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Relevant bibliographies by topics / Anticancer

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Academic literature on the topic 'Anticancer'

Author: Grafiati

Published: 4 June 2021

Last updated: 22 June 2024

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Journal articles on the topic "Anticancer"

1

Ammazzalorso, Alessandra, and Marialuigia Fantacuzzi. "Anticancer Inhibitors." Molecules 27, no. 14 (July 21, 2022): 4650. http://dx.doi.org/10.3390/molecules27144650.

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Dove, Alan. "Anticancer verotoxin." Nature Biotechnology 17, no. 8 (August 1999): 738. http://dx.doi.org/10.1038/11646.

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Reese, David M. "Anticancer drugs." Nature 378, no. 6557 (December 1995): 532. http://dx.doi.org/10.1038/378532c0.

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Worland, PhD, Peter J., Gary S. Gray, PhD, Mark Rolfe, PhD, Karen Gray, PhD, and Jeffrey S. Ross, MD. "Anticancer Antibodies." American Journal of Clinical Pathology 119, no. 4 (April 1, 2003): 472–85. http://dx.doi.org/10.1309/y6lp-c0lr-726l-9dx9.

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Ross, Jeffrey S., Karen Gray, Gary S. Gray, Peter J. Worland, and Mark Rolfe. "Anticancer Antibodies." American Journal of Clinical Pathology 119, no. 4 (April 2003): 472–85. http://dx.doi.org/10.1309/y6lpc0lr726l9dx9.

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LeBrasseur, Nicole. "Anticancer lubrication." Journal of Cell Biology 156, no. 6 (March 11, 2002): 940. http://dx.doi.org/10.1083/jcb1566rr1.

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VanHook, A. M. "Anticancer Cocktails." Science Signaling 7, no. 347 (October 14, 2014): ec284-ec284. http://dx.doi.org/10.1126/scisignal.aaa0425.

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ROUHI, MAUREEN. "ANTICANCER VACCINE." Chemical & Engineering News 75, no. 3 (January 20, 1997): 8. http://dx.doi.org/10.1021/cen-v075n003.p008.

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Bergman, Philip J. "Anticancer Vaccines." Veterinary Clinics of North America: Small Animal Practice 37, no. 6 (November 2007): 1111–19. http://dx.doi.org/10.1016/j.cvsm.2007.06.005.

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Bonetta, Laura. "Anticancer squirt." Nature Medicine 7, no. 8 (August 2001): 891. http://dx.doi.org/10.1038/90920.

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Dissertations / Theses on the topic "Anticancer"

1

Hudnott, Anna Ruth. "Bioreductive anticancer agents." Thesis, University of Exeter, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.302640.

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Braña, García Irene. "Anticancer targeted agent combination." Doctoral thesis, Universitat Autònoma de Barcelona, 2017. http://hdl.handle.net/10803/457506.

