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Artigos de revistas sobre o assunto "Anticancer drug treatment"
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Alven, Sibusiso, e Blessing Atim Aderibigbe. "The Therapeutic Efficacy of Dendrimer and Micelle Formulations for Breast Cancer Treatment". Pharmaceutics 12, n.º 12 (15 de dezembro de 2020): 1212. http://dx.doi.org/10.3390/pharmaceutics12121212.
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Breast cancer is among the most common types of cancer in women and it is the cause of a high rate of mortality globally. The use of anticancer drugs is the standard treatment approach used for this type of cancer. However, most of these drugs are limited by multi-drug resistance, drug toxicity, poor drug bioavailability, low water solubility, poor pharmacokinetics, etc. To overcome multi-drug resistance, combinations of two or more anticancer drugs are used. However, the combination of two or more anticancer drugs produce toxic side effects. Micelles and dendrimers are promising drug delivery systems that can overcome the limitations associated with the currently used anticancer drugs. They have the capability to overcome drug resistance, reduce drug toxicity, improve the drug solubility and bioavailability. Different classes of anticancer drugs have been loaded into micelles and dendrimers, resulting in targeted drug delivery, sustained drug release mechanism, increased cellular uptake, reduced toxic side effects of the loaded drugs with enhanced anticancer activity in vitro and in vivo. This review article reports the biological outcomes of dendrimers and micelles loaded with different known anticancer agents on breast cancer in vitro and in vivo.
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Savinkova, A. V., E. M. Zhidkova, L. R. Tilova, M. D. Lavrova, E. S. Lylova, K. A. Kuzin, A. Yu Portyannikova et al. "VARIANTS AND PERSPECTIVES OF DRUG REPURPOSING FOR CANCER TREATMENT". Siberian journal of oncology 17, n.º 3 (4 de julho de 2018): 77–87. http://dx.doi.org/10.21294/1814-4861-2018-17-3-77-87.
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Recently many new approaches for repurposing or repositioning of the clinically used drugs have been developed. Drug repurposing allows not only to use known schemes for the synthesis of biologically active compounds, but also to avoid multiple studies that are necessary for drug approval process – analysis of pharmacokinetics, carcinogenicity, acute and chronic toxicity, including cardiotoxicity, nephrotoxicity, allergenicity etc. It makes possible to reduce the number of experimental studies as well as costs of investigations. In cancer research drug repurposing includes screening for medicines used nowadays for the treatment of patients with non-cancer diseases which possess anticancer activity or able to enhance the effects of the standard anticancer chemotherapy, and search for new applications of known anticancer drugs for the treatment of different cancer types. Scientific rationale for the search of the compounds with potential anticancer properties among drugs with different applications is based on the multiple cross-talks of signaling pathways, which can inhibit cell proliferation. Modern advances in genomics, proteomics and bioinformatics, development of permanently improving databases of drug molecular effects and high throughput analytical systems allow researchers to analyze simultaneously a large bulk of existing drugs and specific molecular targets. This review describes the main approaches and resources currently used for the drug repurposing, as well as a number of examples.
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Mahmud, Kazi Mustafa, Mahruba Sultana Niloy, Md Salman Shakil e Md Asiful Islam. "Ruthenium Complexes: An Alternative to Platinum Drugs in Colorectal Cancer Treatment". Pharmaceutics 13, n.º 8 (19 de agosto de 2021): 1295. http://dx.doi.org/10.3390/pharmaceutics13081295.
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Colorectal cancer (CRC) is one of the intimidating causes of death around the world. CRC originated from mutations of tumor suppressor genes, proto-oncogenes and DNA repair genes. Though platinum (Pt)-based anticancer drugs have been widely used in the treatment of cancer, their toxicity and CRC cells’ resistance to Pt drugs has piqued interest in the search for alternative metal-based drugs. Ruthenium (Ru)-based compounds displayed promising anticancer activity due to their unique chemical properties. Ru-complexes are reported to exert their anticancer activities in CRC cells by regulating different cell signaling pathways that are either directly or indirectly associated with cell growth, division, proliferation, and migration. Additionally, some Ru-based drug candidates showed higher potency compared to commercially available Pt-based anticancer drugs in CRC cell line models. Meanwhile Ru nanoparticles coupled with photosensitizers or anticancer agents have also shown theranostic potential towards CRC. Ru-nanoformulations improve drug efficacy, targeted drug delivery, immune activation, and biocompatibility, and therefore may be capable of overcoming some of the existing chemotherapeutic limitations. Among the potential Ru-based compounds, only Ru (III)-based drug NKP-1339 has undergone phase-Ib clinical trials in CRC treatment.
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Lee, Jun H., e Anjan Nan. "Combination Drug Delivery Approaches in Metastatic Breast Cancer". Journal of Drug Delivery 2012 (26 de abril de 2012): 1–17. http://dx.doi.org/10.1155/2012/915375.
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Disseminated metastatic breast cancer needs aggressive treatment due to its reduced response to anticancer treatment and hence low survival and quality of life. Although in theory a combination drug therapy has advantages over single-agent therapy, no appreciable survival enhancement is generally reported whereas increased toxicity is frequently seen in combination treatment especially in chemotherapy. Currently used combination treatments in metastatic breast cancer will be discussed with their challenges leading to the introduction of novel combination anticancer drug delivery systems that aim to overcome these challenges. Widely studied drug delivery systems such as liposomes, dendrimers, polymeric nanoparticles, and water-soluble polymers can concurrently carry multiple anticancer drugs in one platform. These carriers can provide improved target specificity achieved by passive and/or active targeting mechanisms.
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P. George, Christy, Shridhar H. Thorat, Parth S. Shaligram, Suresha P. R. e Rajesh G. Gonnade. "Drug–drug cocrystals of anticancer drugs erlotinib–furosemide and gefitinib–mefenamic acid for alternative multi-drug treatment". CrystEngComm 22, n.º 37 (2020): 6137–51. http://dx.doi.org/10.1039/d0ce00353k.
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Drug–drug cocrystals of anticancer drugs erlotinib and gefitinib with furosemide and mefenamic acid, respectively, have been synthesized, characterized and their solubilities and dissolution rates were correlated with crystal structures.
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Moradi-Marjaneh, Reyhaneh, Majid Khazaei, Sima Seifi, Seyed Mahdi Hassanian, Gordon A. Ferns e Amir Avan. "Pharmacogenetics of Anticancer Drug Sensitivity and Toxicity in Colorectal Cancer". Current Pharmaceutical Design 24, n.º 23 (24 de outubro de 2018): 2710–18. http://dx.doi.org/10.2174/1381612824666180727144535.
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Inter-individual differences in drug response are an important cause of failure in anticancer treatment and adverse drug events in cancer patients. Gene polymorphisms related to these outcomes have been investigated in an effort to find new genetic biomarkers to predict toxicity and response to anticancer drugs. Evaluating the value single nucleotide polymorphisms (SNPs) in the genes involved in transportation, activation and metabolism of anticancer drugs provides a promising approach to select the appropriate therapeutic regimes with at least adverse reactions. This review summarizes the current knowledge about the relationship between of SNPs involved in the transportation, activation and metabolism of anticancer drugs and treatment outcomes in colorectal cancer (CRC) patients.
