic agents, capable of selectively killing cancer cells. Inhibition of telomerase is expected to lead toward shortening of telomeres to a critical length, such that replicative senescence and cell death due to irreparable chromosomal damage can result. It has been observed that cancer cells generally have shorter telomeres than the normal replicative cell population, probably because the malignant cells have undergone more divisions. Therefore, the inhibition telomeres of cancer cells after a few cycles of cell division, without the normal cells suffering harmful consequences during therapy. Telomerase is certainly an interesting target on which to continue to study molecules that inhibit its function to obtain a specificity of therapeutic intervention and a reduction of the nonspecific cytotoxicity of chemotherapy.
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Combrink, Margaretha Johanna W., and Johanna Elizabeth Maree. "The Transition From Palliation With Anticancer Treatment to Palliation Without Anticancer Treatment." Journal of Hospice & Palliative Nursing 18, no. 5 (October 2016): 421–28. http://dx.doi.org/10.1097/njh.0000000000000267.

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Ayyad, Rezk R., Ahmed M. Mansour, Ahmed M. Nejm, Yasser Abdel Allem Hassan, and Ahmed R. Ayyad. "An Overview of Antibiotics Used in Cancer Treatment and Drugs that Act as Antimicrotubules." Journal of Progress in Engineering and Physical Science 3, no. 2 (June 2024): 25–32. http://dx.doi.org/10.56397/jpeps.2024.06.04.

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The caner in general is an abnormal growth with no causes and route of transportation in the body, which is the difficult of treatment or limited of its spread. One of the methods of treatment is the chemotherapeutic agents, we will overview on Antibiotics and Antimicrotubules act as Anticancer. The Anticancer Antibiotics are Bleomycin, Dactinomycin, Daunorubicin, Epirubicin, Plicamycin, Doxorubicin, Mitomycin. Antimicrotubules, mostly, they are naturally compounds which inhibit the microtubules which responsible for the cell division and proliferation of the cancer cell specifically as Colchicine, Vincristine, Vinblastine, hence the Antibiotic Anticancers and Antimicrotubules are important to know its importance in cancer treatment.
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Tiwari, Deepanshi, and Mamta Tiwari. "Vincristine: Beyond on anticancer treatment." International Journal of Pharmacognosy and Life Science 1, no. 2 (July 1, 2020): 38–43. http://dx.doi.org/10.33545/27072827.2020.v1.i2a.17.

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&NA;. "Timing of anticancer treatment crucial." Inpharma Weekly &NA;, no. 870 (January 1993): 4. http://dx.doi.org/10.2165/00128413-199308700-00004.

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Nozières, C., C. Damatte-Fauchery, and F. Borson-Chazot. "Thyroid effects and anticancer treatment." Annales d'Endocrinologie 72, no. 3 (June 2011): 198–202. http://dx.doi.org/10.1016/j.ando.2011.04.002.

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Pelicano, H., D. S. Martin, R.-H. Xu, and P. Huang. "Glycolysis inhibition for anticancer treatment." Oncogene 25, no. 34 (August 2006): 4633–46. http://dx.doi.org/10.1038/sj.onc.1209597.

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Dissertations / Theses on the topic "Anticancer treatment"

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DREUSSI, EVA. "Pharmacogenomics of miRNA for personalized anticancer treatment." Doctoral thesis, Università degli Studi di Trieste, 2016. http://hdl.handle.net/11368/2908099.

