Relevant bibliographies by topics / Antitumour

Contents

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

Academic literature on the topic 'Antitumour'

Author: Grafiati
Published: 4 June 2021
Last updated: 20 February 2023

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Journal articles on the topic "Antitumour"

1

Asche, C. "Antitumour Quinones." Mini-Reviews in Medicinal Chemistry 5, no. 5 (May 1, 2005): 449–67. http://dx.doi.org/10.2174/1389557053765556.

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Demeunynck, Martine. "Antitumour acridines." Expert Opinion on Therapeutic Patents 14, no. 1 (January 2004): 55–70. http://dx.doi.org/10.1517/13543776.14.1.55.

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Slack, J. A., and C. Goddard. "Antitumour imidazotetrazines." Journal of Chromatography B: Biomedical Sciences and Applications 337 (January 1985): 178–81. http://dx.doi.org/10.1016/0378-4347(85)80027-x.

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Sreco-Zelenovic, Bojana, Sanja Grabez, Mirjana Popsavin, Vesna Kojic, Jovana Francuz, and Velimir Popsavin. "Synthesis and antiproliferative activity of simplified goniofufurone analogues." Journal of the Serbian Chemical Society, no. 00 (2020): 56. http://dx.doi.org/10.2298/jsc200730056s.

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Several (+)-goniofufurone analogues with simplified structures were designed, synthesized and evaluated for their in vitro antitumour activity against a panel of human tumour cell lines. Dephenylated compounds 2 and 3, demonstrated remarkable antitumour activities, in the cultures of K562 and Raji cells with IC50 values in the range of 3.0-9.3 nM. Each of goniofufurone analogues lacking the tetrahydrofuran ring (4, 5 and 6) strongly inhibited the growth of at least one malignant cell line, with IC50 values in the range of 11-30 nM. Brief SAR analysis showed that the simplified goniofufurone analogues, designed by removing the phenyl group from C-7, or by opening the THF ring, could show stronger antiproliferative effects compared to control molecules. It is noticeable that analogues 2-8 are completely inactive with respect to the normal MRC-5 cell line. These findings, together with their potent antitumor activities, provide a suitable basis for the development of new and selective antitumour drugs.
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Jones, Bryony. "Evading antitumour immunity." Nature Reviews Cancer 16, no. 7 (June 17, 2016): 410. http://dx.doi.org/10.1038/nrc.2016.65.

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Jones, Bryony. "Evading antitumour immunity." Nature Reviews Genetics 17, no. 7 (June 6, 2016): 374. http://dx.doi.org/10.1038/nrg.2016.77.

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Mitra, Roshni, Sarvjeet Singh, and Ashok Khar. "Antitumour immune responses." Expert Reviews in Molecular Medicine 5, no. 3 (January 13, 2003): 1–22. http://dx.doi.org/10.1017/s1462399403005623.

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The role of the immune system in combating tumour progression has been studied extensively. The two branches of the immune response – humoral and cell-mediated – act both independently and in concert to combat tumour progression, the success of which depends on the immunogenicity of the tumour cells. The immune system discriminates between transformed cells and normal cells by virtue of the presence of unique antigens on tumour cells. Despite this, the immune system is not always able to detect and kill cancerous cells because neoplasms have also evolved various strategies to escape immune surveillance. Attempts are being made to trigger the immune system into an early and efficient response against malignant cells, and various therapeutic modalities are being developed to enhance the strength of the immune response against tumours. This review aims to elucidate the tumouricidal role of various components of the immune system, including macrophages, lymphocytes, dendritic cells and complement.
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Westwell, Andrew D. "Novel antitumour molecules." Drug Discovery Today 8, no. 1 (January 2003): 47–50. http://dx.doi.org/10.1016/s1359-6446(02)02551-5.

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Westwell, Andrew D. "Novel antitumour molecules." Drug Discovery Today 8, no. 5 (March 2003): 229–31. http://dx.doi.org/10.1016/s1359-6446(03)02622-9.

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Westwell, A. "Novel antitumour molecules." Drug Discovery Today 8, no. 9 (May 1, 2003): 421–22. http://dx.doi.org/10.1016/s1359-6446(03)02676-x.