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Ostroumova, O. D., D. A. Sychev, A. I. Kochetkov, T. M. Ostroumova, M. I. Kulikova e V. A. De. "Anti-cancer agents and drug-induced hypertension". Medical alphabet, n.º 17 (7 de setembro de 2022): 30–41. http://dx.doi.org/10.33667/2078-5631-2022-17-30-41.
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Arterial hypertension is one of the most common comorbidities in patients with cancer. Moreover, the treatment with anticancer agents can lead to the development of drug-induced arterial hypertension. The aim of this work is to systematize and analyze data about anticancer agents, the use of which can cause the development of drug-induced hypertension, about epidemiology, pathophysiological mechanisms, risk factors, clinical signs, diagnosis and differential diagnosis, treatment and prevention of hypertension associated with the use of anticancer drugs. It was found that anti-cancer drugs often contribute to the development of drug-induced hypertension. The mechanisms that determine the development of hypertension are diverse and may include the development of endothelial dysfunction, an increased arterial stiffness, capillary rarefaction, fluid and electrolyte imbalance, and genetic factors. It is important to remember about drugs that can cause drug-induced hypertension to reduce the risk of developing adverse reactions, and prevent cardiovascular disease. Treatment of drug-induced hypertension, caused by anticancer drugs, often requires immediate discontinuation of drugs, due to adverse reactions that are often life-threatening. In some situations, it is possible to reduce the dose of the drugs and / or prescribe antihypertensive drugs. Arterial hypertension is an important risk factor in the development of cardiovascular events, including stroke, coronary heart disease, heart failure.
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Li, Fan, Xinqing Fu, Qingqing Huo e Wantao Chen. "Research Progress on the Nano-Delivery Systems of Antitumor Drugs". Nano LIFE 10, n.º 01n02 (março de 2020): 2040006. http://dx.doi.org/10.1142/s1793984420400061.
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To date, chemotherapy, the main treatment for malignant tumors, still fails to provide ideal therapeutic efficacy, which is deeply rooted in various physiological barriers, either temporal or spatial, to the delivering of anticancer drugs to solid tumor sites during chemotherapy. In the meantime, the therapeutic efficacy of anticancer drugs is affected by inherent cancer characteristics, drug transport, cellular uptake and other complex interactions. Recently, advances have been constantly achieved on nanoscale drug delivery systems (NDDSs) for anticancer drug delivery, driven by their excellent stability and effectiveness in improving water solubility of anticancer drugs, prolonging systemic circulation time, reducing side effects and improving anticancer effects. This paper presents an overview of the current research status and challenges in applying NDDSs to anticancer drug delivery.
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Fumagalli, Gaia, Cristina Marucci, Michael S. Christodoulou, Barbara Stella, Franco Dosio e Daniele Passarella. "Self-assembly drug conjugates for anticancer treatment". Drug Discovery Today 21, n.º 8 (agosto de 2016): 1321–29. http://dx.doi.org/10.1016/j.drudis.2016.06.018.
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Kim, Tae-Hyun, Gyeong Jin Lee, Joo-Hee Kang, Hyoung-Jun Kim, Tae-il Kim e Jae-Min Oh. "Anticancer Drug-Incorporated Layered Double Hydroxide Nanohybrids and Their Enhanced Anticancer Therapeutic Efficacy in Combination Cancer Treatment". BioMed Research International 2014 (2014): 1–11. http://dx.doi.org/10.1155/2014/193401.
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Objective. Layered double hydroxide (LDH) nanoparticles have been studied as cellular delivery carriers for anionic anticancer agents. As MTX and 5-FU are clinically utilized anticancer drugs in combination therapy, we aimed to enhance the therapeutic performance with the help of LDH nanoparticles.Method. Anticancer drugs, MTX and 5-FU, and their combination, were incorporated into LDH by reconstruction method. Simply, LDHs were thermally pretreated at 400°C, and then reacted with drug solution to simultaneously form drug-incorporated LDH. Thus prepared MTX/LDH (ML), 5-FU/LDH (FL), and (MTX + 5-FU)/LDH (MFL) nanohybrids were characterized by X-ray diffractometer, scanning electron microscopy, infrared spectroscopy, thermal analysis, zeta potential measurement, dynamic light scattering, and so forth. The nanohybrids were administrated to the human cervical adenocarcinoma, HeLa cells, in concentration-dependent manner, comparing with drug itself to verify the enhanced therapeutic efficacy.Conclusion. All the nanohybrids successfully accommodated intended drug molecules in their house-of-card-like structures during reconstruction reaction. It was found that the anticancer efficacy of MFL nanohybrid was higher than other nanohybrids, free drugs, or their mixtures, which means the multidrug-incorporated LDH nanohybrids could be potential drug delivery carriers for efficient cancer treatment via combination therapy.
Teses / dissertações sobre o assunto "Anticancer drug treatment"
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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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Golovko, Olga. "The screening for novel proteasome inhibitors as a treatment of cancer using IncuCyte FLR and fluorometric microculture cytotoxicity assay". Thesis, Uppsala universitet, Institutionen för medicinsk biokemi och mikrobiologi, 2011. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-160700.
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The problem of finding targeted medicine is a central problem in chemotherapy. From this point of view the ubiquitin-proteasome system is a highly promising object in the pharmaceutical approach. Proteasome plays a critical role in cellular protein degradation, cell cycle and apoptosis regulation. Proteasome inhibitors are substances blocking the actions of proteasome. Cancer cells are more sensitive to inhibition of the ubiquitin-proteasome system than normal cells. Therefore proteasome inhibitors have the potential to be successfully used in the cancer treatment. The study aimed to test various substances to identify possible proteasome inhibitors with the IncuCyteTM FLR image system and fluorometric microculture cytotoxicity assay. Using the IncuCyte FLR method allows for detecting changes in the molecular processes of living cells. To make proteasome inhibition visible the model cell line MelJuSoUbG76V-YFP is used which helps to detect alterations in proteasome activity by means of the yellow fluorescent protein enrichment in cells as a response to proteasome inhibition. Fluorometric microculture cytotoxicity assay is a method for the determination of cytotoxicity in human tumor cells. The study showed that substance #25 possessed a proteasome inhibitory capacity in a dose-dependent manner as demonstrated with the IncuCyte FLR image system. According to the fluorometric microculture cytotoxicity assay, substance #1 was the most stable and toxic. Substances #2 and #185 had selective toxicity against cancer cells and lower effects against normal cells. Combining IncuCyte FLR and fluorometric microculture cytotoxicity assay allows finding substances which act as proteasome inhibitors with high toxic effect.
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Brazzale, Chiara. "Gold nanoparticle surface tuning for multimodal treatment of cancer". Doctoral thesis, Università degli studi di Padova, 2016. http://hdl.handle.net/11577/3424441.