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Pharmacogenetics (PGx) aims at the definition of predictive and prognostic genetic biomarkers that can help clinicians in treatment tailoring. In this thesis, we explored two emerging topics in PGx: SNPs affecting the activity and maturation of a class of non coding RNAs, microRNAs (miRNAs), and immunogenetics. Genetic analyses were performed by a medium throughput technology, Veracode technology (Illumina). The clinical model of this study is represented by the locally advanced rectal cancer (LARC). Specifically, the main two aims of this study were: 1. the identification of predictive biomarkers of pathological response to neoadjuvant treatment in LARC patients, defined in terms of tumour regression grade (TRG); 2. the identification of biomarkers of disease free survival (DFS) and overall survival (OS) in LARC patients. To find an answer to these questions, we analyzed two panels of SNPs, selected according to bioinformatic analysis and literature data, on a group of 280 LARC patients homogeneously treated with fluoropyrimidines-based chemoradiotherapy in neo-adjuvant setting. In the first part of this project, we analyzed a panel of 144 SNPs potentially involved in miRNA maturation and activity. With a quite complex statistical strategy, we identified 5 new predictive biomarkers of response to neoadjuvant treatment. Specifically, DROSHA-rs10719 and SMAD3-rs17228212 were unfavourable predictive biomarkers (p=0.0274, p=0.0049), while SMAD3-rs744910, SMAD3-rs745103, and TRBP-rs6088619 showed an opposite effect (p=0.0153, p=0.0471, p=0.0125). Moreover, in patients with complete pathological response (TRG1), SMAD3-rs745103 was significantly associated with DFS (p=0.011). This study underlines the potential key role of SMAD3, factor involved not only in miRNA maturation but also in inflammation and in particular in TGFβ pathway, that is crucial in cancer progression and treatment response. Bearing in mind this interesting results and the huge amount of literature data addressing the high potentiality of immunogenetics in oncology, we analyzed a panel of 192 SNPs in genes involved in immune response in the same group of 280 LARC patients. We investigated another clinical end-point, the 2-year disease-free survival (2yDFS), because it is a strong prognostic biomarker of OS. Firstly, we identified 4 SNPs significantly associated with the 2yDFS. Two of them are located in IL17F (rs641701: OR=5.84, 95% CI=1.52-22.45, p=0.010; rs9463772: OR=3.56, 95% CI=1.22-10.35, p=0.020) and the other ones in STAT3 (rs8069645: OR=0.36, 95% CI=0.13-0.99, p=0.048; rs9867701: OR=3.00, 95% CI=1.09-8.30, p=0.034). Secondly, we studied the potential association of these 4 SNPs with the 10 years overall survival (OS). Interestingly, 3 SNPs remained significant and two of them are located in IL17F gene (IL17F-rs641701: OR=3.23, 95% CI=1.50-6.95, p=0.003; IL17F-rs9463772 OR=2.89, 95% CI=1.49-5.61, p=0.002, and STAT3-rs8069645 OR=0.50, 95% CI=0.25-0.98, p=0.044). We tested these associations in a validation group of 63 LARC patients who underwent radical surgery and adjuvant treatment based on fluoropyrimidines. Surprisingly, IL17F-rs9463772 is still significantly associated with OS (p=0.045), thus we can conclude that this is really a strong prognostic biomarker. To conclude, we performed 2 different PGx projects that led us to identify different predictive and prognostic biomarkers in LARC patients. These data, if confirmed in larger studies, will help clinicians to personalize patients treatment and management.
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Magri, Neal Francis. "Modified taxols as anticancer agents." Diss., Virginia Polytechnic Institute and State University, 1985. http://hdl.handle.net/10919/53892.

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Modifications of the potent anticancer agent taxol were carried out in order to gain an understanding of the chemical reactivity of the drug and the factors which contribute to its biological activity. The C-2' and/or the C-7 hydroxyl groups of taxol were substituted with acetyl, ßalanyl, silyl, succinyl, trichloroethyloxycarbonyl or carbonate linked dibenzylidene protected glucosyl groups. The C-7 position was selectively epimerized under free radical conditions and a 2'-epiacetyltaxol was produced via base catalysed epimerization. The C-2' amide became nucleophilic in the presence of base and could attack a C-2; acyl substituent. The C-13 ester side chain was selectively reduced by borohydride. The 7 position of taxol was selectively oxidized by Jones reagent and longer reaction times also oxidized the 2' position. The D rings of the 7 oxotaxols were readily opened via beta elimination; hydrogenation of the double bond in the enone of the D seco products produced a product in which the C ring was opened. The D ring was also susceptible to electrophilic attack. Reaction of taxol with triethyloxonium tetrafluoroborate or acetyl chloride/HC1 produced D seco taxols. C-7 deoxygenation was not achieved due to steric hindrance at C-7 and the instability of taxol under free radical conditions. Biological testing of modified taxols showed that substitution of the C-2' hydroxyl removed biological activity but that C-2' acyl groups were readily removed vivo. The water soluble 2'-βalanyItaxol possessed in vivo activity equal to that of taxol. Substitution of the C-7 hydroxyl did not inhibit the ability of a taxol derivative to polymerize tubulin but did decrease in vivo activity; epimerization of C-7 decreased in vivo activity slightly. A 2'-oxotaxol was found to be less active than, but still comparable to, its nonoxidized analogue. All taxol derivatives having a 7-oxo group and/or not possessing a D ring lost almost all biological activity.
Ph. D.
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Coldman, Andrew James. "The development of resistance to anticancer agents." Thesis, University of British Columbia, 1986. http://hdl.handle.net/2429/26975.