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Las toxicidades limitantes de dosis fuero una neutropenia febril grado 4 (en el brazo de docetaxel) y una neutropenia grado 3 en el brazo de gemcitabina. La combinación de carlumab no tuvo un impacto El cáncer es una enfermedad altamente frecuente y con alta mortalidad. El desarrollo de fármacos contra el cáncer se ha caracterizado por su ineficiencia, con una de las tasas de aprobación de fármacos más baja entre las diferentes especialidades médicas. El principal motivo de esta baja tasa de éxito es la falta de eficacia de los nuevos fármacos que entran al desarrollo clínico. Se han planteado diferentes estrategias para mejorar la eficiencia del desarrollo de fármacos, incluyendo la combinación de fármacos antitumorales, el desarrollo en paralelo de biomarcadores y la optimización del diseño de los ensayos clínicos usando modelización basada en farmacocinética y farmacodinamia Esta tesis es un compendio de dos artículos que evalúan estrategias para optimizar el desarrollo de fármacos mediante la combinación de agentes antitumorales. El primer proyecto es la evaluación preclínica en xenoinjertos derivados de pacientes (PDX) la combinación de inhibidores de PI3K-mTOR con diferentes agentes antitumorales y el segundo es el ensayo clínico fase I evaluando carlumab, un anticuerpo anti CCL2, en combinación con diferentes quimioterapias en pacientes con tumores sólidos avanzados. Proyecto 1: se seleccionaron tres modelos de PDX con deficiencia en PTEN: un PDX de cáncer de mama triple negativo (TNBC), otro de carcinoma de ovario de bajo grado KRAS G12R mutado y otro de adenocarcinoma de pulmón con mutaciones en KRAS G12C y TP53 R181P. En estos modelos se evaluaron dos inhibidores de PI3K-mTOR—PF-04691502 and PF-05212384— en combinación con cisplatino, paclitaxel o dacomitinib. La adición de los inhibidores de PI3K-mTOR a cisplatino o paclitaxel aumentó la actividad de la quimioterapia en los modelos de TNBC y LGSOC; sin embargo, no se objetivó este efecto en modelo de adenocarcinoma de pulmón con mutación de KRAS y TP53. Se objetivó modulación farmacodinámica de pAKT y pS6 en los grupos tratados con inhibidores de PI3K-mTOR. Nuestra investigación sugiere que añadir un inhibidor de PI3K-mTOR puede aumentar el efecto inhibitorio sobre el crecimiento de la quimioterapia en modelos PDX con deficiencia en PTEN. Sin embargo, este beneficio no se observó en el modelo de adenocarcinoma KRAS y TP53 mutado. En el futuro se deberá ahondar en el papel de la pérdida de PTEN en la actividad de estas combinaciones. Proyecto 2: se trata de un ensayo clínico fase Ib evaluando carlumab, un anticuerpo monoclonal contra CCL-2, en combinación con cuatro regímenes de quimioterapia (docetaxel, gemcitabina, carboplatino + paclitaxel y doxorrubicina liposomal pegilda (PLD). En este estudio participaron 53 pacientes en los que o bien los agentes quimioterápicos eran parte del tratamiento convencional o no tenían otras opciones de tratamiento convencional: docetaxel (n=15), gemcitabina (n=12), carboplatino + paclitaxel (n=12) y PLD (n=14). Las toxicidades limitantes de dosis incluyeron una neutropenia febril grado 4 (en el brazo de docetaxel) y una neutropenia grado 3 (en el brazo de gemcitabina). De acuerdo a los brazos de tratamiento, las toxicidades grado 3 o mayores más frecuentes fueron: neutropenia (6/15) y neutropenia febril (4/15) en el brazo de docetaxel, neutropenia (2/12) en el brazo de gemcitabina, neutropenia (4/12), trombocitopenia (4/12) y anemia (2/12) en el brazo de carboplatino-paclitaxel y anemia (3/14) y mucositis (2/14) en el brazo de PLD. Se objetivo una respuesta parcial y 18 estabilizaciones de la enfermedad (38%). La adición de carlumab no tuvo cambios relevantes en el perfil farmacocinético de ninguna de las quimioterapias evaluadas. Los niveles de CCL2 libres descendieron inmediatamente tras el tratamiento con carlumab, pero aumentaron con las administraciones posteriores, sugiriendo que carlumab secuestraba CCL2 de manera temporal. No se objetivaron anticuerpos anti-droga que justificasen dicho efecto. No se objetivaron cambios en las células tumorales circulantes ni en las células circulantes endoteliales. En 3 de 19 pacientes evaluables se objetivó una reducción del 30% en los niveles de N-telopeptido de colágeno tipo I en orina (uNTx). Carlumab es seguro administrado a dosis de 10 o 15 mg/kg en combinación con quimioterapia convencional y tiene buena tolerancia. Sin embargo, no se alcanza una inhibición sostenida de CCL2, ni se han objetivado un número de respuestas significativas.
Cancer is a highly frequent disease associated to high mortality. Drug development in Oncology has shown to be inefficient, having one of the lowest success rate of drugs entering in phase I trials that finally achieves marketed authorization. The main reason for this high failure rate is lack of efficacy. Different strategies have been adopted to improved anti-cancer drug development with the aim of improving patient care. This strategies include the combinatorial use of agents, biomarker co-development, and optimization of clinical trial design with the use of pharmacokinetic-pharmacodynamic modeling. This thesis is presented as compendium of work integrating two projects; the first project preclinically evaluates the combination of two PI3K-mTOR inhibitors and chemotherapy or the pan-HER inhibitor dacomitinib in patient derived xenografts. The second project evaluates de monoclonal antibody anti-CCL2 carlumab in patient derived xenografts. Project 1: Three PDXs were selected for their lack of PTEN expression by immunohistochemistry: a triple-negative breast cancer (TNBC), a KRAS G12R low-grade serous ovarian cancer (LGSOC), and KRAS G12C and TP53 R181P lung adenocarcinoma (LADC). Two dual PI3K-mTOR inhibitors were evaluated—PF-04691502 and PF-05212384—in combination with cisplatin, paclitaxel, or dacomitinib. The addition of PI3K-mTOR inhibitors to cisplatin or paclitaxel increased the activity of chemotherapy in the TNBC and LGSOC models; whereas no added activity was observed in the LADC model. Pharmacodynamic modulation of pS6 and pAKT was observed in the group treated with PI3K-mTOR inhibitor. Our research suggests that the addition of a PI3K-mTOR inhibitor may enhance tumor growth inhibition when compared to chemotherapy alone in PTEN-deficient PDXs. However, this benefit was absent in the KRAS and TP53 mutant LADC model. The role of PTEN deficiency in the antitumor activity of these combinations should be further investigated in the clinic. Project 2 is a first-in-human phase 1b study of carlumab with one of four chemotherapy regimens (docetaxel, gemcitabine, paclitaxel+carboplatin, and pegylated liposomal doxorubicin HCl [PLD]). Fifty-three patients with advanced solid tumors for which ≥1 of these regimens was considered standard of care or for whom no other treatment options existed participated in the study: docetaxel (n=15), gemcitabine (n=12), paclitaxel or carboplatin (n=12), or PLD (n=14). Dose-limiting toxicities included one grade 4 febrile neutropenia (docetaxel arm) and one grade 3 neutropenia (gemcitabine arm). The most common drug-related grade ≥3 adverse events were docetaxel arm—neutropenia (6/15) and febrile neutropenia (4/15); gemcitabine arm—neutropenia (2/12); paclitaxel+carboplatin arm—neutropenia, thrombocytopenia (4/12 each), and anemia (2/12); and PLD arm—anemia (3/14) and stomatitis (2/14). One partial response and 18 (38 %) stable disease responses were observed. Combination treatment with carlumab had no clinically relevant pharmacokinetic effect on any of the chemotherapeutic agents tested. Free CCL2 declined immediately post-treatment with carlumab but increased with further chemotherapy administrations in all arms, suggesting that carlumab could sequester CCL2 for only a short time. Neither antibodies against carlumab nor consistent changes in circulating tumor cells (CTCs) or circulating endothelial cells (CECs) enumeration were observed. Three of 19 evaluable patients showed a 30 % decrease from baseline urinary cross-linked N-telopeptide of type I collagen (uNTx). Carlumab could be safely administered at 10 or 15 mg/kg in combination with standard-of-care chemotherapy and was well-tolerated, although no long-term suppression of serumCCL2 or significant tumor responses were observed.

