Relevant bibliographies by topics / Doxorubicin

Academic literature on the topic 'Doxorubicin'

Author: Grafiati
Published: 4 June 2021
Last updated: 30 July 2024

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Journal articles on the topic "Doxorubicin"

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Rahmani, Talia Putri, Yahdiana Harahap, and Denni Joko Purwanto. "A review of the relationship between Doxorubicin and Doxorubicinol, CBR1 polymorphism, and cardiotoxicity." Pharmacy Education 24, no. 6 (June 14, 2024): 105–15. http://dx.doi.org/10.46542/pe.2024.246.105115.

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Background: Doxorubicin is a chemotherapy drug given to breast cancer patients. However, its administration is limited by its cardiotoxicity. The CBR1 enzyme in the liver catalyses doxorubicin to doxorubicinol, which also contributes to its cardiotoxicity. The polymorphism of the CBR1 enzyme affects doxorubicin and doxorubicinol levels in the body. Objective: To review the effect of CBR1 polymorphisms on the levels of doxorubicin and doxorubicinol after administration of doxorubicin. Methods: Relevant studies from selected databases were examined; Three main studies with 20 support studies were reviewed. Results: The recommended methods were the analysis of doxorubicin and doxorubicinol levels using the Dried Blood Spot biosampling technique, which uses the ultra-high-performance liquid chromatography-tandem mass spectrometry (LCMS/MS), and the evaluation of the genetic profile of CBR1 using Polymerase Chain Reaction. Conclusion: Four CBR1 genetic polymorphisms have been shown to reduce doxorubicinol levels in the body, which is associated with decreased CBR1 activity and expression. Thus, the conversion of doxorubicin to doxorubicinol is reduced. Therefore, individuals who experience CBR1 polymorphisms have a lower risk of cardiotoxicity after the administration of doxorubicin.
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Fan, L., J. Y. Guo, C. I. Wong, R. Lim, H. L. Yap, Y. M. Khoo, P. Iau, B. C. Goh, H. S. Lee, and S. C. Lee. "Genetic variants in human carbonyl reductase 3 (CBR3) and their influence on doxorubicin pharmacokinetics in Asian breast cancer patients." Journal of Clinical Oncology 25, no. 18_suppl (June 20, 2007): 2505. http://dx.doi.org/10.1200/jco.2007.25.18_suppl.2505.

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2505 Background: Human carbonyl reductase 3 (CBR3) is one of the main metabolizing enzymes to extensively reduce doxorubicin to its major active metabolite, doxorubicinol in normal and tumor tissues. Recently, the CBR3 958G>A (V244M) genetic variant has been described to alter function in vitro. We postulate that CBR3 genetic variants could contribute to the inter-individual variability of doxorubicin pharmacokinetics in breast cancer patients. Methods: We studied 101 female breast cancer patients (66 Chinese, 26 Malay, 7 Indian and 2 of other ethnic origins) who were treated with doxorubicin at 75mg/m2 every 3 weeks. Comprehensive sequencing of the 3 exons of CBR3, including the splice-site junctions was performed. Plasma concentrations of doxorubicin and doxorubicinol were analyzed during the first doxorubicin cycle. Results: Five CBR3 coding region variants (239G>A, 483C>T, 507C>T, 598G>A and 958G>A) were detected, of which 239G>A, 598G>A and 958G>A were non-synonymous. 598G>A was novel, and was found in 1 Malay patient who was heterozygous. The genotype distributions of 239G>A and 958G>A were 36%/30%/34%, and 40%/36%/24% respectively for GG/AG/AA. The 239GG variant was associated with significantly higher AUC of doxorubicinol and AUC ratio of doxorubicinol to doxorubicin than the AG and AA variants (AUC of doxorubicinol 2.18±1.37ug/ml*h (GG) vs 2.04±2.11ug/ml*h (AG), p=0.05, and 1.55±0.61ug/ml*h (AA), p=0.004; AUC ratio of doxorubicinol to doxorubicin 1.90±1.29 (GG) vs 1.72±1.34 (AG), p=0.025, and 1.45±0.67 (AA), p=0.006). Patients with the 958AA variant had significantly higher AUC of doxorubicinol than those with the 958GG variant (2.29±1.60ug/ml*h vs 1.56±0.60ug/ml*h, p=0.009). The 239GG variant was more common in our population than in Caucasians (36% vs 20%. p=0.027), while the 958AA variant was more common than reported in Caucasians (24% vs 8%, p=0.014) and Japanese (24% vs 7%, p=0.016). Conclusions: CBR3 genetic variants may influence the pharmacokinetics of doxorubicin and its major metabolite doxorubicinol. Inter-ethnic differences in frequencies of CBR3 genetic variants exist and may account for differences in pharmacokinetics and pharmacodynamics of doxorubicin between different populations. No significant financial relationships to disclose.
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Choi, Won-Gu, Dong Kyun Kim, Yongho Shin, Ria Park, Yong-Yeon Cho, Joo Young Lee, Han Chang Kang, and Hye Suk Lee. "Liquid Chromatography–Tandem Mass Spectrometry for the Simultaneous Determination of Doxorubicin and its Metabolites Doxorubicinol, Doxorubicinone, Doxorubicinolone, and 7-Deoxydoxorubicinone in Mouse Plasma." Molecules 25, no. 5 (March 10, 2020): 1254. http://dx.doi.org/10.3390/molecules25051254.