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In the last decades colloidal decorated gold nanoparticles (GNPs) have been studied as platform for drug and gene delivery, for diagnostic and other biomedical applications. These metal nanoparticles are intriguing because of their unique physico-chemical properties that can be exploited for multimodal and combined treatment of cancer. In the present thesis work gold nanoparticles were decorated with a targeting ligand (Folate-PEG) to combine an active and a passive targeting aiming to enhance the selective accumulation within the tumour site. Deep studies have been done to investigate the effect of surface Folate density on the internalization efficiency of gold nanoparticles. Afterwards intracellular trafficking studies were performed to clarify the uptake mechanism and investigate lysosomal delivery. Confocal microscopy and TEM analysis showed in good agreement that Folate targeted gold nanoparticles are internalized via a clathrin-independent pathway. Another purpose of the project have concerned the exploitation of GNPs as sensitizers in the sonodynamic therapy. This is a non-invasive approach which consists in cancer tissue irradiation with focused ultrasounds (HIFU) to trigger cavitation phenomena leading to irreversible destruction of the target tissue. The combination of the ultrasound exposure and the pre-incubation of cells with Folate targeted particles induced a significant and selective cell death. The concept of multimodal targeting was extended to the development of pH responsive targeted gold nanoparticles, using a pH sensitive polymer able to respond with morphological alterations to environmental pH changes. The cell uptake results confirmed that the “hiding” and “reveal” of targeting agents on GNP surface is modulated by the sensitive polymer. As a result there is an enhanced site-selective GNP accumulation in the cancer tissue, according to a cooperative exploitation of phenotypic and environmental features of the tumour. In conclusion, the present thesis work is proposed as proof-of-concept to show that by finely tuning the surface properties of nanosystems, site-selectivity can be significantly enhanced, thus reducing the disposition of drug nanocarriers in off-target tissues.Lo scopo del presente progetto di dottorato è stato quello di produrre e caratterizzare dal punto di vista chimico-fisico e biologico un nanocarrier per il direzionamento selettivo di farmaci antitumorali a tumori sovraesprimenti il recettore per l’acido folico. Sono stati compiuti studi approfonditi per verificare come la densità dell’agente di targeting influenzasse l’efficienza d’internalizzazione del sistema. Inoltre studi di trafficking intracellulare hanno verificato come particelle d’oro direzionate con agente di targeting Folato-PEG vengano internalizzate mediante meccanismo clatrina-indipendente. Si è inoltre indagata la capacità di nanoparticelle d’oro come sensibilizzanti alla terapia sonodinamica al fine di poter combinare un trattamento farmacologico ad un approccio fisico. Un ulteriore sviluppo del progetto ha riguardato la modifica di nanoparticelle d’oro direzionate con Folato-PEG con una seconda componente pH responsiva in grado di passare da una conformazione estesa a pH fisiologico di 7.4 ad una forma idrofobica globulare a pH 6.5, condizione tipica del tessuto tumorale. In questo modo é possibile modulare il mascheramento/esposizione dell’agente di targeting e ridurre il bio-riconoscimento aspecifico a favore della sito-specificità. Tra gli sviluppi futuri del progetto, vi è la decorazione di nanoparticelle d’oro con un polimero dotato di gruppi idrazinici coniugati a Doxorubicina mediante legame idrazonico. In virtù delle proprietà del legame idrazonico, la Doxorubicina sarà rilasciata esclusivamente nei comparti endosomiali e lisosomiali, in seguito all'uptake cellulare mediato dal recettore FR per l’acido folico.
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Pardella, Elisa. "Therapy-induced stromal senescence promotes prostate cancer progression and aggressiveness". Doctoral thesis, Università di Siena, 2021. http://hdl.handle.net/11365/1128061.
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Although chemotherapy still represents the gold-standard treatment option for cancer cure, it often results in several long-term negative side effects, including cancer relapse and acquired resistance to the therapy. Docetaxel is the preferred anticancer drug for several tumor types, including metastatic castrate-resistant prostate cancer. However, it exhibits only modest efficacy and many patients who received Docetaxel treatment experience tumor progression and chemotherapy insensitivity. Therefore, identifying the molecular mechanisms that associate anticancer therapy with its negative bystander effects is an urgent need in order to develop novel strategies targeting chemotherapy vulnerabilities. Interestingly, a possible link is provided by therapy-induced cellular senescence. Indeed, a recent body of evidence highlights that several antineoplastic agents promote the senescent phenotype in both stromal and tumor cells. Despite it has been originally identified as a tumor-suppressive mechanism, many findings underline that cellular senescence sustains tumor growth and dissemination. The tumor-promoting effects of cellular senescence are mainly mediated by secreted factors, that exert profound paracrine effects through the generation of a pro-inflammatory and immunosuppressive microenvironment. For instance, it is well known that cancer progression and aggressiveness are strongly supported by the bi-directional crosstalk between cancer cells and the surrounding tumor microenvironment, that favors cancer cell migration and invasion, neo-angiogenesis and homing of distant organs. In this scenario, stromal cells exert a promoting role in cancer progression providing tumor with energy sources, growth factors and cytokines.
In this study, we found that Docetaxel treatment strongly promotes the senescent phenotype in stromal prostate fibroblasts, as revealed by a sharp increase in numerous senescence markers, including SA-β-Galactosidase activity, γ-H2AX nuclear foci, and p53 expression. We also provided evidence that Docetaxel treatment induces the senescence-associated secretory phenotype (SASP) in prostate stromal fibroblasts, by increasing the levels of pro-inflammatory cytokines (IL-6, IL-8), growth factors (VEGF-A) and matrix-metalloproteinases (MMP-2 and MMP-3). The clinical relevance of the senescence-inducing effects of Docetaxel in the stromal compartment of prostate cancer was determined analyzing the accumulation of lipofuscin aggregates in tissue specimens from 20 patients with prostate cancer, 10 of whom received neo-adjuvant Docetaxel chemotherapy before radical prostatectomy. Remarkably, we found that lipofuscin staining is significantly higher in patients treated with Docetaxel therapy and preferentially accumulates in the stromal compartment of prostate cancer tissues. Besides, this study underlined that Docetaxel-induced senescent stromal cells exhibit a strong mitochondrial dysfunction, characterized by increased mitochondrial mass and oxidative stress, reduced mitochondrial membrane potential, and morphological changes of the mitochondrial structure. Moreover, we observed that the anticancer drug promotes metabolic alterations in senescent prostate fibroblasts, including increased extracellular acidification rate and lactate secretion, suggesting that senescent cells may shift towards a more glycolytic metabolism to meet their energetic demands, as a consequence of impaired mitochondria. We then investigated the role of the paracrine factors and metabolites secreted by senescent fibroblasts on prostate cancer aggressiveness by incubating PC3 tumor cells with conditioned media from control or senescent fibroblasts. We highlighted that therapy-induced stromal senescence supports the increase in the invasive and migratory abilities, and clonogenic and stemness potential of prostate cancer cells. Interestingly, these effects are directly correlated to stromal senescence. Indeed, clearance of senescent fibroblasts through administration of ABT263, a senolytic drug, reverts the malignant phenotype of prostate cancer cells. The results obtained in this study highlight that the long-term adverse effects of Docetaxel therapy could be correlated to its ability to induce the senescent phenotype in the stromal compartment, thus generating a supportive tumor microenvironment, that further promotes prostate cancer progression and aggressiveness. In addition, this study shed new light on the use of senolytic drugs to improve Docetaxel efficacy and overcome its detrimental bystander effects in prostate cancer.