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Rijt, Sabine H. van. "Osmium arene anticancer complexes." Thesis, University of Warwick, 2010. http://wrap.warwick.ac.uk/3213/.

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Drawbacks associated with anticancer chemotherapeutic cisplatin include tumour drug resistance, non-effectiveness against all tumours and lack of tumour-specificity resulting in severe side-effects (e.g. nausea, hair loss and kidney toxicity). The use of other metals such as transition metals rutheniumandosmium, may address the problems associated with platinum drugs and have received increased interest over the years. In this thesis the biological activity and aqueous solution chemistry of half-sandwichosmium (II) compounds of the type [(arene)OsII(X)(YZ)] n+ is explored. Chelating ligands containing nitrogen or nitrogen and oxygen donor atoms (N, NandN, O-chelatingligands) are investigated. It is shown that the chelating ligand has a large effect on the aqueous reactivity of the complexes. The introduction of functional groups on the chelate allowed for the ‘fine-tuning’ of the aqueous reactivity and nucleobase binding of the complexes. Also the nature of the coordinating arene was found to have an important effect on their biological activity. This could be rationalised by increased hydrophobicity with more extended arenes such as biphenylandtetrahydroanthracene, resulting in increased cellular uptake and increased cytotoxicity. Conjugating cell penetrating peptides to the complexes resulted in improved biological properties and opened a new way for functionalisation of the compounds. Several compounds reported in this thesis exhibit promising activity in the ovarian, colon and lung cancer cell lines and some could overcome cisplatin resistance in ovarian cisplatin resistant cell lines. Initial studies revealed cell death via apoptosis and the possible involvement of mitochondria in the apoptotic pathway. These results point to a novel pathway of activation for these complexes which is advantageous for addressing chemoresistance and effectiveness to oher types of cancers. This work shows that the biological properties of these compounds can be tuned by choice of ligands and also provides initial evidence for a novel pathway of activation.

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Pettersson, Hanna Ilse. "Quinolinequinones as anticancer agents." Thesis, University of Exeter, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.249038.

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Coverdale, James P. C. "Catalytic organometallic anticancer complexes." Thesis, University of Warwick, 2017. http://wrap.warwick.ac.uk/99039/.