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Doxorubicin, an anthracycline antitumor antibiotic, acts as a cancer treatment by interfering with the function of DNA. Herein, liquid chromatography-tandem mass spectrometry was for the first time developed and validated for the simultaneous determination of doxorubicin and its major metabolites doxorubicinol, doxorubicinone, doxorubicinolone, and 7-deoxydoxorubicinone in mouse plasma. The liquid–liquid extraction of a 10 μL mouse plasma sample with chloroform:methanol (4:1, v/v) and use of the selected reaction monitoring mode led to less matrix effect and better sensitivity. The lower limits of quantification levels were 0.5 ng/mL for doxorubicin, 0.1 ng/mL for doxorubicinol, and 0.01 ng/mL for doxorubicinone, doxorubicinolone, and 7-deoxydoxorubicinone. The standard curves were linear over the range of 0.5–200 ng/mL for doxorubicin; 0.1–200 ng/mL for doxorubicinol; and 0.01–50 ng/mL for doxorubicinone, doxorubicinolone, and 7-deoxydoxorubicinone in mouse plasma. The intra and inter-day relative standard deviation and relative errors for doxorubicin and its four metabolites at four quality control concentrations were 0.9–13.6% and –13.0% to 14.9%, respectively. This method was successfully applied to the pharmacokinetic study of doxorubicin and its metabolites after intravenous administration of doxorubicin at a dose of 1.3 mg/kg to female BALB/c nude mice.
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Tonetti, M., A. B. Astroff, W. Satterfield, A. De Flora, U. Benatti, and J. R. DeLoach. "Pharmacokinetic properties of doxorubicin encapsulated in glutaraldehyde-treated canine erythrocytes." American Journal of Veterinary Research 52, no. 10 (October 1, 1991): 1630–35. http://dx.doi.org/10.2460/ajvr.1991.52.10.1630.