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The mechanism of resistance of tumor cells to chemotherapeutic agents is explored using probabilistic methods where it is assumed that resistant cells arise spontaneously with a defined frequency. The resistance process is embedded in a discrete time Markov branching process which models the growth of the tumor and contains three seperate cell types: stem, transitional and end cells. Using the asymptotic properties of such models it is shown that the proportion of each type of cell converge to constants almost surely. It is shown that the parameters relating to stem cell behaviour determine the asymptotic behaviour of the system. It is argued that for biologically likely parameter values, cure of the tumor will occur if, and only if, all stem cells are eliminated. A model is developed for the acquisition of resistance by stem cells to a single drug. Probability generating functions are derived which describe the behaviour of the process after an arbitrary sequence of drug treatments. The probability of cure, defined as the probability of ultimate extinction of the stem cell compartment, is characterised as the central quantity reflecting the success of therapeutic intervention. Expressions for this function are derived for a number of experimental situations. The effects of variation in the parameter values are examined. The model is extended to the case where two anticancer drugs are available and formulae for the probability of cure are developed. The problem of therapeutic scheduling is examined and under situations where drugs are of "equal" effectiveness, but may not be given together, it is shown that the mean number of tumor cells is minimised by sequential alternation of the drugs. The models are applied to data collected on the L1210 leukemia treated by the drugs Cyclophosphamide and Arabinosylcytosine. In both cases the analysis of the data provide evidence that resistant cells arise spontaneously with a frequency of approximately 10⁻⁷ per division. When applied to human breast cancer, the model indicates that neoadjuvant therapy is unlikely to greatly influence the likelihood that the patient will die from the growth of drug-resistant cells.
Science, Faculty of
Statistics, Department of
Graduate
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Fumagalli, G. "DRUG-CONJUGATES FOR SELF-ASSEMBLED NANOPARTICLES IN ANTICANCER TREATMENT." Doctoral thesis, Università degli Studi di Milano, 2018. http://hdl.handle.net/2434/542496.

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This dissertation is an overview on the functionalization of known anticancer compounds in order to form different drug-conjugates able to self-assemble in water to form nanoparticles. This approach is useful to improve the drug delivery properties and pharmacokinetic profile of anticancer drugs. All the described conjugates, except for the ones illustrated in chapter 5, have the same general structure: the anticancer drug is connected to the self-assembly inducer trough a linker. Chapter 1 regards a general introduction about nanomedicine, the advantages of the use of nanotechnology-based systems in cancer treatment and the benefits of nano- formulated drugs in the improvement of drug-delivery. Furthermore, nanoparticles are presented with a focus on their classification, characterization and preparation techniques. Chapter 2 regards the preparation of different types of self-assembled nanoparticles using various anticancer compounds and dyes but with the same lipophilic tail as self- assembling inducer: squalene. Different natural anticancer compounds such as paclitaxel, cyclopamine and doxorubicin and dyes, as fluorescein and tetramethylrhodamine, were functionalized to obtain squalene-based conjugates. Both hetero-nanoparticles composed by two drug-conjugates and drug- and dye-conjugates were prepared and tested. Chapter 3 is focused on the importance of the self-assembly inducer and describes the preparation of new conjugates containing an active moiety as self-assembly inducer. In particular, in this section, is described the preparation of conjugates composed by aloin or podophyllotoxin as active compounds and 4-(1,2-diphenylbut-1-en-1-yl) aniline, an analog of the know anticancer compound tamoxifen, as self-assembly inducer. Chapter 4 highlights the influence of the linker between the active compound and the self-assembly inducer to obtain an effective release of the free drug. In particular, it is described the synthesis of a new self-immolative linker able to trigger the drug release in particular conditions, specifically in the presence of a lipase. This linker was used for the preparation of two conjugates containing the known anticancer compound N- desacetylthiocolchicine. Chapter 5 concerns the preparation of dual drug-conjugates able to form nanoparticles without the presence of a self-assembly inducer. These conjugates have a symmetrical structure: two molecules of the same drug are linked by a chain able to guarantee the drug release in particular conditions. The natural anticancer compounds involved in the preparation of this type of conjugates are paclitaxel, epothilone A, podophyllotoxin and camptothecin and the linker used contain a disulfide moiety able to be cleaved in cellular environment.
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Zhang, Wen. "Identification of novel pyruvate dehydrogenase kinase 1 (PDK1) inhibitors for anticancer therapeutics." Thesis, University of Macau, 2018. http://umaclib3.umac.mo/record=b3953604.

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Cadorette, Veronica R. "Chemical investigation of Dicranum fulvum for anticancer activity." Thesis, Virginia Tech, 1989. http://hdl.handle.net/10919/44706.

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Biological screening of extracts of various bryophytes showed that the species Dicranum fulvum gave extracts with activity in both in vitro and in vivo bioassays. This plant was thus selected for extraction and fractionation, monitored by iin vitro bioassays.