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Dissertations / Theses on the topic "Antitumour"

1

Mokdsi, George. "Antitumour Metallocenes." Thesis, The University of Sydney, 2000. http://hdl.handle.net/2123/794.

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This thesis reports a study of the chemical stability and coordination chemistry of several antitumour metallocenes Cp2MCl2 (Cp = h5-C5H5; M = Ti 1, V 2, Nb 3, Mo 4), as well as derivatives of Cp2TiCl2 1, with nucleic acids, nucleic acid constituents and proteins. These studies were carried out in order to identify the biologically active species and more fully understand the molecular level mechanism of action of the antitumour metallocenes, in particular Cp2TiCl2 1, which is currently undergoing phase II clinical trials. The interactions of Cp2MoCl2 4 with four oligonucleotides were studied by 1H and 31P NMR spectroscopy. In 50 mM salt solutions of Cp2MoCl2 4, hydrolysis of the halide ligands occurred to give a solution with pD -2, containing a species in which both Cp rings remain metal bound for 24 h. At pD -7, partial hydrolysis of the Cp rings (-30percent) occurred after 24 h. Addition of an aqueous solution of Cp2MoCl2 4 in 50 mM salt to the self-complementary sequence d(CGCATATGCG)2, maintaining the pD at 6.0-7.0, showed no evidence for the formation of a metallocene-oligonucleotide complex and only peaks arising from hydrolysis of Cp2MoCl2 4 were detected. A similar result was obtained in titration experiments with the single stranded sequence d(ATGGTA) at pD 6.5-7.0. However, at pD 3.0, new signals assigned to a molybdocene-oligonucleotide complex(es), which was stable for hours at pD 3.0, were detected; while at pD -7 the complex is destabilised and only peaks arising from hydrolysis of Cp2MoCl2 4 were detected. Titration experiments at low pD with Cp2MoCl2 4 and the dinucleotide dCG were consistent with formation of a complex arising due to coordination of molybdenum to guanine N7 and/or cytosine N3. The results obtained showed that stable oligonucleotide adducts were not formed in 50 mM salt at pD -7 and hence it is highly unlikely that formation of molybdocene-DNA adducts in vivo is the primary action that is responsible for the antitumour properties of Cp2MoCl2 4. The rate of hydrolysis of the aromatic rings of Cp2TiX2 (X equals Cl 1, OCOCH2NH3Cl 27) and the dimethylsubstituted derivatives (MeCp)2TiX2 (X equals Cl 34, OCOCH2NH3Cl 41), in aqueous solutions at pD 2-8 was studied by 1H NMR spectroscopy. Rapid hydrolysis of both the halide/glycine and Cp ligands in Cp2TiX2 (X equals Cl 1, OCOCH2NH3Cl 27) occurred and predominantly gave a precipitate at pD -7. In contrast, under the same experimental conditions, the predominant species present in aqueous solutions of (MeCp)2TiX2 (X equals Cl 34, OCOCH2NH3Cl 41) at pH 2-8 contained both MeCp rings metal bound. At pD < 5, Cp2TiX2 (X equals Cl 1, OCOCH2NH3Cl 27) and (MeCp)2TiX2 (X equals Cl 34, OCOCH2NH3Cl 41) formed similar complex(es) with purine nucleotides. However, at pD >5, stable adducts between nucleotides and Cp2TiX2 (X equals Cl 1, OCOCH2NH3Cl 27) were not formed. In contrast, (MeCp)2TiX2 (X equals Cl 34, OCOCH2NH3Cl 41) formed complex(es) with 5'-dAMP or 5'-dGMP, which were stable for 24 h. These results suggest that formation of stable chelates between (MeCp)2TiX2 (X equals Cl 34, OCOCH2NH3Cl 41) and nucleic acid constituents in vivo is possible. However, the methyl substituted derivatives 34 and 41 did not show any antitumour activity against EAT in mice when administered in either 10percentDMSO/90percentsaline or in water at pH 6.2-6.4, which suggests that the labile Cp-Ti bond present in Cp2TiCl2 1 is required for antitumour activity. The synthesis of a range of Cp substituted titanocene derivatives was investigated in an attempt to prepare derivatives with modified Cp stability in comparison to the methyl substituted derivatives. The synthesis of derivatives (CpCH2Y)2TiCl2 where Y equals ?CHO 43, ?CONMe2 44, ?NO2 45, (RCp)2TiCl2 where R equals ?COMe 46, ?COOMe 47 or ?CONMe2 48, (CpNMe2)2TiCl2 62 and (Cp(CH2)2NMe2)2TiCl2 63 was unsuccessful, due to the presence of coordinating substituents on the Cp rings and poor stability in polar, protic solvents. Hence, these derivatives were excluded from further studies. The rate of hydrolysis of the Cp rings of Cp2TiX2 (X equals Cl 1, OCOCCl3 22 and OCOCH2NH3Cl 27) in aqueous solutions, 10percentDMSO/90percentD2O and 100percent DMSO was monitored by 1H NMR spectroscopy. Rapid hydrolysis of both the carboxylate and Cp ligands of Cp2TiX2 (OCOCCl3 22 and OCOCH2NH3Cl 27) occurred in DMSO to give biologically inactive species. The rate of these reactions were concentration dependent as dilution of these samples with saline or water to give the therapeutic conditions of 10percentDMSO/90percentD2O slowed the hydrolysis chemistry. In contrast, samples of Cp2TiX2 (X equals Cl 1 and OCOCH2NH3Cl 27) dissolved in water, gave solutions containing the presumed antitumour active species in which the halide or glycine ligands have been hydrolysed but the Cp rings remain metal bound. Thus, charged X ligands may be incorporated into Cp2TiX2 and will give comparable activity to Cp2TiCl2 1 provided the samples are administered in water. The antitumour metallocenes Cp2MCl2 (M equals Ti 1, V 2, Nb 3, Mo 4) and the inactive derivative (MeCp)2TiCl2 34 were found to inhibit the relaxation of supercoiled plasmid DNA pBR322 by human topoisomerase II in vitro. These results implicated the inhibition of topoisomerase II in the mechanism of antitumour activity although there was no direct correlation between the in vitro results with biological activity against EAT in vivo. UV spectroscopy confirmed that the metallocenes Cp2MCl2 (M equals Ti 1, Mo 4) became associated with and were stabilised to hydrolysis by calf thymus DNA but not with human serum albumin. ICP-AES was used to measure the amount of metal associated with either DNA or human serum albumin after incubation with Cp2MCl2 (M equals Ti 1, Nb 3, Mo 4) and dialysis of these solution. The results confirmed that DNA stabilises or becomes associated with the metallocenes. However, errors associated with the ICP-AES measurements did not allow these results to be quantified. 1H NMR spectroscopy was used to show that the antitumour metallocene Cp2MoCl2 4 formed an adduct with glutathione 72 in the pH range 3-7 through the sulfur donor group. In comparison, the antitumour metallocenes Cp2MCl2 (M equals Ti 1, Nb 3) showed limited adduct formation with glutathione 72 at pH -3 and no adducts were detected at pH > 5.5.
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2