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SUMMARY Canine erythrocytes were loaded with the antineoplastic drug doxorubicin and then treated with 0.16% glutaraldehyde. This procedure has been previously shown to slow down the efflux of doxorubicin from erythrocytes and to result in the selective targeting of the carrier erythrocytes to liver. Three dogs were treated each with 2 different schedules of iv bolus administration of doxorubicin (0.4 mg/kg of body weight): free drug and doxorubicin encapsulated in glutaraldehyde-treated erythrocytes. The 2 treatments yielded consistent differences in the plasma pharmacokinetic properties of doxorubicin and of its only metabolite, doxorubicinol. A triphasic exponential decay of doxorubicin plasma concentrations was observed on injection of the free drug. Conversely, in the case of erythrocyte-encapsulated doxorubicin, 4 phases of plasma concentrations of doxorubicin were found. The plasma concentrations of doxorubicinol, after a steady increase during the first hour, followed patterns of decay comparable to those of the parent drug. On the basis of the kinetic variables calculated with the 2 administration schedules, area under curve concentrations of plasma doxorubicin were 136 μg·h/L (free infusion) and 734 μ-g·h/L (erythrocyte-encapsulated drug). Significant alterations of hematologic and hematochemical factors were not observed in the 3 dogs during and after the 2 treatments. On the basis of our findings, doxorubicin-loaded and glutaraldehyde-treated erythrocytes may potentially be used in the treatment of systemic and hepatic tumors in dogs.
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Bartlett, N. L., B. L. Lum, G. A. Fisher, N. A. Brophy, M. N. Ehsan, J. Halsey, and B. I. Sikic. "Phase I trial of doxorubicin with cyclosporine as a modulator of multidrug resistance." Journal of Clinical Oncology 12, no. 4 (April 1994): 835–42. http://dx.doi.org/10.1200/jco.1994.12.4.835.

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PURPOSE To study the effects of cyclosporine (CsA), a modulator of multidrug resistance (MDR), on the pharmacokinetics and toxicities of doxorubicin. PATIENTS AND METHODS Nineteen patients with incurable malignancies entered this phase I trial. Initially patients received doxorubicin alone (60 or 75 mg/m2) as a 48-hour continuous intravenous (i.v.) infusion. Patients whose tumors did not respond received CsA as a 2-hour loading dose of 6 mg/kg and a 48-hour continuous infusion of 18 mg/kg/d with doxorubicin. Target CsA levels were 3,000 to 4,800 ng/mL (2.5 to 4.0 mumol/L). Doxorubicin doses were reduced to 40% of the prior dose without CsA, and then escalated until myelosuppression equivalent to that resulting from doxorubicin alone was observed. Doxorubicin pharmacokinetics were analyzed with and without CsA. RESULTS Thirteen patients received both doxorubicin alone and the combination of doxorubicin and CsA. Mean CsA levels were more than 2,000 ng/mL for all cycles and more than 3,000 ng/mL for 68% of cycles. Dose escalation of doxorubicin with CsA was stopped at 60% of the doxorubicin alone dose, as four of five patients at this dose level had WBC nadirs equivalent to those seen with doxorubicin alone. Nonhematologic toxicities were mild. Reversible hyperbilirubinemia occurred in 68% of doxorubicin/CsA courses. The addition of CsA to doxorubicin increased grade 1 and 2 nausea (87% v 47%) and vomiting (50% v 10%) compared with doxorubicin alone. There was no significant nephrotoxicity. Paired pharmacokinetics were studied in 12 patients. The addition of CsA increased the dose-adjusted area under the curve (AUC) of doxorubicin by 55%, and of its metabolite doxorubicinol by 350%. CONCLUSION CsA inhibits the clearance of both doxorubicin and doxorubicinol. Equivalent myelosuppression was observed when the dose of doxorubicin with CsA was 60% of the dose of doxorubicin without CsA. Understanding these pharmacokinetic interactions is essential for the design and interpretation of clinical trials of MDR modulation, and should be studied with more potent MDR modulators.
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Darrabie, Marcus D., Antonio Jose Luis Arciniegas, Jose Gabriel Mantilla, Rajashree Mishra, Miguel Pinilla Vera, Lucia Santacruz, and Danny O. Jacobs. "Exposing cardiomyocytes to subclinical concentrations of doxorubicin rapidly reduces their creatine transport." American Journal of Physiology-Heart and Circulatory Physiology 303, no. 5 (September 1, 2012): H539—H548. http://dx.doi.org/10.1152/ajpheart.00108.2012.