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Half-sandwich complexes of ruthenium, iridium, and more recently osmium, have shown promise as anticancer agents. Many of these ‘piano-stool’ complexes appear to target the redox balance in cells. Separately, similar complexes have been investigated for the catalysis of hydrogenation reactions, with many examples achieving high turnover frequencies and enantioselectivities. This thesis is concerned with achieving in cell catalysis to increase drug potency and generate selectivity for cancer cells. A series of eighteen Os(II) and Ir(III) complexes, of the type [M(ηx-arene)(diamine)] (Os-arene: p-cymene, biphenyl, or m-terphenyl; Ir-arene: Cp*, CpxPh, or CpxBip), were synthesised and fully characterised. The structures were derived from a Ru(II) transfer hydrogenation catalyst [Ru(η6-p-cymene)(TsDPEN)], TsDPEN = N-tosyl-diphenyl-ethylenediamine. The complexes were isolated as 16-electron amido catalysts, which were highly stable in solution and upon storage, unlike their 16-electron Ru(II) counterparts, and were highly active for asymmetric transfer hydrogenation of ketones. Os complexes afforded enantiomerically-pure alcohols with high conversion and enantioselectivity (> 99%) at rates exceeding those of the existing Ru catalyst. Two Os and Ir complexes were explored for the conversion of NADH to its oxidised form (NAD+) under physiologically-relevant conditions. Antiproliferative activities determined in 14 human cell lines correlated with experimentally-determined hydrophobicities. Typically, Os catalysts were found to be more active than their Ir counterparts, though were internalised by cancer cells to a lesser degree, suggestive of a more potent in-cell mechanism of action. Structural modifications identified an apparent inert site of substitution on the sulfonamide substituent. Furthermore, their potency towards cancer cells was increased in combination with L-buthionine sulfoximine, an inhibitor of glutathione synthesis. Acute in vivo toxicities were determined in zebrafish, and all compounds investigated exhibited lower toxicities than the Pt anticancer drug, cisplatin. The complexes were shown to generate reactive oxygen species (ROS) in cancer cells, and similarly generated ROS in zebrafish. Transfer hydrogenation catalysis was explored under physiologically-relevant conditions using sodium formate as a biologically-compatible hydride source. Osmium complexes catalysed the reduction of pyruvate, a key metabolite in cells, to either L-lactate or D-lactate, selectively (ca. 83% ee). Upon co-administration of the catalyst and sodium formate, cancer cell proliferation was decreased by up to 13× (relative to cells treated with the catalyst alone), while no sodium formate effect was determined in non-cancerous cells. Importantly, the treatment of cells with a particular enantiomer of the Os catalyst and sodium formate facilitated the in cell reduction of pyruvate to D-lactate, providing, to the best of my knowledge, the first example of a synthetic catalyst carrying out asymmetric transfer hydrogenation chemistry in cells.

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May, Christopher. "Synthesis of anticancer compounds." Thesis, Imperial College London, 1987. http://hdl.handle.net/10044/1/47237.

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McGowan, Geraldine. "Platinum picoline anticancer complexes." Thesis, University of Edinburgh, 2005. http://hdl.handle.net/1842/11119.

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The 2-picoline (2-methylpyridine) complex, cis-[PtCl₂(NH₃)(2-pic)] (AMD473), is promising new generation platinum antitumour agent currently in clinical trials and highly active cisplatin resistant cell-lines. The antitumour activity of trans platinum complexes has attracted renewed interest since it has been shown that some trans compounds, in particular those possessing planar amine ligands, are anticancer-active. Therefore, three trans isomers, trans-[PtCl₂(NH₃)(2-pic)] (1), trans-[PtCl₂(NH₃)(3-pic)] (2) and trans-[PtCl₂(NH₃)(4-pic)] (3), were synthesised and characterised. The crystal structure of 1 shows steric hindrance induced by the 2-methyl group towards an axial approach to Pt, while its 3-pic (2) and 4-pic (3) analogues are less sterically hindered. Notable however, is that in the solid state complex 1 is less sterically-hindered than its cis isomer. ¹⁵N-labelling of complexes 1-3 allowed both the hydrolysis rates and pK_a values of the complexes to be determined using 2D[¹H, ¹⁵N] NMR spectroscopy. Adducts of cis- and trans-(PtCl₂(NH₃)(2-pic)] with neutral 9-ethylguanine (9-EtGH) and anionic (N1-deprotonated) 9-ethylguanine (9-EtG) were prepared and their structures determined by X-ray crystallography. Platinum is coordinated at the guanine N7 position with a head-to-tail arrangement of the bases in all cases. Two of the complexes exhibited intermolecular triple hydrogen bonding between neutral and deprotonated guanine ligands. In addition, adducts of cis- and trans-[PtCl₂(NH₃)(2-pic)] with guanosine and 2’-deoxyguanosine were prepared and characterised in solution by NMR spectroscopy and ESI mass spectrometry. The complexes cis-[Pt(NH₃)(2-pic)(Guo)₂]²⁺, and cis- and trans-(Pt(NH₃)(2-pic)(2’-dGuo)₂]²⁺ were assigned as head-to-tail conformations, on the basis of their NOE cross-peaks. The reaction of cis-[Pt(¹⁵NH₃)(2-pic)(OH₂)₂]²⁺ and guanosine (Guo) was followed by 2D [¹H, ¹⁵N] NMR spectroscopy and was found to proceed through two mono(guanosine) intermediate species to yield the dominant product cis-[Pt(¹⁵NH₃)(2-pic)(Guo)₂]²⁺. Initial guanosine substitution trans to 2-picoline was faster than substitution cis to 2-picoline due to steric hindrance, but the rates of the second guanosine substitution were similar. The binding of ¹⁵N-labelled-1 to a self-complementary DNA duplex, d(TATGGTACCATA)₂, was investigated using 1D ¹H and 2D [¹H, ¹⁵H] NMR spectroscopy. The first aquation step appeared to be the rate-limiting step in the formation of the monofunctional adducts. Several DNA products were observed but could not be identified unambiguously. The rate constants for reactions between ¹⁵N-laabelled 1 and guanosine 5’-monophosphate (5’-GMP) were determined via 2D NMR studies, and compared to those previously reported for cis-[PtCl₂(NH₃)(2-pic)].