Mokdsi, George. "Antitumour Metallocenes." University of Sydney. Chemistry, 2000. http://hdl.handle.net/2123/794.

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This thesis reports a study of the chemical stability and coordination chemistry of several antitumour metallocenes Cp2MCl2 (Cp = h5-C5H5; M = Ti 1, V 2, Nb 3, Mo 4), as well as derivatives of Cp2TiCl2 1, with nucleic acids, nucleic acid constituents and proteins. These studies were carried out in order to identify the biologically active species and more fully understand the molecular level mechanism of action of the antitumour metallocenes, in particular Cp2TiCl2 1, which is currently undergoing phase II clinical trials. The interactions of Cp2MoCl2 4 with four oligonucleotides were studied by 1H and 31P NMR spectroscopy. In 50 mM salt solutions of Cp2MoCl2 4, hydrolysis of the halide ligands occurred to give a solution with pD -2, containing a species in which both Cp rings remain metal bound for 24 h. At pD -7, partial hydrolysis of the Cp rings (-30percent) occurred after 24 h. Addition of an aqueous solution of Cp2MoCl2 4 in 50 mM salt to the self-complementary sequence d(CGCATATGCG)2, maintaining the pD at 6.0-7.0, showed no evidence for the formation of a metallocene-oligonucleotide complex and only peaks arising from hydrolysis of Cp2MoCl2 4 were detected. A similar result was obtained in titration experiments with the single stranded sequence d(ATGGTA) at pD 6.5-7.0. However, at pD 3.0, new signals assigned to a molybdocene-oligonucleotide complex(es), which was stable for hours at pD 3.0, were detected; while at pD -7 the complex is destabilised and only peaks arising from hydrolysis of Cp2MoCl2 4 were detected. Titration experiments at low pD with Cp2MoCl2 4 and the dinucleotide dCG were consistent with formation of a complex arising due to coordination of molybdenum to guanine N7 and/or cytosine N3. The results obtained showed that stable oligonucleotide adducts were not formed in 50 mM salt at pD -7 and hence it is highly unlikely that formation of molybdocene-DNA adducts in vivo is the primary action that is responsible for the antitumour properties of Cp2MoCl2 4. The rate of hydrolysis of the aromatic rings of Cp2TiX2 (X equals Cl 1, OCOCH2NH3Cl 27) and the dimethylsubstituted derivatives (MeCp)2TiX2 (X equals Cl 34, OCOCH2NH3Cl 41), in aqueous solutions at pD 2-8 was studied by 1H NMR spectroscopy. Rapid hydrolysis of both the halide/glycine and Cp ligands in Cp2TiX2 (X equals Cl 1, OCOCH2NH3Cl 27) occurred and predominantly gave a precipitate at pD -7. In contrast, under the same experimental conditions, the predominant species present in aqueous solutions of (MeCp)2TiX2 (X equals Cl 34, OCOCH2NH3Cl 41) at pH 2-8 contained both MeCp rings metal bound. At pD < 5, Cp2TiX2 (X equals Cl 1, OCOCH2NH3Cl 27) and (MeCp)2TiX2 (X equals Cl 34, OCOCH2NH3Cl 41) formed similar complex(es) with purine nucleotides. However, at pD >5, stable adducts between nucleotides and Cp2TiX2 (X equals Cl 1, OCOCH2NH3Cl 27) were not formed. In contrast, (MeCp)2TiX2 (X equals Cl 34, OCOCH2NH3Cl 41) formed complex(es) with 5'-dAMP or 5'-dGMP, which were stable for 24 h. These results suggest that formation of stable chelates between (MeCp)2TiX2 (X equals Cl 34, OCOCH2NH3Cl 41) and nucleic acid constituents in vivo is possible. However, the methyl