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Marwah, Mandeep Kaur. "Development of a novel deformable liposomal formulation for the dermal drug delivery of anticancer agents in the treatment of non-melanoma skin cancers". Thesis, Aston University, 2017. http://publications.aston.ac.uk/37493/.
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The incidence of skin cancer is increasing and conventional treatments such as surgery are not suitable for all patients. This study aimed to develop an elastic liposomal gel to be applied directly to the tumour for the controlled release of anti-cancer agents to the dermal layer. The proposed anti-cancer flavonoids EGCG and naringenin as well as the novel potent cytotoxic agent MTL-004 were loaded into the bilayer of liposomes. Furthermore, aqueous gels HEC and HPMC were investigated as carriers for the liposomes to be applied topically. Liposomes loaded with either Tween 80, Tween 20 or sodium cholate were found to have increased elastic properties, liposomes with an average size of 400 nm were able to pass through a pore size of 100 nm. Release studies from liposomes loaded with either EGCG, naringenin and MTL-004 as well as varying ratios of Tween 20 were carried out. Within 24 hours, EGCG liposomes loaded with 0% or 10% w/w Tween 20 gave a release of 13.7 ± 1.1 % and 94.4 ± 4.9 % respectively; naringenin liposomes loaded with 0% or 10% w/w Tween 20 gave a release of 109.7 ± 5.0 % and 48.5 ± 2.1 % respectively; MTL-004 liposomes loaded with 0% or 10% w/w Tween 20 gave a release of 59.8 ± 1.2 % and 74.0 ± 1.8 % respectively. This indicates a compounds individual physiochemical properties influences release of compound from liposomes. EGCG, naringenin and MTL-004 loaded liposomes added into the aqueous gel HEC or HPMC gels may have had an additive effect in terms of retarding drug release. Release was faster from HEC gels and liposomes formulated with Tween 20. In vitro cellular uptake of liposome uptake into HDFa and HaCat cells was apparent. Thus it appears elastic liposomes are useful in enhancing drug penetration into dermal cells and furthermore may be useful in the development of a controlled release formulation.
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Shaw, Yeng-Jeng. "Small molecule-based drug design of anticancer agents that target protein kinase B / AKT, Bcl-xL and DNA methyltransferases for the treatment of prostate cancer". Columbus, Ohio : Ohio State University, 2005. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1128693982.
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Yaacoub, Katherine. "c-FLIP as a potent anticancer target : Enhancement of cancer cell apoptosis by compounds identified through virtual screening". Thesis, Rennes 1, 2017. http://www.theses.fr/2017REN1B011/document.
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FLIP (FLICE inhibitory protein) est une protéine anti-apoptotique qui a des identités de séquence partagées avec la protéine pro-apoptotique caspase-8. FLIP se trouve en compétence avec caspase-8 pour se fixer sur la protéine adaptatrice FADD, ce qui empêche l’activation de caspase-8 bloquant ainsi l'apoptose. Lors du développement des molécules interférant avec des protéines anti-apoptotiques, la recherche d'inhibiteurs de la protéine FLIP qui est surexprimée dans un très grand nombre de cancers, a échoué. Cela s'explique en partie par le fait que peu d'information structurelle de FLIP est actuellement disponible TRAIL est une cytokine de la famille TNFα. Elle est décrite pour activer des voies de signalisation conduisant à la mort cellulaire par apoptose. TRAIL a montré un grand intérêt dans la thérapie anticancéreuse, grâce à sa capacité d’induire la mort des cellules tumorales sans aucun effet sur les cellules normales. Cependant, l’efficacité de TRAIL est limitée par plusieurs mécanismes moléculaires. Un de ces mécanismes est la surexpression de FLIP qui fait compromettre l’utilisation thérapeutique de TRAIL. Le but principal de ce projet est de développer des nouvelles molécules capables d’inhiber la protéine FLIP dans les cellules tumorales, sans aucun effet sur la protéine homologue caspase-8. Après modélisation des protéines FLIP et caspase-8 sur la base de la structure cristallographique de FLIP viral et FADD respectivement, des premières expériences d’ancrage ou “docking” utilisant une banque de composés chimiques du «National Cancer Institute NCI » ont été réalisées. Les 9 molécules les plus intéressantes, étant comme sélectives pour FLIP et non caspase 8, ont été sélectionnées et testées sur des lignées de cancer de poumons surexprimant la protéine FLIP. Une co-administration de chacune des molécules inhibitrices de FLIP avec TRAIL a été faite pour vérifier la restauration de la voie apoptotique dans les cellules cancéreuses. Un test moléculaire de « Pull down assay » a été fait afin de confirmer l’inhibition de l’interaction de FLIP avec FADD. Finalement, l’évaluation de l’activité enzymatique des caspases a été étudiée pour vérifier la réactivation de la voie apoptotique après la combinaison de TRAIL avec les inhibiteurs de c-FLIP. En conclusion, la combinaison de TRAIL avec les inhibiteurs de FLIP aboutit à la restauration de la voie apoptotique dans des cellules cancéreuses. Ces composés nouvellement identifiés, peuvent servir ultérieurement comme des potentiels éléments des stratégies utilisées dans le domaine du traitement du cancerFLIP (FLICE Inhibitory Protein) is an anti-apoptotic protein which shares sequencesimilarity with the pro-apoptotic protein caspase-8. FLIP competes with caspase-8 for binding to the adaptor protein FADD (Fas-associated death domain), thus it inhibits caspase-8 activation, thereby blocking apoptosis. During the development of molecules interfering with anti-apoptotic proteins, searching for inhibitors of FLIP protein which is overexpressed in a very large number of cancers, has failed. This is partly due to the fact that little FLIP structural information is available at present. TRAIL is a member of TNFα superfamily. It has been described to activate the apoptotic signaling pathways. TRAIL showed great interest in anti-cancer therapy, due to its ability to induce tumor cell death without any effect on normal cells. However, the efficacy of TRAIL is limited by several molecular mechanisms. One of these mechanisms is the overexpression of FLIP which is able to compromise the therapeutic use of TRAIL. The main goal of this project is to develop novel inhibitory molecules able to interfere with FLIP in tumor cells without any effect on the homologous protein caspase 8. After the construction of FLIP and caspase-8 proteins on the basis of the crystallographic structure of the viral FLIP and FADD respectively, the first docking experiments using a chemical library of the National Cancer Institute NCI have been carried out. The most interesting molecules, being selective for FLIP versus caspase 8, were selected and tested on lung cancer cell lines that overexpress FLIP protein. Co-administration of FLIP inhibitors with TRAIL was performed to verify the restoration of the apoptotic pathway in cancer cells. A molecular test of "Pull down assay" was done in order to confirm the inhibition of the FLIP/FADD interaction. Finally, the evaluation of caspases activity was carried out to confirm the reactivation of the apoptotic machinery after TRAIL/FLIP-inhibitors combination. In conclusion, the combination of TRAIL with FLIP inhibitors resulted in apoptosis restoration in resistant tumor cells. These newly identified compounds may serve later as potential elements in cancer treatment field
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Serafin, Antonio Mendes. "Cell biological responses of prostatic tumour cell lines to irradiation and anticancer drugs". Thesis, Stellenbosch : Stellenbosch University, 2003. http://hdl.handle.net/10019.1/53321.