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Liu, Zhe. "Organometallic iridium anticancer complexes." Thesis, University of Warwick, 2011. http://wrap.warwick.ac.uk/52292/.

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Cisplatin has been used to treat various types of cancers for over 30 years, however, a number of serious side-effects of cisplatin have stimulated the quest for other metal-based anticancer agents. Iridium complexes are generally thought to be too inert to possess high reactivity, and therefore, there are only a few previous reports of the antitumour activity of iridium complexes. In this thesis a wide range of organometallic IrIII cyclopentadienyl complexes of the type [(η5-Cpx)Ir(XY)Cl]0/+ (where Cpx = pentamethylcyclopentadienyl (Cp*), tetramethyl(phenyl)cyclopentadienyl (Cpxph) or tetramethyl(biphenyl)cyclopentadienyl (Cpxbiph), XY = N,N-, N,O- or C N-chelating ligand) has been synthesised and characterised. All the complexes hydrolyse rapidly in aqueous solution. Complexes with N,N-chelating ligands readily form adducts with 9-ethylguanine but not 9-ethyladenine; C N- or N,O-chelated complexes bind to both purines. Guanine residues are preferential binding sites for 1,10-phenanthroline complexes on plasmid DNA. Replacement of the neutral N,N-bound chelating ligand by the negatively-charged C,N-bound analogues can improve biological activity. In addition, cytotoxic potency towards A2780 human ovarian cancer cells increases with phenyl substitution on Cp*: Cpxbiph > Cpxph > Cp*. This can be rationalised by increased hydrophobicity with more extended phenyl ring, resulting in increased cellular uptake and increased intercalative ability. Notably, several complexes exhibited submicromolar anticancer activity. The interconversion of 1,4-NADH and NAD+ through hydride-transfer reactions in the presence of cyclopentadienyl IrIII aqua complexes was studied. It is shown that the IrIII aqua complexes not only converts NAD+ to 1,4-NADH using formate as the hydride source, but can also catalyse the reverse reaction with hydride donation from 1,4-NADH to a iridium centre, recovered by protonation of bound hydride with generation of H2. This work demonstrates how the aqueous chemistry, nucleobase binding and anticancer activity of the IrIII cyclopentadienyl complexes can be controlled and fine-tuned by the modification of the chelating and cyclopentadienyl ligands. The results suggest that this new class of organometalic Ir(III) complexes is well suited for development as anticancer agents.

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Arbaeen, Abrar Fawzi S. "Platinum anticancer drug shortages." Thesis, The University of Sydney, 2019. http://hdl.handle.net/2123/21128.