substituted derivatives 34 and 41 did not show any antitumour activity against EAT in mice when administered in either 10percentDMSO/90percentsaline or in water at pH 6.2-6.4, which suggests that the labile Cp-Ti bond present in Cp2TiCl2 1 is required for antitumour activity. The synthesis of a range of Cp substituted titanocene derivatives was investigated in an attempt to prepare derivatives with modified Cp stability in comparison to the methyl substituted derivatives. The synthesis of derivatives (CpCH2Y)2TiCl2 where Y equals ?CHO 43, ?CONMe2 44, ?NO2 45, (RCp)2TiCl2 where R equals ?COMe 46, ?COOMe 47 or ?CONMe2 48, (CpNMe2)2TiCl2 62 and (Cp(CH2)2NMe2)2TiCl2 63 was unsuccessful, due to the presence of coordinating substituents on the Cp rings and poor stability in polar, protic solvents. Hence, these derivatives were excluded from further studies. The rate of hydrolysis of the Cp rings of Cp2TiX2 (X equals Cl 1, OCOCCl3 22 and OCOCH2NH3Cl 27) in aqueous solutions, 10percentDMSO/90percentD2O and 100percent DMSO was monitored by 1H NMR spectroscopy. Rapid hydrolysis of both the carboxylate and Cp ligands of Cp2TiX2 (OCOCCl3 22 and OCOCH2NH3Cl 27) occurred in DMSO to give biologically inactive species. The rate of these reactions were concentration dependent as dilution of these samples with saline or water to give the therapeutic conditions of 10percentDMSO/90percentD2O slowed the hydrolysis chemistry. In contrast, samples of Cp2TiX2 (X equals Cl 1 and OCOCH2NH3Cl 27) dissolved in water, gave solutions containing the presumed antitumour active species in which the halide or glycine ligands have been hydrolysed but the Cp rings remain metal bound. Thus, charged X ligands may be incorporated into Cp2TiX2 and will give comparable activity to Cp2TiCl2 1 provided the samples are administered in water. The antitumour metallocenes Cp2MCl2 (M equals Ti 1, V 2, Nb 3, Mo 4) and the inactive derivative (MeCp)2TiCl2 34 were found to inhibit the relaxation of supercoiled plasmid DNA pBR322 by human topoisomerase II in vitro. These results implicated the inhibition of topoisomerase II in the mechanism of antitumour activity although there was no direct correlation between the in vitro results with biological activity against EAT in vivo. UV spectroscopy confirmed that the metallocenes Cp2MCl2 (M equals Ti 1, Mo 4) became associated with and were stabilised to hydrolysis by calf thymus DNA but not with human serum albumin. ICP-AES was used to measure the amount of metal associated with either DNA or human serum albumin after incubation with Cp2MCl2 (M equals Ti 1, Nb 3, Mo 4) and dialysis of these solution. The results confirmed that DNA stabilises or becomes associated with the metallocenes. However, errors associated with the ICP-AES measurements did not allow these results to be quantified. 1H NMR spectroscopy was used to show that the antitumour metallocene Cp2MoCl2 4 formed an adduct with glutathione 72 in the pH range 3-7 through the sulfur donor group. In comparison, the antitumour metallocenes Cp2MCl2 (M equals Ti 1, Nb 3) showed limited adduct formation with glutathione 72 at pH -3 and no adducts were detected at pH > 5.5.
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Gate, Ernest N. "Investigations on new antitumour agents." Thesis, Aston University, 1985. http://publications.aston.ac.uk/12512/.