Isolation was guided by a combination of bioassay and chemical methods, and led to the isolation of three compounds, betulin, 9,l9- cyclolanostâ 23â eneâ 3,25â diol, and B-sitosterol. Purification was achieved by open column, flash column, gel filtration, thin layer chromatography, the chromatotron and crystallization.

The isolated compounds were identified by comparisons of spectroscopic data with those of authentic samples and the matching of experimental and literature melting points and optical rotations.


Master of Science
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Soler, Vives Marta. "Peptide conjugates containing chlorambucil or tetradentate aminopyridine ligands for anticancer treatment." Doctoral thesis, Universitat de Girona, 2015. http://hdl.handle.net/10803/285974.

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Nowadays, the search for new drugs against cancer is one of the major goals to improve the quality of life of patients. The development of more selective treatments against cancer cells may lead to a significant reduction of the side-effects, being one of the most important topics in current research. In this regard, cell-penetrating peptides (CPPs) have been described to efficiently transport therapeutic molecules across the cell membrane. Furthermore, some metal complexes based on platinum (cisplatin and derivatives) are used in current chemotherapy. Despite their efficacy, these drugs display high toxicity. Thus, the design of novel complexes based on non-toxic metals (iron or manganese) is currently under way. These complexes could induce an irreversible oxidative stress through reactive oxygen species (ROS) at the subcellular level. Consequently, this might result in the alteration of the redox homeostasis and in cell death via apoptosis.The main objective of this thesis is the transport of iron or manganese complexes based on aminopyridine ligands into cancer cells through their conjugation to a non-toxic cell-penetrating peptide. Towards this aim, in one hand an undecapeptide (BP16) has been identified as a novel cell-penetrating peptide. On the other hand, it has been developed a straightforward synthetic methodology to conjugate the tetradentate aminopyridine ligands Me2PyTACN and (S,S’)-BPBP to peptide derivatives. Using this methodology, conjugates incorporating the aforementioned ligands and a tetrapeptide sequence have been prepared. These conjugates have been metallated with iron, manganese and other metals, and the resulting metallopeptides have been characterized and studied as DNA nucleases. Next, following the previous synthetic methodology, the Me2PyTACN and (S,S’)-BPBP ligands have been conjugated to the cell-penetrating peptide BP16 with the aim of being efficiently internalized into cancer cells. The resulting conjugates exhibit high cytotoxic activity similar to that observed by well-known anticancer drugs. Besides, BP16 displays high efficient drug delivery properties since it is able to enhance the uptake of the anticancer agent chlorambucil, improving its cytotoxicity against cancer cells between 6- to 10-fold. These high cytotoxic activities correlated with the high cellular uptake observed by the resulting conjugates, which it has been attributed to BP16. Based on the sum of these results, we have shown that BP16 is able to significantly enhance the cellular uptake of redox-active complexes and other well-known drugs. In brief, this study establishes that the synergy between the cytotoxic activity provided by metal complexes and their efficient transport into the cells could be useful to develop more selective therapies as well as novel anticancer treatments.
La recerca de nous fàrmacs per combatre el càncer representa un factor clau per millorar la qualitat de vida dels pacients. El desenvolupament de tractaments més selectius per les cèl•lules canceroses pot donar lloc a una reducció significativa dels efectes secundaris, essent aquest el tema principal de molts projectes de recerca. En aquest sentit, s’han descrit pèptids capaços de transportar els fàrmacs allà on es requereix que actuïn. Aquests pèptids es coneixen com a cell-penetrating peptides (CPPs). D’altra banda, en quimioteràpia s’utilitzen complexos metàl•lics basats en metalls com el platí (cisplatí i derivats). Tot i ser efectius, aquests fàrmacs presenten una elevada toxicitat, per la qual cosa s’està estudiant el disseny de complexos de metalls no tòxics, com el ferro o el manganès. Aquests complexos metàl•lics poden induir un estrès oxidatiu irreversible a nivell cel•lular gràcies a l’alta producció d’espècies reactives d’oxigen. En conseqüència, la pròpia alteració de l’homeòstasi redox de la cèl•lula pot causar la seva mort cel•lular per apoptosi.L’objectiu principal d’aquesta tesi doctoral és el transport de complexos de ferro o manganès basats en lligands de tipus aminopiridina dins les cèl•lules canceroses mitjançant la seva conjugació a un cell-penetrating peptide. Per assolir aquest objectiu, en primer lloc, s’ha identificat el pèptid d’onze aminoàcids BP16 com a cell-penetrating peptide. En segon lloc, s’ha desenvolupat una metodologia sintètica per a conjugar els lligands tetradentats de tipus aminopiridina Me2PyTACN i (S,S’)-BPBP a un derivat peptídic. Mitjançant aquesta metodologia s’han preparat conjugats incorporant aquests lligands i una seqüència de quatre aminoàcids. Aquests conjugats s’han metal•lat amb ferro, manganès i altres metalls, i els metal•lopèptids obtinguts s’han caracteritzat i estudiat com a nucleases de DNA. A continuació, seguint la metodologia sintètica anterior, els lligands Me2PyTACN i (S,S’)-BPBP s’han conjugat al cell-penetrating peptide BP16 amb l’objectiu de que siguin transportats dins les cèl•lules canceroses. Els conjugats resultants presenten activitat citotòxica elevada, comparable a la de fàrmacs anticancerígens utilitzats avui en dia. A més, paral•lelament, també s’ha comprovat que el pèptid BP16 és capaç de transportar de manera efectiva el fàrmac anticancerigen clorambucil, incrementant entre 6 i 10 vegades la seva activitat citotòxica enfront les cèl•lules canceroses. Aquestes altes activitats citotòxiques estan directament correlacionades amb una major internalització cel•lular dels conjugats resultants, proporcionada pel pèptid BP16. Així doncs, el pèptid BP16 permet millorar significativament la internalització cel•lular de complexos redox actius i d’altres fàrmacs. Amb caràcter general, aquest estudi estableix que la sinèrgia entre l’activitat citotòxica de complexos anticancerígens i el seu transport eficient a nivell cel•lular pot ser útil per desenvolupar teràpies més selectives i nous tractaments contra el càncer.
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Cozzi, Sarah-Jane. "Molecular targets of anticancer PKC activators in the treatment of melanoma /." [St. Lucia, Qld.], 2005. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe19185.pdf.