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The platinum-based chemotherapy drugs cisplatin, carboplatin, and oxaliplatin remain, despite their long-term use, as integral components in the treatment of more than 25 different human cancers. As such, shortages in their supply can have serious health and societal impacts on both the outcome and welfare of patients and on the healthcare systems as a whole. As all three drugs are no longer under patent protection, they are supplied in Australia, the U.S. and the U.K. by between four and 17 different pharmaceutical companies, which reduces the risk of drug shortages. Determining the number and impact of platinum drug shortages in various regions of the world is difficult because legislation to monitor shortages has only been passed recently. All three drugs have suffered from shortages since 2017 with the most common shortage being due to discontinuation of the drug by the company. Other causes include production disruptions, changes in customer demand, problems in supply such as transport and storages, and other reasons. The median duration of drug shortage is 22 days (shortest and longest supply shortages are 3 and 79 days, respectively). Shortages appear to be rare in developed western countries and western European countries, but more common in eastern European countries where platinum drugs are never available or are available only half of the time. This project highlights the lack of information available on platinum drug shortages and the end to further examine platinum drug shortages in regions that are more likely to be impacted, such as Africa, south-east Asia, central and southern America, and the Middle East.

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Sandler, Joel Stuart. "Anticancer compounds from marine invertebrates /." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2005. http://wwwlib.umi.com/cr/ucsd/fullcit?p3247792.

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Books on the topic "Anticancer"

1

Sotiris, Missailidis, ed. Anticancer therapeutics. Chichester: John Wiley & Sons, 2008.

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Grimm, Stefan, ed. Anticancer Genes. London: Springer London, 2014. http://dx.doi.org/10.1007/978-1-4471-6458-6.

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Ojima, Iwao, Gregory D. Vite, and Karl-Heinz Altmann, eds. Anticancer Agents. Washington, DC: American Chemical Society, 2001. http://dx.doi.org/10.1021/bk-2001-0796.

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Todd, Adam, Paul W. Groundwater, and Jason H. Gill. Anticancer Therapeutics. Chichester, UK: John Wiley & Sons, Ltd, 2018. http://dx.doi.org/10.1002/9781118696194.

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Missailidis, Sotiris, ed. Anticancer Therapeutics. Chichester, UK: John Wiley & Sons, Ltd, 2008. http://dx.doi.org/10.1002/9780470697047.

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Károly, Lapis, Eckhardt S, and International Union Against Cancer, eds. Anticancer drug research. Budapest: Akadémiai Kiadó, 1987.

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Georg, Gunda I., Thomas T. Chen, Iwao Ojima, and Dolatrai M. Vyas, eds. Taxane Anticancer Agents. Washington, DC: American Chemical Society, 1994. http://dx.doi.org/10.1021/bk-1995-0583.

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Goldstein, Lori J., and Robert F. Ozols, eds. Anticancer Drug Resistance. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2632-2.

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Reddy, L. Harivardhan, and Patrick Couvreur, eds. Macromolecular Anticancer Therapeutics. New York, NY: Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-0507-9.

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Macromolecular anticancer therapeutics. New York: Springer Verlag, 2009.

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Book chapters on the topic "Anticancer"

1

Schacter, Lee, Marcel Rozencweig, Claude Nicaise, Renzo Canetta, Susan Kelley, and Laurie Smaldone. "Anticancer Drugs." In Early Phase Drug Evaluation in Man, 644–54. London: Macmillan Education UK, 1990. http://dx.doi.org/10.1007/978-1-349-10705-6_49.

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Schwab, Matthias, Elke Schaeffeler, and Hiltrud Brauch. "Anticancer Drugs." In Metabolism of Drugs and Other Xenobiotics, 365–78. Weinheim, Germany: Wiley-VCH Verlag GmbH & Co. KGaA, 2012. http://dx.doi.org/10.1002/9783527630905.ch13.

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Saeidnia, Soodabeh. "Anticancer Antibiotics." In New Approaches to Natural Anticancer Drugs, 51–66. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-14027-8_4.

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Saeidnia, Soodabeh. "Anticancer Terpenoids." In New Approaches to Natural Anticancer Drugs, 67–92. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-14027-8_5.

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Isnard-Bagnis, Corinne, Vincent Launay-Vacher, Svetlana Karie, and Gilbert Deray. "Anticancer drugs." In Clinical Nephrotoxins, 511–35. Boston, MA: Springer US, 2008. http://dx.doi.org/10.1007/978-0-387-84843-3_22.

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Ramon, Anne Laure, and Claude Malvy. "Anticancer Oligonucleotides." In Macromolecular Anticancer Therapeutics, 539–68. New York, NY: Springer New York, 2009. http://dx.doi.org/10.1007/978-1-4419-0507-9_16.

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Zhao, Le, Zengyi Shao, and Jacqueline V. Shanks. "Anticancer Drugs." In Industrial Biotechnology, 237–69. Weinheim, Germany: Wiley-VCH Verlag GmbH & Co. KGaA, 2016. http://dx.doi.org/10.1002/9783527807833.ch8.

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De Conno, F., and K. Foley. "Anticancer therapy." In Cancer Pain Relief, 33–35. Dordrecht: Springer Netherlands, 1995. http://dx.doi.org/10.1007/978-94-011-0099-1_16.