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Thesis (PhD)--Stellenbosch University, 2003.ENGLISH ABSTRACT: The "classic" prostate cell lines, DU145, PC-3 and LNCaP, have served as a valuable cell biological model for research into prostate cancer. However, their relevance may be limited because they derive from metastatic, and not from primary normal and tumour epithelium. The cell lines (1532T, 1535T, 1542T, 1542N and BPH-l) have been derived from primary benign and malignant human tumour prostate epithelium and may be more representative. Using these cell lines I have examined the role of basic cell damage responses (repair, checkpoint activation, apoptosis and associated signalling proteins, and the influence of androgen status) in cell inactivation, and its relevance to treatment. Numerous studies have suggested that loss of p53 function leads to resistance to chemotherapeutic agents and irradiation. It is shown here that the p53-inactive cell lines are, in fact, the most sensitive to chemotherapeutic agents such as etoposide, vinblastine and estramustine, whilst the p53 wild-type cell line, LNCaP, is the most radiosensitive. Notwithstanding the effects of p53 degradation by the HPV -16 E6 viral protein, the results on chemosensitivity raises the possibility that different chemotherapeutic agents may have different p53-dependent effects in different tumour cells. Androgen deprivation is demonstrated to sensitise prostate cancer cells to chemotherapeutic agents and it is shown that the hormone independent cell lines are the most chemosensitive. The LNCaP cell line displayed an increased resistance to apoptosis induced by etoposide and gamma irradiation, suggesting that androgens are capable of protection against both these DNA damaging agents. The major factors determining radiosensitivity in human tumour cell lines are known to be DNA double-strand break (dsb) induction and repair. In the prostate cell lines I find that cellular radiosensitivity correlates with the number of DNA double-strand breaks measured within 2 hours of irradiation, and that the more radioresistant cell lines show better repair competence. Conclusions as to the influence of androgen dependence on radiosensitivity and repair are not possible at this stage since only the LNCaP cell line was androgen sensitive. The fact that the 2 hour repair period can separate radiosensitive from radioresistant cells in 2 groups of human tumour cell lines highlights the role of non-homologous end-joining repair. This has implications for therapy, and is consistent with the clinical observation that prostate tumours can be successfully controlled by low dose rate-brachytherapy. To evaluate the role of apoptosis, cells were exposed to TD50 concentrations of chemotherapeutic drugs, and 60Co y-irradiation. Apoptosis was found to be low, overall, and ranged from 0.1% - 12.1%,3.0% - 6.0% and 0.1% - 8.5% for etoposide, estramustine and vinblastine, respectively. The percentage of cells undergoing druginduced apoptosis was, on average, higher in the tumour cell lines than in the normal cell lines. Gamma irradiation-induced apoptosis levels ranged from 1.3% - 7%. The LNCaP cell line yielded the lowest percentage of apoptotic cells after exposure. The l532T cell line yielded the highest percentage of apoptotic cells after exposure. Apoptotic propensity did not rank the cell lines according to their radiosensitivity. Immunoblotting demonstrated that the apoptosis-associated proteins, bax and bcl-2, are expressed at a basal level in all the cell lines tested, but no increase was detected after exposure to TD50 doses of etoposide, vinblastine and estramustine. The ratio of bax and bcl-2 also was not altered by DNA damage. No evidence was found that a correlation may exist between reproductive cell death and the expression of genes which control apoptosis. My results show that apoptosis is not a major mechanism of drug- or radiation-induced cell death in prostate cell lines. In conclusion, loss of p53 function and loss of androgen dependence was not found to be correlated with resistance of tumours to chemotherapeutic drugs. Cellular radiosensitivity was found to be correlated with the number of DNA double-strand breaks remaining after 2 hours of repair. The more radioresistant cell lines showed better repair competence. Apoptosis and genes affecting apoptosis, such as p53 and members of the bcl-2 family, do not seem to contribute significantly to the sensitivity of prostate cancer cells to anticancer drugs and irradiation.
AFRIKAANSE OPSOMMING: Die klassieke prostaat sellyne, DU145, PC-3 en LNCaP, het 'n waardevolle bydrae gemaak in die sel biologiese model in prostaat kanker. Die toepaslikheid daarvan mag egter beperk wees, aangesien hierdie sellyne afkomstig is van metastatiese, en nie van primêr normale en tumor epiteel nie. Die sellyne 1532T, 1535T, 1542T, 1542N en BPH-I is afkomstig van primêre benigne en maligne menslike prostaat tumor epiteel en mag moontlik meer verteenwoordigend wees. Deur van hierdie sellyne gebruik te maak, is die rolondersoek van die reaksie op basiese selskade (d.w.s. herstel, beheerpunt aktivering, apoptose en verwante sein proteïene, en die invloed van androgeen status) tydens die proses van sel inaktivering, asook die toepaslikheid ten opsigte van behandeling. Volgens verskeie studies lei die verlies aan p53 funksie tot weerstandigheid teen chemoterapeutiese middels en bestraling. Die resultate van hierdie studie toon dat die p53-onaktiewe sellyne egter die sensitiefste is vir chemoterapeutiese middels, soos etoposied, vinblastien en estramustien, terwyl die p53 natuurlike-tipe sellyn, LNCaP, die meeste radiosensitief is. Ten spyte van die invloed van p53 afbraak deur die HPV -16 E6 virale proteïen, dui die resultate van chemosensitiwiteit op die moontlikheid dat verskillende chemoterapeutiese middels verskillende p53-afhanklike effekte op verskillende tumorselle mag hê. Dit is bewys dat onttrekking van androgeen prostaat kankerselle sensitiseer teen chemoterapeutiese middels en dat hormoon-onafhanklike sellyne die hoogste chemosensitiwiteit vertoon. Die LNCaP sellyn vertoon 'n verhoogde weerstandigheid teen apoptose wat deur etoposied en y-bestraling geïnduseer is, wat 'n aanduiding is dat androgene beskerming kan bied teen beide hierdie DNA beskadigingsfaktore. Die belangrikste faktore wat die radiosensitiwiteit in menslike tumorselle bepaal, IS bekend dat dit die dubbelbande van DNA verbreek en herstel. Hierdie studie het aangetoon dat in prostaat sellyne die sellulêre radiosensitiwiteit korreleer met die aantal DNA dubbelband verbrekings binne 2 uur na bestraling, en dat die meer radioweerstandige sellyne beter herstelvermoë vertoon. Gevolgtrekkings oor die invloed van androgeen se afhanklikheid van radiosensitiwiteit en herstel kan egter nie op hierdie stadium gemaak word nie, aangesien slegs die LNCaP sellyn androgeenafhanklik was. Die feit dat die 2 uur herstelperiode 'n skeiding kan maak tussen radiosensitiewe en radioweerstandige selle in twee groepe menslike tumor sellyne, onderstreep die rol van herstel van nie-homoloë endverbindings. Dit hou implikasies in vir terapie, en stem ooreen met die kliniese waarnemings dat prostaat tumore suksesvol gekontroleer kan word deur lae intensiteit dosis bragiterapie. Ten einde die rol van apoptose te ondersoek, is selle blootgestel aan TD50 konsentrasies chemoterapeutiese middels, asook 60Co y-bestraling. Apoptose was oor die algemeen laag, en het gestrek van 0.1% tot 12.1%,3.0% tot 6.0% en 0.1% tot 8.5% vir etoposied, estramustien en vinblastien onderskeidelik. Die persentasie selle wat middel geïnduseerde apoptose ondergaan het, was gemiddeld hoër in tumor sellyne as in normale sellyne. Die waardes van apoptose geïnduseer deur y-bestraling het gewissel van 1.3% tot 7.0%. Die LNCaP sellyn het die laagste persentasie apoptotiese selle na bestraling gelewer, terwyl die 1532 r sellyn die hoogste persentasie gelewer het. Die volgorde van die radiosensitiwiteit van die sellyne was nie waarneembaar in hulle geneigdheid tot apoptose nie. Immunoblots het aangetoon dat die apoptose-geassosieerde proteïene, bax en bcl-2, uitgeskei word teen 'n basisvlak in al die sellyne wat getoets is, maar dat geen verhoogde uitskeiding waarneembaar was na blootstelling aan TD50 dosisse etoposied, vinblastien en estramustien nie. Die verhouding van bax en bcl-2 is ook nie beïnvloed deur DNA beskadiging nie. Dit blyk daarom dus onwaarskynlik dat daar 'n korrelasie bestaan tussen reproduktiewe seldood en die uitskeiding van gene wat apoptose beheer. Die resultate dui daarop dat apoptose me 'n belangrike meganisme vir middel- of bestralingsgeïnduseerde seldood in prostaat sellyne is nie.