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Lewis, Andrew Martin. "The synthesis and biological evaluation of a novel anticancer small molecule." Thesis, University of Cambridge, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.607805.

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Cassim, Layla. "Melatonin and anticancer therapy interactions with 5-Fluorouracil." Thesis, Rhodes University, 2008. http://hdl.handle.net/10962/d1003224.

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On the basis of clinical studies, some researchers have advocated that the neurohormone and antioxidant melatonin, shown to possess intrinsic anticancer properties, be used as co-therapy in cancer patients being treated with the antineoplastic agent 5-fluorouracil, as increased patient survival times and enhanced quality of life have been observed. The focus of this research was thus to investigate the mechanisms of this seemingly beneficial drug interaction between 5-fluorouracil and melatonin. Metabolism studies were undertaken, in which it was established that there is no hepatic metabolic drug interaction between these agents by cytochrome P450, and that neither agent alters the activity of this enzyme system. Co-therapy with melatonin is thus unlikely to alter plasma levels of 5-fluorouracil by this mechanism. Novel mechanisms by which 5-fluorouracil is toxic were elucidated, such as the induction of lipid peroxidation, due to the formation of reactive oxygen species; decreases in brain serotonin, dopamine and norepinephrine levels, possibly leading to depression; hippocampal shrinkage and morphological alterations and lysis of hippocampal cells, which may underlie cognitive impairment; and a reduction in the nociceptive threshold when administered acutely. All these deleterious effects are attenuated by the co-administration of melatonin, suggesting that the agent exhibits antidepressive and analgesic properties, in addition to its known antioxidative and free radical-scavenging abilities. This suggests that melatonin cotherapy can significantly decrease 5-fluorouracil-induced toxicity, but this may also exert a protective effect on cancer cells and thus compromise the anticancer efficacy of 5-fluorouracil. It was, furthermore, found that stimulation of indoleamine 2,3-dioxygenase activity, mediated by increases in superoxide anion and interferon-γ levels, may underlie resistance to 5-fluorouracil therapy. Melatonin was shown to increase superoxide anion levels in vivo, and this is believed to be by conversion to the metabolite and known oxidant 6- hydroxymelatonin. This highlights that the possible deleterious effects of melatonin metabolites should be studied further. Serum corticosterone levels and cytokine profiles are unaltered by both 5-FU and melatonin, suggesting that these agents may be used by HIV infected individuals without promoting the progression to AIDS. It can thus be concluded that melatonin co-therapy is potentially useful in countering 5-fluorouracil toxicity.
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Books on the topic "Anticancer treatment"

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Chʻang, Min-i. Anticancer medicinal herbs. [Beijing, China]: Hunan Science and Technology Publishing House, 1992.

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Servan-Schreiber, David. Anticancer: A new way of life. New York: Viking, 2009.