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Doxorubicin is commonly used to treat leukemia, lymphomas, and solid tumors, such as soft tissue sarcomas or breast cancer. A major side effect of doxorubicin therapy is dose-dependent cardiotoxicity. Doxorubicin's effects on cardiac energy metabolism are emerging as key elements mediating its toxicity. We evaluated the effect of doxorubicin on [14C]creatine uptake in rat neonatal cardiac myocytes and HL-1 murine cardiac cells expressing the human creatine transporter protein. A significant and irreversible decrease in creatine transport was detected after an incubation with 50–100 nmol/l doxorubicin. These concentrations are well below peak plasma levels (5 μmol/l) and within the ranges (25–250 nmol/l) for steady-state plasma concentrations reported after the administration of 15–90 mg/m2 doxorubicin for chemotherapy. The decrease in creatine transport was not solely because of increased cell death due to doxorubicin's cytotoxic effects. Kinetic analysis showed that doxorubicin decreased Vmax, Km, and creatine transporter protein content. Cell surface biotinylation experiments confirmed that the amount of creatine transporter protein present at the cell surface was reduced. Cardiomyocytes rely on uptake by a dedicated creatine transporter to meet their intracellular creatine needs. Our findings show that the cardiomyocellular transport capacity for creatine is substantially decreased by doxorubicin administration and suggest that this effect may be an important early event in the pathogenesis of doxorubicin-mediated cardiotoxicity.
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Maureen Okwudiri Onyebuenyi, Nsikak-Abasi Udokang, Ita Sunday Out, and Gbaranor Barina Kekii. "Assessment of the ameliorative potential of A. cepa and its fractions on doxorubicin-induced cardiotoxicity in Wistar rats." Open Access Research Journal of Biology and Pharmacy 9, no. 3 (December 30, 2023): 021–40. http://dx.doi.org/10.53022/oarjbp.2023.9.2.0057.

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The assessment of the ameliorative potentials of A. cepa and its fractions on doxorubicin-induced cardiotoxicity in Wistar rats was evaluated in this study. 45 Wistar rats of both sexes were randomly divided into 9 groups of 5 animals each; as follows: group I, served as control and received 10 ml/kg body weight of 0.9% saline, group II, 10mg/kg body weight of doxorubicin, group III, 4 mg/kg body weight of vitamin E plus Dox. Group IV, 1000mg/kg body weight of crude extracts of A. cepa plus Dox. Group V, 1000mg/kg body weight of n-hexane fraction of A. cepa plus Dox. Group VI, 1000mg/kg body weight of DCM fraction of A. cepa plus Dox. Group VII, 1000mg/kg body weight of EA fraction of A.cepa plus Dox. Group VIII, 1000mg/kg body weight of methanol fraction of A. cepa plus Dox, and group IX, combinations of 1000mg/kg, 4mg/kg 10mg/kg body weight of crude extract of A. cepa, vitamin E and Dox respectively for 16 days. Groups I and II treatments lasted 14 days, while treatments for groups III-VIII lasted 16 days (making 14 day for respective treatments and addition 2 days for doxorubin administered once 48 hourly) before sacrificing. All substances in this study were administered orally except doxorubicin that was done intravenously. The results showed that doxorubicn administration (group II) significantly (p<0.05) elevated troponin and NO levels; CK and LDH activities, compared to the control group indicating cardiotoxicity. This cardiotoxic effect of doxorubincin was significantly reversed by administration of vitamin E, crude extract, DCM, n-hexane to groups III, IV, V and VI respectively. A significant (p<0.05) reduction of only NO was recorded with EA fraction, compared with group II (dox). Methanol fraction (group VIII) further escalated doxorubicin-induced cardiotoxicity with a significantly (p<0.05) elevated myoglobulin and NO levels and CK activity. But the combined treatment with vitamin E, Crude extract and dox significantly (p<0.05) reduced cardiotoxic markers in this study except myoglobulin where a significant (p<0.05) elevation was recorded. It can be concluded that fresh A. cepa leaves extract possesses cardio-protective properties and may be a suitable cardio-protector against drug-induced cardiotoxicity in crude extract form, fractions of DCM and n-hexane but definitely not with methanol fraction as shown in this study.
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Gergely, Szabolcs, Csaba Hegedűs, Petra Lakatos, Katalin Kovács, Renáta Gáspár, Tamás Csont, and László Virág. "High Throughput Screening Identifies a Novel Compound Protecting Cardiomyocytes from Doxorubicin-Induced Damage." Oxidative Medicine and Cellular Longevity 2015 (2015): 1–12. http://dx.doi.org/10.1155/2015/178513.