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Booker, Victoria. "Investigating the occurrence and fate of anticancer drugs in sewage treatment works and the wider aquatic environment". Thesis, Lancaster University, 2015. http://eprints.lancs.ac.uk/82556/.
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The occurrence of pharmaceuticals in wastewater and the wider environment is of growing concern. This thesis focuses on anticancer drugs - a group of biologicallypotent and often recalcitrant set of chemicals whose fate and impact on the wider freshwater environment is poorly studied. The aims of this thesis were to prioritise a group of anticancer drugs for environmental monitoring programmes (from the many drugs in use), based on their consumption and fate during wastewater treatment; to undertake a national and regional survey of two commonly used anticancer drugs, cyclophosphamide (CP) and ifosfamide (IF) in wastewater and river water; to assess the performance of a river-based chemical fate model through comparisons with field observations; and to conduct a mass balance for CP in wastewater treatment plants to assess chemical fate during the different stages of wastewater treatment. Given the large number of anticancer drugs currently in use (>70) a decision support process was developed to ascertain a short list of drugs which are most likely to persist and be released with treated effluent to environmental waters. To do this, accurate consumption data were compiled from a hospital survey in NW England and combined with urinary excretion rates derived from clinical studies. Physical– chemical property data were then compiled along with likely chemical fate and persistence during and after wastewater treatment. A shortlist of 15 chemicals (from 65), including CP and IF, was prioritised based on their consumption, persistency and likelihood of occurrence in surface waters and supported by observational studies where possible. The ecological impact of these ‘prioritised’ chemicals however is uncertain as the measured concentrations in surface waters generally fall below standard toxicity thresholds, although there is evidence that exposure of aquatic organisms to some of these chemicals may induce low-dose genotoxic effects. This prioritised sub-list of anticancer drugs should prove useful for developing environmental screening programmes and targeted toxicity assays. To assess the occurrence of anticancer drugs in wasterwaters both CP and IF were measured in raw influent and final effluent waters from fourteen STPs located across England using a sensitive analytical method. CP was detected in both wastewater influent and effluent with mean (SD) concentration of 4.1 ng/L (4.8) and 6.6 ng/L (6.5), respectively, in agreement to measured ranges from a limited number of studies conducted in Europe and elsewhere. IF was only detected in four wastewater samples with the highest concentration being observed in wastewater effluent at 0.77 ng/L (cv = 24.3% (n=3)) and possibly reflecting the relatively lower consumption of this drug relative to CP. Additional monitoring was conducted in the rivers Calder, Darwen and Ribble (North West UK) with CP present at 5 of the 6 river locations with concentrations ranging from 0.41 to 3.71 ng/L. All these rivers receive treated wastewater effluent from sewage treatment works serving different population sizes, with CP measured in river water some ~20 miles downstream of the nearest STP, indicating the widespread dispersal and persistence of this chemical. CP and IF were measured systematically down the Rivers Aire and Calder in NE England and the results compared to a GIS-based water quality model (LF2000- WQX) used to predict CP and IF distributions in the two rivers, using regional consumption data and subsequent release quantities from STPs. CP was detected in 90% of river samples, apart from rural/uplands sites located at the source of the River Aire and Calder, respectively. CP presented the highest concentration, ranging from 0.17 to 4.53 ng/L (average 1.14 ng/L). IF was seldom detected in the sampled sites and concentrations ranged from < LOD to 1.82 ng/L (average 0.51 ng/L). Model results showed a fair agreement to the measured data for CP in the River Aire, discrepancies arise as the river progressed further downstream where the modelled data was lower than the measured data. A significant input of CP from Leeds STP at A7 (STP-1) saw the continuing rise in CP despite the increase in river flow. At the lower end of the Calder (pre-confluence with the River Aire) a spike in CP is detected far beyond the modelled value. A risk assessment was carried out to establish the potential adverse effects of anticancer drugs in the river catchment. All calculated risk quotients were below 1, showing no significant risk to aquatic organisms. However, long term toxicity studies for these chemicals are needed to define the environmental stress produced by their continuous exposure and induction. The fate and removal efficiency of cyclophosphamide (CP) and ifosfamide (IF) were investigated in two conventional sewage treatment plants (STP-S and STP-C) during different stages of waste water treatment. Overall average concentrations of CP were 1.17±1 ng/L in the two plants, which is lower than recent measurements conducted elsewhere. Grab-samples were coordinated with the hydraulic residence time of wastewater in each of the treatment stages in order to monitor changes in CP concentrations in the same parcel of water as it passed through the STP. Interestingly, concentrations of CP were observed to increase from raw influent to final tertiarytreated effluent and this is likely to be attributable to the degradation of a CPmetabolite and subsequent ‘liberation’ of the parent CP as the metabolite passes through the various sewage treatment processes. This observation, apparent in both studied STPs, has implications for chemical fate modelling of anti-cancer drugs, especially if STP influent loads are used to predict subsequent fluxes to receiving waters rather than final effluent values. Moreover, this increase in concentrations made a mass balance difficult to achieve, but highlighted that elimination/removal of CP in wastewater during primary to tertiary processing is very low (<20%). The calculated fluxes of CP with final effluent discharge were 3.16- 6.48 g/year for STP-S and 4.56 -51.57 g/year for STP-C and highlight that STPs are a continuing source of highly water-soluble, recalcitrant anticancer drugs to the environment.