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Convention, United States Pharmacopeial. Fact sheets on anticancer drugs. [Washington, D.C.?]: National Cancer Institute [distributor], 1994.

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Servan-Schreiber, David. Anticancer: A new way of life. New York: Viking, 2010.

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Servan-Schreiber, David. Anticancer: A new way of life. New York: Viking, 2009.

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Servan-Schreiber, David. Anticancer: A new way of life. New York: Viking, 2009.

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Link, Wolfgang. Principles of Cancer Treatment and Anticancer Drug Development. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-18722-4.

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Cho, William C. S. Evidence-based Anticancer Materia Medica. Dordrecht: Springer Science+Business Media B.V., 2011.

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Stephen, Neidle, and Waring Michael J, eds. Molecular aspects of anticancer drug-DNA interactions. Basingstoke: Macmillan, 1993.

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Parfenov, E. A. Biometals and ligands for anticancer drug design. Commack, N.Y: Nova Science Publishers, 1998.

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Book chapters on the topic "Anticancer treatment"

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Zimmermann, Jürg, Pascal Furet, and Elisabeth Buchdunger. "STI571: A New Treatment Modality for CML?" In Anticancer Agents, 245–59. Washington, DC: American Chemical Society, 2001. http://dx.doi.org/10.1021/bk-2001-0796.ch015.

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Koul, Bhupendra. "Plants with Anticancer Potential." In Herbs for Cancer Treatment, 193–1174. Singapore: Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-32-9147-8_4.

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Baxter, Andy, and John Montana. "The Discovery and Development of Second-Generation Matrix Metalloproteinase Inhibitors for the Treatment of Cancer." In Anticancer Agents, 260–81. Washington, DC: American Chemical Society, 2001. http://dx.doi.org/10.1021/bk-2001-0796.ch016.

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Wani, Mohmmad Younus, and Manzoor Ahmad Malik. "Treatment Modalities." In Gold and its Complexes in Anticancer Chemotherapy, 17–34. Singapore: Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-33-6314-4_3.

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Ciner, Aaron T., Richard J. Gralla, Kostas N. Syrigos, and Sam H. Ahmedzai. "Pulmonary Toxicities of Anticancer Treatment." In The MASCC Textbook of Cancer Supportive Care and Survivorship, 201–15. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-90990-5_13.

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Schabel, F. M. "Rationale for Perioperative Anticancer Treatment." In Perioperative Chemotherapy, 1–10. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-82432-6_1.

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Weekes, Colin D., and Manuel Hidalgo. "Targeted Therapeutics in Cancer Treatment." In Principles of Anticancer Drug Development, 403–61. New York, NY: Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-7358-0_15.

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Powis, G. "Liver Disease and Anticancer Drug Treatment." In Drugs and the Liver: High Risk Patients and Transplantation, 99–104. Dordrecht: Springer Netherlands, 1993. http://dx.doi.org/10.1007/978-94-011-1994-8_16.

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Feng, Tao, and Yanli Zhao. "Clinical Anticancer Drugs for Cancer Treatment." In Nanomaterial-Based Drug Delivery Carriers for Cancer Therapy, 7–13. Singapore: Springer Singapore, 2016. http://dx.doi.org/10.1007/978-981-10-3299-8_2.

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Mravec, Boris. "Influencing Late Effects of Anticancer Treatment." In Neurobiology of Cancer, 693–94. Cham: Springer Nature Switzerland, 2024. http://dx.doi.org/10.1007/978-3-031-68590-3_56.

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Conference papers on the topic "Anticancer treatment"

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Cherdyntseva, N., N. Litviakov, F. Ivanova, E. Denisov, P. Gervas, and E. Cherdyntsev. "The molecular aspects of personalized anticancer treatment." In PHYSICS OF CANCER: INTERDISCIPLINARY PROBLEMS AND CLINICAL APPLICATIONS (PC’16): Proceedings of the International Conference on Physics of Cancer: Interdisciplinary Problems and Clinical Applications 2016. Author(s), 2016. http://dx.doi.org/10.1063/1.4960229.

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"PAMAM Dendrimers as anti-HER2 Positive Breast Cancer Treatment." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0176.