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Sibaud, Vincent, Robert Baran, Bianca Maria Piraccini, Mario E. Lacouture, and Caroline Robert. "Anticancer Therapies." In Baran & Dawber's Diseases of the Nails and their Management, 604–16. Chichester, UK: John Wiley & Sons, Ltd, 2018. http://dx.doi.org/10.1002/9781119323396.ch17.

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Ganguly, A. K., and Sesha Sridevi Alluri. "Anticancer Drugs." In Medicinal Chemistry, 89–101. Boca Raton: CRC Press, 2021. http://dx.doi.org/10.1201/9781003182573-4.

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Conference papers on the topic "Anticancer"

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"14th International Congress on Targeted Anticancer Therapies (TAT 2016)." In 14th International Congress on Targeted Anticancer Therapies (TAT 2016). Frontiers Media SA, 2016. http://dx.doi.org/10.3389/978-2-88919-879-5.

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Turánek, Jaroslav, Michaela Škrabalová, and Pavlína Knötigová. "Antimicrobial and anticancer peptides." In XIth Conference Biologically Active Peptides. Prague: Institute of Organic Chemistry and Biochemistry, Academy of Sciences of the Czech Republic, 2009. http://dx.doi.org/10.1135/css200911128.

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Mangalagiu, Violeta, Dumitrela Diaconu, Costel Moldoveanu, Gheorghita Zbancioc, Ramona Danac, Dorina Amariucai-Mantu, Vasilichia Antoci, and Ionel Mangalagiu. "Hybrid and chimeric nitrogen heterocycles with biological activity." In Scientific seminar with international participation "New frontiers in natural product chemistry". Institute of Chemistry, Republic of Moldova, 2023. http://dx.doi.org/10.19261/nfnpc.2023.ab01.

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Nitrogen heterocycles, especially azine and azole derivatives, are highly valuable scaffolds in medicinal chemistry, being the core components of a large variety of drugs with variously biological activity such as antiplasmodial and antimalarial, antitubercular, antibacterial, antifungal, anticancer, analgesic, antidepressant, anxiolytics, antihypertensive, anticoagulants, diuretics, etc. As a result, obtaining of such entities continues to arouse a strong interest from academia and industry. As part of our ongoing research in the area of nitrogen heterocyclic derivatives, we present herein some representative results obtained by our group in the field of hybrid and chimeric azahetrocycles compounds with antimicrobial and anticancer activity. Chemistry, anticancer, antibacterial, antifungal and antituberculosis activity of compounds is presented. Some of the hybrid and chimeric structures possess a good anticancer and/or antimicrobial activity.

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Ciorteanu, Roxana Elena, Monica Sardaru, Dumitrela Diaconu, Ionel Mangalagiu, and Ramona Danac. "Synthesis and anticancer properties of new indolizinic derivatives." In Scientific seminar with international participation "New frontiers in natural product chemistry". Institute of Chemistry, Republic of Moldova, 2023. http://dx.doi.org/10.19261/nfnpc.2023.ab25.

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Natural compounds with indolizine scaffolds have demonstrated numerous biological activities and have found use in medical research laboratories. Thys, the unique indolizine scaffold became an important system for the development of new drug candidates in medicinal chemistry. [1,2] Several indolizines with excellent anticancer activity and tubulin polymerization inhibitory potency have been reported recently, and our group contributed also to the field. [1,3] The goal of this study was the design, synthesis and anticancer evaluation of several new derivatives with symmetrical or unsymmetrical substituted 7,7’-(ethene-1,2-diyl)bisindolizine structure, and several new 6-, 7- or 8-substituted indolizine derivatives. Mono and bisindolizines were synthesized in good yields via [3+2] dipolar cycloaddition of the in situ generated ylides, from corresponding N-pyridinium salts to ethyl propiolate. Part of the new derivatives were tested for their anticancer activity by screening against NCI’s 60 human tumour cell lines panel and the results are presented herein. In vitro experiments regarding tubulin interaction were performed for the active compounds.

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Chandrasekhar, H. Raghu, P. Vasanth Raj, J. Venkata Rao, and N. Udupa. "Anticancer activity of hypericum mysorense." In 2009 International Conference on Biomedical and Pharmaceutical Engineering (ICBPE). IEEE, 2009. http://dx.doi.org/10.1109/icbpe.2009.5384082.

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Lowe, Henry Isaac Cloore, Ngeh J. Toyang, Charah Watson, and Joseph Bryant. "Abstract 1754: Cycloartane anticancer activity." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-1754.