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Skelton, Lorraine Ann. "Pyridyl quinazolines as potential antitumour agents." Thesis, Institute of Cancer Research (University Of London), 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.294789.

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Shi, Dong-Fang. "The medicinal chemistry of antitumour benzazoles." Thesis, University of Nottingham, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.283645.

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Langnel, David Antoine Fernand. "New synthetic routes to antitumour imidazotetrazines." Thesis, University of Nottingham, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.311742.

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Shahbakhti, Hassan. "Structure/activity relationships of antitumour diazridinylquinones." Thesis, University of Salford, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.308289.

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Ayuko, Washington O. "Free radicals as potential antitumour agents." Thesis, Aston University, 1991. http://publications.aston.ac.uk/12521/.

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The aim of this work was to use extremely low concentrations of free radical generating compounds as a 'catalyst' to trigger endogenous free radical chain reactions in the host and to selectively eliminate neoplastic cells in the host. To test the hypothesis, a number of free radical generating compounds were screened on several malignant cell lines in vitro to select model compounds that were used against tumour models in vivo. 2,2-Diphenyl-1-picrylhydrazyl (DPPH) and its derivatives were selected at the model compounds for in vivo experiments in view of their high cytotoxic potency against several malignant cell lines in vitro. The water soluble derivative, 2,2-diphcnyl-l-(2', 4'-dinitro-6'-sulphophenyl) hydrazyl (DDSH) given by subcutaneous injections demonstrated significant antitumour activities against the MAC 16 murine colon adcnocarcinoma implanted subcuta-ncously in male NMRI mice at nanomolar concentration range. 40-60% of long term survival of over 60 days was achieved (compared with control survival of 20 days) with total tumour elimination. This compound was also active against both P388 leukaemia in male BDF1 mice and TLX5 lymphoid tumour in male CBA/CA mice at a similar concentration range. However, some of these animals died suddenly after treatment with no evidence of disease present at post mortem. The cause of death was unknown but thought to be related to the treatment. There was significant increase in scrum level of malondialdchydc (MDA) following treatment, but did not correlate to the antitumour activities of these compounds. Induction of supcroxide dismutasc (SOD), and glutathione peroxidase (GPx) occurred around day 8 after the administration of DDSH. Histological sections of MAC16 tumours showed areas of extensive massive hacmorrhagic necrosis and vascular collapse associated with perivas-cular cell death following the administration of nanomolar concentration of DDSH which was probably compatible with the effects of free radicals. It was concluded that the antitumour activities of these compounds may be related to free radical and cytokinc production.
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Horspool, Keith R. "Structure-activity studies on antitumour imidazotetrazinones." Thesis, Aston University, 1988. http://publications.aston.ac.uk/12550/.