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Background: Poly (amidoamine) dendrimers (PAMAMs) are widely used in drug delivery systems and gene transfection as drug carriers. They also exert several biological effects like modulating gene expression, particularly EGFR (ErbB1) signaling pathway, which raises the question of whether these polymers can also inhibit the phosphorylation of HER2 (ErbB2) in breast cancer. However, this area hasn’t been investigated before. Methods: In this study, we evaluated the anticancer effects of different generations and surface chemistries of PAMAMs on HER2 positive breast cancer cells (SkBr3 and ZR-75 cell lines). Cell viability and morphological changes were evaluated upon treatment with PAMAMs. In addition, their effect on colony formation in soft agar was assessed. Additionally, western blot was performed to understand the underlying mechanisms of action. Results: PAMAMs anticancer effects were found to follow a specific trend, as they were more significant in cationic polymers and in higher generations. Cationic PAMAMs reduced cell viability of HER2 positive breast cancer cells up to 5.1% in SkBr3 and to 28% in ZR75 (p<0.001), in a dose and time-dependent manner. Cationic polymers also resulted in changing the morphology in the examined cell lines, as well as inhibiting colony formation in soft agar compared to controls (p<0.001). The mechanism of action was found to be mediated by inhibiting the phosphorylation of erbB2 and JNK1/2/3. Conclusion: These anticancer effects of PAMAM dendrimers make them promising molecules, which can add benefit to current anti-HER2 treatments and be employed successfully in different biomedical applications.
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Eka Putra, Gusti Ngurah Putu, Leaf Huang, and Yih-Chih Hsu. "Cisplatin encapsulated nanoparticle as a therapeutic agent for anticancer treatment." In SPIE BiOS, edited by Wei R. Chen. SPIE, 2016. http://dx.doi.org/10.1117/12.2214695.

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Rahman, N. A. A., M. N. Adon, and Abdul M. M. Jamil. "The Impact of Pulse Electric Field Treatment and Selected Bioactive Compound Extract toward Anticancer Treatment." In 2018 9th IEEE Control and System Graduate Research Colloquium (ICSGRC). IEEE, 2018. http://dx.doi.org/10.1109/icsgrc.2018.8657599.

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Nita, E., M. Nekulova, M. Gomez, T. Hupp, and K. Ball. "PO-170 Dissecting the role of IFITM1 in response to anticancer treatment." In Abstracts of the 25th Biennial Congress of the European Association for Cancer Research, Amsterdam, The Netherlands, 30 June – 3 July 2018. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/esmoopen-2018-eacr25.692.

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Quidville, Virginie, Samar Alsafadi, Aïcha Goubar, Catherine Durieu, Sonia Baconnais, Eric LeCam, Philippe Dessen, Stephan Vagner, and Fabrice Andre. "Abstract 1623: The spliceosome as a new therapeutic target for anticancer treatment." 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.am2011-1623.

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Fernandez, Eric, Jianxiong Pang, Chris Snell, Cathy Derow, Frances Brightman, Christophe Chassagnole, and Robert Jackson. "Abstract 5147: drugCARD: a database of anticancer treatment regimens and drug combinations." 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.am2013-5147.

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Ma, Liang, Jeremy Barker, Changchun Zhou, Biaoyang Lin, and Wei Li. "A Perfused Two-Chamber System for Anticancer Drug Screening." In ASME 2010 International Manufacturing Science and Engineering Conference. ASMEDC, 2010. http://dx.doi.org/10.1115/msec2010-34326.

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A cell culture microfluidic device has been developed to test the cytotoxicity of anticancer drugs while reproducing multi-organ interactions in vitro. Cells were cultured in separate chambers representing the liver and tumor. The two chambers were connected through a channel to mimick the blood flow. Glioblastoma (GBM) cancer cells (M059K) and hepatoma cells (HepG2) were cultured in the tumor and the liver chambers, respectively. The cytotoxic effect of cancer treatment drug Temolozomide (TMZ) was tested using this two chamber system. The experimental results showed that with the liver cells, the cancer cells showed much higher viability than those without the liver cells. This indicates that the liver metabolism has strong effect on the toxicity of the anticancer drug. The results demonstrated that the perfused two chamber cell culture system has the potential to be used as a platform for drug screening in a more physiologically realistic environment.
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Ahmed, Elham, Abdul Khan, Kirti S. Prabhu, Kodappully Siveen, Zafar Nawaz, Hatem Zayed, and Shahab Uddin. "Sanguinarine Mediated Anti-Tumor activity Via Targeting JAK/STAT3 Pathway in Thyroid Cancer." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0155.