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Li, Jiao, Pamela Crowell, and Jake Yue Chen. "Construct anticancer drug-drug correlation network." In the 2009 ACM symposium. New York, New York, USA: ACM Press, 2009. http://dx.doi.org/10.1145/1529282.1529444.

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Domínguez Martín, Eva María, Ana María Díaz Lanza, Patrícia Rijo, and Célia Faustino. "Anticancer Hybrid Combinations with phenolic compounds." In 5th International Electronic Conference on Medicinal Chemistry. Basel, Switzerland: MDPI, 2019. http://dx.doi.org/10.3390/ecmc2019-06319.

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Satya, Kulsum Hashmi, Sakshi Gupta, Armeen Siddique, and Seema Joshi. "Vanadium Complexes as Potential Anticancer Agents." In ASEC 2023. Basel Switzerland: MDPI, 2023. http://dx.doi.org/10.3390/asec2023-15263.

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Isyaka, M., M. Langat, E. Mas-Claret, T. Hodges, M. Brabner, J. Munisi, B. Mbala, and D. Mulholland. "Anticancer Diterpenoids from African Croton Species." In GA – 70th Annual Meeting 2022. Georg Thieme Verlag KG, 2022. http://dx.doi.org/10.1055/s-0042-1759135.

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Reports on the topic "Anticancer"

1

Cheng, Yi-Qiang, Cheng Wang, Shane Wesener, and Viahwakanth Potharla. Engineer Novel Anticancer Bioagents. Fort Belvoir, VA: Defense Technical Information Center, October 2010. http://dx.doi.org/10.21236/ada535365.

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Seol, Dai-Wu. TRAIL-Based Anticancer Drug Development. Fort Belvoir, VA: Defense Technical Information Center, July 2002. http://dx.doi.org/10.21236/ada407205.

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Hammond, Scott M. MicroRNA Inhibitors as Anticancer Therapies. Fort Belvoir, VA: Defense Technical Information Center, August 2007. http://dx.doi.org/10.21236/ada475785.

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Peterson, Blake R. Anticancer Inhibitors of AR-Mediated Gene Expression. Fort Belvoir, VA: Defense Technical Information Center, November 2006. http://dx.doi.org/10.21236/ada463403.

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Howard, David, Peter Bach, Ernst Berndt, and Rena Conti. Pricing in the Market for Anticancer Drugs. Cambridge, MA: National Bureau of Economic Research, January 2015. http://dx.doi.org/10.3386/w20867.

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Klein, Mark. Development of Novel p16INK4a Mimetics as Anticancer Therapy. Fort Belvoir, VA: Defense Technical Information Center, October 2014. http://dx.doi.org/10.21236/ada615123.

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Inoue, Takashi, and Mamoru Narukawa. Anti-tumor efficacy of anti-PD-1/PD-L1 antibodies in combination with other anticancer drugs in solid tumors: a systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, October 2022. http://dx.doi.org/10.37766/inplasy2022.10.0004.

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Review question / Objective: The aim of this systematic review is to compare the combination of PD-1/PD-L1 inhibitors plus other anticancer drugs and monotherapies of PD-1/PD-L1 inhibitors in terms of antitumor efficacy in the solid tumors to better inform clinical practice. To this end, the proposed systematic review will address the following question: Which is the best choice to enhance response rate in subjects with solid tumors, PD-1/PD-L1 inhibitors plus cytotoxic agents or PD-1/PD-L1 inhibitors plus other targeted anticancer drugs? Condition being studied: Cancer is the leading cause of death worldwide, accounting to approximately 9.6 million deaths worldwide in 2018. The clinical efficacy of immune checkpoint inhibitors (CPIs) including PD-1/PD-L1 inhibitors has been proven; however, it is also known that their efficacy as monotherapy is limited, with a response rate of 20% or less in solid tumors. The combination of CPIs and anticancer agents has been actively attempted in solid tumors area.

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Hu, Xiaoyi. Human Methionine Aminopeptidase 1 (MetAP1) as a New Anticancer Target. Fort Belvoir, VA: Defense Technical Information Center, April 2005. http://dx.doi.org/10.21236/ada436150.

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Zhang, Jian-Ting. Molecular Study of Interactions between P-Glycoprotein and Anticancer Drugs. Fort Belvoir, VA: Defense Technical Information Center, August 1995. http://dx.doi.org/10.21236/ada300162.

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Biswas, Kaustav, and Samuel J. Danishefsky. Synthesis of Epothilone Analogs: Toward the Development of Potent Anticancer Drugs. Fort Belvoir, VA: Defense Technical Information Center, August 2002. http://dx.doi.org/10.21236/ada409475.

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