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Rafferty, Karen. "Novel organometallic compounds as potential antitumour agents." Thesis, University of Leeds, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.487773.

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Books on the topic "Antitumour"

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1938-, Gielen M., ed. Tin-based antitumour drugs. Berlin: Springer-Verlag, 1990.

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Gielen, M., ed. Tin-Based Antitumour Drugs. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-74191-3.

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V, Wilman Derry E., ed. The chemistry of antitumour agents. London: Blackie, 1990.

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Gate, Ernest Nicholas. Investigations on new antitumour agents. Birmingham: University of Aston in Birmingham. Department of Pharmaceutical Sciences, 1985.

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Wilman, Derry E. V., ed. The Chemistry of Antitumour Agents. Dordrecht: Springer Netherlands, 1990. http://dx.doi.org/10.1007/978-94-009-0397-5.

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Horspool, Keith Ronald. Structure-activity studies on antitumour imidazotetrazionones. Birmingham: Aston University. Departmentof Pharmaceutical Sciences, 1988.

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Shahbakhti, Hassan. Structure/activity relationships of antitumour diaziridinylquinones. Salford: University of Salford, 1996.

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Blackman, Claire. Studies on carbinolamine-containing triazine antitumour agents. Portsmouth: University of Portsmouth, 1994.

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Hickman, John Angus. Studies of the mechanism of action of antitumour compounds. Birmingham: Aston University. Department of Pharmaceutical Sciences, 1989.

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Gdarah, Khaled M. The synthesis of some nucleoside analogues as antitumour agents. Uxbridge: Brunel University, 1993.

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Book chapters on the topic "Antitumour"

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Suarato, A. "Antitumour anthracyclines." In The Chemistry of Antitumour Agents, 30–62. Dordrecht: Springer Netherlands, 1990. http://dx.doi.org/10.1007/978-94-009-0397-5_2.

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Rees, R. C., and S. A. Ali. "Antitumour Lymphocyte Responses." In Immunological Aspects of Cancer, 11–50. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4613-2557-4_2.

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Schiller, Erich. "Antitumour Drug Therapy." In Free Radicals and Inhalation Pathology, 739–52. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-642-18619-6_21.

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Denny, W. A. "Acridine-based antitumour agents." In The Chemistry of Antitumour Agents, 1–29. Dordrecht: Springer Netherlands, 1990. http://dx.doi.org/10.1007/978-94-009-0397-5_1.

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Coleman, Robert E., and Philippe Clézardin. "Antitumour Effects of Bisphosphonates." In Textbook of Bone Metastases, 345–50. Chichester, UK: John Wiley & Sons, Ltd, 2006. http://dx.doi.org/10.1002/0470011610.ch26.

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Gielen, Marcel. "Tin-Based Antitumour Drugs." In Main Group Elements and their Compounds, 446–52. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-52478-3_37.

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Keppler, B. K. "The Role of Non-Platinum Complexes in Cancer Therapy." In Tin-Based Antitumour Drugs, 1–68. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-74191-3_1.

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Crowe, Alan J. "Tin Compounds and their Potential as Pharmaceutical Agents." In Tin-Based Antitumour Drugs, 69–114. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-74191-3_2.

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Cardarelli, Nate F. "The Role of Tin Hormones in Senescence: A Hypothesis." In Tin-Based Antitumour Drugs, 115–46. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-74191-3_3.

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Duffield, J. R., C. R. Morris, D. M. Morrish, J. A. Vesey, and D. R. Williams. "The Speciation and Bioavailability of Tin in Biofluids." In Tin-Based Antitumour Drugs, 147–67. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-74191-3_4.