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Sanguinarine (SNG), a natural compound with an array of pharmacological activities, has promising therapeutic potential against a number of pathological conditions, including malignancies. This research aimed to investigate the antiproliferative and anti-cancer potential of SNG against two well characterized papillary thyroid cancer (PTC) cell lines, BCPAP and TPC-1 .In both cell lines , SNG was able to inhibit cell proliferation in time and dose dependent manner. Western blot analysis revealed increased expression of apoptosis and autophagy markers , caspase-3,cleaved caspase-3 , P62, and LC3. SNG modulate its anticancer effect through ROS production, because NAC was able to reverse SNG effect. Interestingly, co-treatment of PTC with SNG and cisplatin amplified anticancer activity. Finally, SNG treatment of PTC spheroid suppressed its growth with downregulation of stemness markers including ALDH2 and SOX2 markers. In conclusion, SNG enhanced the anti cancer activity against PTC cells and the effect is amplified when cisplatin is added.
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Theofilos, Dimitrios, Charalampos Marketos, Danai Bisirtzoglou, Athanasios Zetos, Antigoni Sakelaropoulou, and George Politis. "Is surgical treatment a motivator factor for smoking cessation? Experience in an anticancer hospital." In Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.pa1205.

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Reports on the topic "Anticancer treatment"

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Feltmate, Colleen. Application of Nanotechnology in the Targeted Release of Anticancer Drugs in Ovarian Cancer Treatment. Fort Belvoir, VA: Defense Technical Information Center, December 2007. http://dx.doi.org/10.21236/ada486569.

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Feltmate, Colleen. Application of Nanotechnology in the Targeted Release of Anticancer Drugs in Ovarian Cancer Treatment. Fort Belvoir, VA: Defense Technical Information Center, December 2006. http://dx.doi.org/10.21236/ada481424.

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Venedicto, Melissa, and Cheng-Yu Lai. Facilitated Release of Doxorubicin from Biodegradable Mesoporous Silica Nanoparticles. Florida International University, October 2021. http://dx.doi.org/10.25148/mmeurs.009774.

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Cervical cancer is one of the most common causes of cancer death for women in the United States. The current treatment with chemotherapy drugs has significant side effects and may cause harm to healthy cells rather than cancer cells. In order to combat the potential side effects, nanoparticles composed of mesoporous silica were created to house the chemotherapy drug doxorubicin (DOX). The silica network contains the drug, and a pH study was conducted to determine the conditions for the nanoparticle to disperse the drug. The introduction of disulfide bonds within the nanoparticle created a framework to efficiently release 97% of DOX in acidic environments and 40% release in neutral environments. The denotation of acidic versus neutral environments was important as cancer cells are typically acidic. The chemistry was proved with the incubation of the loaded nanoparticle into HeLa cells for a cytotoxicity report and confocal imaging. The use of the framework for the anticancer drug was shown to be effective for the killing of cancerous cells.
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Chen, Xiaole, Peng Wang, Yunquan Luo, Yi-Yu Lu, Wenjun Zhou, Mengdie Yang, Jian Chen, Zhi-Qiang Meng, and Shi-Bing Su. Therapeutic Efficacy Evaluation and Underlying Mechanisms Prediction of Jianpi Liqi Decoction for Hepatocellular Carcinoma. Science Repository, September 2021. http://dx.doi.org/10.31487/j.jso.2021.02.04.sup.

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Objective: The aim of this study was to assess the therapeutic effects of Jianpi Liqi decoction (JPLQD) in hepatocellular carcinoma (HCC) and explore its underlying mechanisms. Methods: The characteristics and outcomes of HCC patients with intermediate stage B who underwent sequential conventional transcatheter arterial chemoembolization (cTACE) and radiofrequency ablation (RFA) only or in conjunction with JPLQD were analysed retrospectively. The plasma proteins were screened using label-free quantitative proteomics analysis. The effective mechanisms of JPLQD were predicted through network pharmacology approach and partially verified by ELISA. Results: Clinical research demonstrated that the Karnofsky Performance Status (KPS), traditional Chinese medicine (TCM) syndrome scores, neutropenia and bilirubin, median progression-free survival (PFS), and median overall survival (OS) in HCC patients treated with JPLQD were superior to those in patients not treated with JPLQD (all P<0.05). The analysis of network pharmacology, combined with proteomics, suggested that 52 compounds targeted 80 potential targets, which were involved in the regulation of multiple signaling pathways, especially affecting the apoptosis-related pathways including TNF, p53, PI3K-AKT, and MAPK. Plasma IGFBP3 and CA2 were significantly up-regulated in HCC patients with sequential cTACE and RFA therapy treated with JPLQD than those in patients not treated with JPLQD (P<0.001). The AUC of the IGFBP3 and CA2 panel, estimated using ROC analysis for JPLQD efficacy evaluation, was 0.867. Conclusion: These data suggested that JPLQD improves the quality of life, prolongs the overall survival, protects liver function in HCC patients, and exhibits an anticancer activity against HCC. IGFBP3 and CA2 panels may be potential therapeutic targets and indicators in the efficacy evaluation for JPLQD treatment, and the effective mechanisms involved in the regulation of multiple signaling pathways, possibly affected the regulation of apoptosis.
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