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Kotadia, Nayna. "A Study on the Protein Interaction with Different Platinum Compounds". TopSCHOLAR®, 2008. http://digitalcommons.wku.edu/theses/8.
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Since the discovery of anti-tumor activity of cisplatin in 1960, significant progress has been made in treating metastatic or advanced cancer with cisplatin and platinum compounds. Platinum compounds covalently bind to DNA and disrupt DNA function. They are also known to bind with amino acids like methionine, histidine and cysteine to form cisplatin-protein adducts which are responsible for most of its cytotoxicity and side effects. Recent articles on cisplatin-protein have shown that adding bulky adjuncts to cisplatin or using different platinum compounds varies the degree and extent of reaction thus possibly reducing cisplatin resistance and side effects.
One of the proteins to study is cytochrome C, which is an intermediate in apoptosis (a controlled form of cell death used to kill cells in the process of development or in response to infection or DNA damage). Cytochrome C activates caspase 9, a cysteine protease, which in turn goes on to activate caspases 3 and 7, which are responsible for destroying the cell from within.
In this study, we tried to examine how various platinum compounds like cis-Pt(NH3)2Cl2, cis-Pt(NH3)2(NO3)2, Pt(en)(NO3)2, Pt(Me4en)(NO3)2, Pt(NH3)2 (oxalate), Pt(en)(oxalate),Pt(Me4en)(oxalate), which have different ligands/bulk, react with cytochrome C in different physiological conditions.
This research project subsequently focused on three main aspects: 1) to determine whether the concentration of platinum compounds made a difference in the reaction rate, 2) to determine whether the pH of the buffer shows any difference in the reaction rate, 3) to determine how the ligands coordinated to the platinum affected the rate. We used 1) HPLC with vitamin B12 (cyanocobalamin) as an internal standard. 2) Separate samples of platinum compounds with bovine serum albumin were then subjected to dialysis and were then sent to the Materials Characterization Center for analysis by ICP-AES spectroscopy.
In summary, the following conclusions are stated: •The leaving group, pH, bulk and the concentration play a very vital role in determining the reaction rate for platinum-cytochrome C interactions. •Chlorides form excellent leaving groups followed by oxalates then nitrates. •Pt(en) reacts faster than Pt(NH3)2 which reacts faster than Pt(Me4en). •Nitrates, Pt(en) and few oxalate form multiple products showing non-specific binding. Only cis-Pt(NH3)2Cl2 and Pt(Me4en)(oxalate) formed predominately a single product showing target specific binding. •cis-Pt(NH3)2Cl2 showed an increased reaction rate at lower pH while cis-Pt(NH3)2(NO3)2 and Pt(Me4en)(NO3)2 showed higher reactions at higher pH. •Despite platinum compound was present in significant molar excess relative to cytochrome C, at the end of 21 hrs there was a significant amount of unreacted cytochrome C left except in case of cis-Pt(en)Cl2 which reacted with the whole cytochrome C in less than ten minutes. •We saw the rate of reaction in order of cis-Pt(en)Cl2 > Pt(en)(oxalate) > cis-Pt(NH3)2Cl2 > Pt(en)(NO3)2 > cis-Pt(NH3)2(NO3)2 > cis-Pt(NH3)2(oxalate) > Pt(Me4en)(oxalate) > Pt(Me4en)(NO3)2
Livros sobre o assunto "Anticancer drug treatment"
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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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Manuel, Hidalgo. Principles of anticancer drug development. New York: Springer, 2011.
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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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1946-, Lippert Bernhard, ed. Cisplatin: Chemistry and biochemistry of a leading anticancer drug. Zürich: Verlag Helvetica Chimica Acta, 1999.
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Avendaño, Carmen. Medicinal chemistry of anticancer drugs. Amsterdam: Elsevier, 2008.
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J, Houghton Peter, e Houghton Janet A, eds. Preclinical and clinical modulation of anticancer drugs. Boca Raton: CRC Press, 1993.
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1945-, Ojima Iwao, Vite Gregory D, Altmann Karl-Heinz, American Chemical Society. Division of Organic Chemistry, American Chemical Society. Division of Medicinal Chemistry e American Chemical Society Meeting, eds. Anticancer agents: Frontiers in cancer chemotherapy. Washington, DC: American Chemical Society, 2001.
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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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Lipp, H. P. Prevention and management of anticancer drug toxicity: The significance of clinical pharmacokinetics. Jena: Univ.-Verlag, 1995.
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Snapka, Robert M. The SV40 replicon model for analysis of anticancer drugs. Austin, TX: R.G. Landes, 1996.
Encontre o texto completo da fonteCapítulos de livros sobre o assunto "Anticancer drug treatment"
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Paalzow, L. K. "Therapeutical Drug Monitoring of Anticancer Drugs". In Drug Delivery in Cancer Treatment III, 85–96. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-75938-3_7.
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Paalzow, Lennart K. "Pharmacokinetic Aspects of Drug-Drug and Drug-Plastic Interactions with Anticancer Drugs". In Drug Delivery in Cancer Treatment II, 15–29. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-74709-0_3.
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Weekes, Colin D., e 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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Carden, Craig P., Hendrik-Tobias Arkenau e Johann S. de Bono. "Optimising the Development of Antibodies as Treatment for Cancer". In Principles of Anticancer Drug Development, 535–67. New York, NY: Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-7358-0_19.
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Link, Wolfgang. "Cancer Drug Resistance". In Principles of Cancer Treatment and Anticancer Drug Development, 77–85. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-18722-4_3.
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Bahnson, Robert R., Alakananda Basu e John S. Lazo. "The role of metallothioneins in anticancer drug resistance". In Cancer Treatment and Research, 251–60. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4615-3872-1_12.
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Feng, Tao, e 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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Link, Wolfgang. "Drug Discovery and Development". In Principles of Cancer Treatment and Anticancer Drug Development, 87–136. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-18722-4_4.
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Link, Wolfgang. "Economic and Social Implications of Modern Drug Discovery". In Principles of Cancer Treatment and Anticancer Drug Development, 137–39. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-18722-4_5.
Texto completo da fonteTrabalhos de conferências sobre o assunto "Anticancer drug treatment"
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Ma, Liang, Jeremy Barker, Changchun Zhou, Biaoyang Lin e 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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"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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Fernandez, Eric, Jianxiong Pang, Chris Snell, Cathy Derow, Frances Brightman, Christophe Chassagnole e 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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Zhang, Wujie, Kyle Gilstrap, Laying Wu, Melissa A. Moss, Qian Wang, Xiongbin Lu e Xiaoming He. "Controlled Release and Intracellular Delivery of Small Molecules Using Thermally Responsive Pluronic F127-Chitosan Nanocapsules". In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53517.