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Conference papers on the topic "Antitumour"

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Xuan Yuan, Defang Li, Hongmei Chen, Chao Sun, Na Chen, Xiaoyu Chen, Zhenhua Wang, and Qiusheng Zheng. "Isoliquiritigen Enhances Antitumour Activity of Cyclophosphamid." In 2010 International Conference on Bioinformatics and Biomedical Technology. IEEE, 2010. http://dx.doi.org/10.1109/icbbt.2010.5478984.

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Welchinskaya, Elena. "CHEMISTRY AND ANTITUMOUR ACTIVITY OF 5-BROMOURACILE’S DERIVATIVES." In CBU International Conference on Integration and Innovation in Science and Education. Central Bohemia University, 2013. http://dx.doi.org/10.12955/cbup.2013.45.

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Diez Fernandez, R., F. Fernandez Fraga, M. Moreno Garcia, and T. Molina Garcia. "4CPS-279 Cancer pain management approach considering potential drug interactions in patients receiving oral antitumour treatment." In 25th Anniversary EAHP Congress, Hospital Pharmacy 5.0 – the future of patient care, 23–28 March 2021. British Medical Journal Publishing Group, 2021. http://dx.doi.org/10.1136/ejhpharm-2021-eahpconf.111.

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Jacq, Xavier, Lisa Smith, Elaine Brown, Adina Hughes, Rajesh Odedra, Dan Heathcote, Jen Barnes, et al. "Abstract 1823: AZ20, a novel potent and selective inhibitor of ATR kinase with in vivo antitumour activity." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-1823.

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Cheng, L., J. Wang, and R. Liu. "Abstract P1-04-01: A novel oncolytic herpes simplex virus, GD116, has enhanced antitumour efficacy in human breast cancer." In Abstracts: 2017 San Antonio Breast Cancer Symposium; December 5-9, 2017; San Antonio, Texas. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.sabcs17-p1-04-01.

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Rahman, Khondaker M., Isabel G. Hijon, Colin H. James, and David E. Thurston. "Abstract 2321: Pyrrolobenzodiazepine (PBD) antitumour agents as chemical probes to determine the number of base pairs required for DNA minor groove structure." 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.am2011-2321.

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Berzaghi, Rodrigo, Vera SC Maia, Felipe V. Pereira, Filipe Manegatti De Melo, Luiz R. Travassos, and Luiz R. Travassos. "Abstract A146: The role of SOCS-1 in stimulating melanoma development through tyrosine-kinase receptors and MAPK pathways and prevents antitumour immunity by PD-L1 expression." In Abstracts: CRI-CIMT-EATI-AACR Inaugural International Cancer Immunotherapy Conference: Translating Science into Survival; September 16-19, 2015; New York, NY. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/2326-6074.cricimteatiaacr15-a146.

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Banerjee, Susana, Thierry André, Dominique Berton, Susan L. Ellard, Begoña Jimenez, Vanessa Samouëlian, Lucy Gilbert, et al. "2022-RA-945-ESGO Antitumour activity of dostarlimab by PD-L1 and tumour mutation burden in patients with mismatch repair deficient and proficient tumours in the GARNET trial." In ESGO 2022 Congress. BMJ Publishing Group Ltd, 2022. http://dx.doi.org/10.1136/ijgc-2022-esgo.878.

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Ruzanova, V. S. "THE PERSONALIZED TECHNOLOGY OF CANCER TREATMENT "KARANAHAN" HAS THREE VECTORS OF THERAPEUTIC EFFECT." In I International Congress “The Latest Achievements of Medicine, Healthcare, and Health-Saving Technologies”. Kemerovo State University, 2023. http://dx.doi.org/10.21603/-i-ic-117.

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The aim of this work was to test the technology of treatment of malignant tumors "Karanahan" on the Lewis lung carcinoma model and to prove the existence of the third antitumor therapeutic vector of this technology – activation of antitumor immunity.
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Tikhonov, Sergey, Nataliya Tikhonova, N. V. Merzlyakova, and A. S. Ozhgihina. "PEPTIDES AS A FUNCTIONAL INGREDIENT FOR PREVENTIVE PRODUCTS." In I International Congress “The Latest Achievements of Medicine, Healthcare, and Health-Saving Technologies”. Kemerovo State University, 2023. http://dx.doi.org/10.21603/-i-ic-133.