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Nanoscale particulate systems have been studied as the delivery vehicle of various drugs and therapeutic agents for decades with promising outcomes. Recently, nano-particulate systems that are responsive to one or more environmental stimuli (such as temperature, pH, and electromagnetic field) are attracting increasing attention because they allow drug delivery and release to be done in a more controllable fashion [1]. The thermally (temperature) responsive nanoparticles are of particular interest to many researchers because the temperature controlled release of the encapsulated drug can be conveniently done with either thermo (using supraphysiologic temperatures) or cryo (using sub-zero temperature) therapies, minimally invasive energy-based surgical techniques that have been widely studied as potential alternatives to radical surgical intervention for the treatment of cancer and other diseases. Moreover, a significantly improved outcome of cancer treatment has been reported by combining thermotherapy (using supraphysiologic temperatures) and anticancer drug encapsulated in thermally responsive nanoparticles [2]. Here, we report thermally responsive nanocapsules that can be combined with cryotherapy for cancer treatment.
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Nikkhah, Mehdi, Jeannine S. Strobl e Masoud Agah. "Study the Effect of Anticancer Drugs on Human Breast Cancer Cells Using Three Dimensional Silicon Microstructures". In ASME 2008 International Mechanical Engineering Congress and Exposition. ASMEDC, 2008. http://dx.doi.org/10.1115/imece2008-66680.
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In this paper we report development of three dimensional silicon microenvironments in order to test the morphological changes and adhesion properties of human breast cancer cells after treatment with different anticancer drugs such as Trichostatin A (TSA), suberoylanilide hydroxamic acid (SAHA) and Scriptaid. Our results indicate that the cancer cells reorganize their cytoskeleton structure after treatment with TSA and Scriptaid. However, SAHA does not change the behavior of the cells inside the three dimensional microstructures while TSA and Scriptaid evoked striking changes in the cells morphology. TSA and Scriptaid drugs cause the cells to stretch inside the isotropic microchambers to avoid contact with curved sidewalls in contrast to their originally rounded shape. The proposed microstructures can be used to evaluate mechanical properties and the pathological grade of various cancer cell lines after different conditions i.e. drug exposure.
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Sarker, Sunandita, Yiannis S. Chatzizisis, Srivatsan Kidambi e Benjamin S. Terry. "Design and Development of a Novel Drug Delivery Catheter for Atherosclerosis". In 2018 Design of Medical Devices Conference. American Society of Mechanical Engineers, 2018. http://dx.doi.org/10.1115/dmd2018-6869.
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Atherosclerosis is a chronic progressive cardiovascular disease that results from plaque formation in the arteries. It is one of the leading causes of death and loss of healthy life in modern world. Atherosclerosis lesions consist of sub-endothelial accumulations of cholesterol and inflammatory cells [1]. However, not all lesions progress to the final stage to cause catastrophic ischemic cardiovascular events [2]. Early identification and treatment of high-risk plaques before they rupture, and precipitate adverse events constitutes a major challenge in cardiology today. Numerous investigations have confirmed that atherosclerosis is an inflammatory disease [3] [4] [5]. This confirmation has opened the treatment of this disease to many novel anti-inflammatory therapeutics. The use of nanoparticle-nanomedicines has gained popularity over recent years. Initially approved as anticancer treatment therapeutics [6], nanomedicine also holds promise for anti-inflammatory treatment, personalized medicine, target-specific treatment, and imaging of atherosclerotic disease [7]. The primary aim of this collaborative work is to develop and validate a novel strategy for catheter-directed local treatment of high-risk plaque using anti-inflammatory nanoparticles. Preselected drugs with the highest anti-inflammatory efficacy will be incorporated into a novel liposome nanocarrier, and delivered in-vivo through a specially designed catheter to high-risk atherosclerotic plaques. The catheter has specially designed perfusion pores that inject drug into the blood stream in such a controlled manner that the streamlines carry the nanoparticles to the stenotic arterial wall. Once the particles make it to the arterial wall, they can be absorbed into the inflamed tissue. In this paper, we discuss the design and development of an atraumatic drug delivery catheter for the administration of lipid nanoparticles.
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Wu, Jie, Shixiong Xu, Quan Long, Michael W. Collins, Carola S. Koenig, Gaiping Zhao, Yuping Jiang e Anwar R. Padhani. "Simulation of Blood Perfusion in Tumour Microvasculature". In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176335.
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Solid tumor has become one of the most serious diseases that threaten mankind’s health and life all over the world. It is well recognized that structural and functional abnormalities of tumor vascularity and the subsequent microenvironment and cellular adaptive consequences creates a great barrier for drug delivery in solid tumors, contributing to treatment resistance. Hence, the investigation of microcirculatory dynamics in solid tumors has important significance for improving the effectiveness of many anticancer therapies.
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Taketani, Akinori, Mika Ishigaki, Bibin Bintan Andriana e Hidetoshi Sato. "Raman endoscopy for real time monitoring of anticancer drug treatment in colorectal tumors of live model mice". In SPIE BiOS, editado por Gerard L. Coté. SPIE, 2014. http://dx.doi.org/10.1117/12.2038939.
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Marković, Maja. "Controlled release of caffeine from three dimensional networks based on poly(metacrylic acid) and casein - analysis of the effect of caffeine concentration on release process". In 35th International Congress on Process Industry. SMEITS, 2022. http://dx.doi.org/10.24094/ptk.022.019.
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Everyday demands for safer and more efficient therapy for many diseases, especially serious ones such as various types of cancer, put various challenges in front of modern science. One of them lies in the fact that numerous anticancer drugs are poorly-water soluble and therefore their encapsulation and controlled release are quite demanding processes. In the present study, we deepened our research of carrier based on hydrophilic poly(methacrylic acid) modified with amphiphilic casein, in which poorly water-soluble model drug caffeine was encapsulated (PMAC-Caf hydrogels). It was investigated how neutralization degree of methacrylic acid (MAA) and amount of encapsulated caffeine affected swelling behavior of the PMAC-Caf hydrogels and caffeine release. Easy, one pot, simultaneous synthesis of the carrier and the encapsulation of caffeine is presented, obtaining thereby as prepared PMAC-Caf drug delivery system that could respond to the specific demands of the targeted delivery of the poorly water-soluble drug - protecting it in the environment which simulated human stomach and releasing it in the environment which simulated human intestines. Changing the synthesis parameters (neutralization degree of MAA and/or amount of encapsulated caffeine) we achieved controlled release of caffeine, indicating that the number of the required doses of the drug in the treatment and its side effects could be reduced. Results showed that the PMAC-Caf drug delivery systems have huge potential for controlled release of poorly water-soluble drugs.
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Nalabothula, Narasimharao, Douglas D. Ross e France Carrier. "Abstract 5498: Prognostic tools to predict the efficacy of anticancer drug treatment targeting Chromatin DNA or enzymes acting on DNA". In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-5498.
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Venedicto, Melissa, e Cheng-Yu Lai. Facilitated Release of Doxorubicin from Biodegradable Mesoporous Silica Nanoparticles. Florida International University, outubro de 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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Feltmate, Colleen. Application of Nanotechnology in the Targeted Release of Anticancer Drugs in Ovarian Cancer Treatment. Fort Belvoir, VA: Defense Technical Information Center, dezembro de 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, dezembro de 2006. http://dx.doi.org/10.21236/ada481424.
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