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Clinical studies indicate that products from cow colostrum are well tolerated by the human body, non-toxic and safe for consumption. The aim of this study is to study the antitumor properties of isolated individual peptides from corvine colostrum on the cell line of rat glioblastoma C6. The study revealed that peptide R1 has antitumor activity, therefore it can be used as a functional ingredient in food products.
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Reports on the topic "Antitumour"

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Georgieva, Ani, Katerina Todorova, Ivan Iliev, Valeriya Dilcheva, Ivelin Vladov, Svetlozara Petkova, Reneta Toshkova, et al. In Vitro Antitumour Activity of Hemocyanins Isolated fromHelix aspersaandHelix lucorumin Human Bladder Car cinoma Cells. "Prof. Marin Drinov" Publishing House of Bulgarian Academy of Sciences, September 2021. http://dx.doi.org/10.7546/crabs.2021.09.10.

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Conejo-Garcia, Jose R. Reprogramming Antitumor Immune Responses with microRNAs. Fort Belvoir, VA: Defense Technical Information Center, October 2012. http://dx.doi.org/10.21236/ada585107.

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Conejo-Garcia, Jose R. Reprogramming Antitumor Immune Responses with microRNAs. Fort Belvoir, VA: Defense Technical Information Center, October 2013. http://dx.doi.org/10.21236/ada595676.

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Wang, He, Jun Chen, Xiaoling Wang, and Jun Dang. Neoadjuvant immune checkpoint inhibitor in combination with chemotherapy or chemoradiotherapy in resectable esophageal cancer: A systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, June 2022. http://dx.doi.org/10.37766/inplasy2022.6.0052.

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Review question / Objective: It remains unclear whether addition of immune checkpoint inhibitor (ICI) to neoadjuvant chemoradiotherapy (nCRT) or neoadjuvant chemotherapy (nCT) can increase antitumor efficacy in resectable esophageal cancer (EC). we performed the systematic review and meta-analysis to assess antitumor efficacy and safety of nICRT and nICT, and made a comparison with nCRT and nICT. We used pathological complete response (pCR) as the primary outcomes of interest. Condition being studied: Initial findings from a number of phase 1 or 2 trials have supported the tolerability and/or antitumor efficacy of ICI plus nICRT (nICRT) and nICT (nICT). However, the superiority of this combination strategy remains uncertain due to lack of randomized control trials (RCTs) with long-term outcomes. Moreover, there are still outstanding questions such as the selection of nICRT or nICT, the ideal predictive biomarkers, and timing of surgical resection.
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Rayhim, Rayhana, and Jeannie S. Strobl. Augmentation of the Differentiation Response to Antitumor Antimalarials. Fort Belvoir, VA: Defense Technical Information Center, July 2004. http://dx.doi.org/10.21236/ada432050.

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Hill, Ann. Vaccine Vector for Sustained High-Level Antitumor CTL Response. Fort Belvoir, VA: Defense Technical Information Center, January 2011. http://dx.doi.org/10.21236/ada546083.

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Basu, Sayani. Monoclonal Antibody Therapy: A New Hope in Cancer Treatment. Natur Library, November 2020. http://dx.doi.org/10.47496/nl.blog.14.

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The remarkable specificity, high efficacy and the ability to elicit an antitumor response indicate that monoclonal antibody therapy offers promise in the treatment of malignancy and appears to be clinically relevant
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Fenton, Bruce M. Potentiation of Prostate Cancer Radiotherapy Using Antiangiogenic and Antitumor Therapies. Fort Belvoir, VA: Defense Technical Information Center, October 2007. http://dx.doi.org/10.21236/ada478113.

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Li, Chun. Radiation-Induced Chemosensitization: Potentiation of Antitumor Activity of Polymer-Drug Conjugates. Fort Belvoir, VA: Defense Technical Information Center, April 2002. http://dx.doi.org/10.21236/ada406209.

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Fenton, Bruce M. Potentiation of Prostate Cancer Radiotherapy Using Combined Antiangiogenic and Antitumor Therapies. Fort Belvoir, VA: Defense Technical Information Center, October 2005. http://dx.doi.org/10.21236/ada446439.

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