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Antracyclines are effective antitumor agents. One of the most commonly used antracyclines is doxorubicin, which can be successfully used to treat a diverse spectrum of tumors. Application of these drugs is limited by their cardiotoxic effect, which is determined by a lifetime cumulative dose. We set out to identify by high throughput screening cardioprotective compounds protecting cardiomyocytes from doxorubicin-induced injury. Ten thousand compounds of ChemBridge’s DIVERSet compound library were screened to identify compounds that can protect H9C2 rat cardiomyocytes against doxorubicin-induced cell death. The most effective compound proved protective in doxorubicin-treated primary rat cardiomyocytes and was further characterized to demonstrate that it significantly decreased doxorubicin-induced apoptotic and necrotic cell death and inhibited doxorubicin-induced activation of JNK MAP kinase without having considerable radical scavenging effect or interfering with the antitumor effect of doxorubicin. In fact the compound identified as 3-[2-(4-ethylphenyl)-2-oxoethyl]-1,2-dimethyl-1H-3,1-benzimidazol-3-ium bromide was toxic to all tumor cell lines tested even without doxorubicine treatment. This benzimidazole compound may lead, through further optimalization, to the development of a drug candidate protecting the heart from doxorubicin-induced injury.
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Harahap, Yahdiana, Maria Juanita, and Baitha Palanggatan Maggadani. "ANALYTICAL METHOD VALIDATION OF DOXORUBICIN AND DOXORUBICINOL IN VOLUMETRIC ABSORPTIVE MICROSAMPLING BY LIQUID CHROMATOGRAPHY-TANDEM MASS SPECTROMETRY." Journal of Southwest Jiaotong University 56, no. 5 (October 30, 2021): 424–32. http://dx.doi.org/10.35741/issn.0258-2724.56.5.38.

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Doxorubicin is a broad-spectrum anthracycline antibiotic which has antineoplastic activity. Doxorubicin can cause cardiotoxic effects due to the formation of doxorubicinol as its main metabolite. One of the latest bio sampling methods, Volumetric Absorptive Microsampling (VAMS), has various advantages which include blood sampling by finger-prick, hematocrit does not influence it, and it can be stored at room temperature. This study aims to determine the optimum analysis conditions and sample preparation method in VAMS with daunorubicin as an internal standard, and to develop sensitive, specific measurements as well as validate the analytical method using Ultra High Performance Liquid Chromatography-Tandem Mass Spectrometry (UPLC-MS/MS). Analytical quantification analysis using mass spectrometry with a mass analyzer type is a triple quadrupole with a positive type of electrospray ionization (ESI). The separation was carried out with the Acquity® UPLC BEH C18 column (2.1 x 100 mm; 1.7 μm), with a flow rate of 0.2 mL/min, and gradient elution using 0.1% formic acid in water and 0.1% formic acid in acetonitrile for 7 minutes. Multiple reaction monitoring (MRM) values were set at m/z 544.22 > 396.9 for doxorubicin; m/z 546.22 > 398.9 for doxorubicinol; and m/z 528.5 > 362.95 for daunorubicin. Sample preparation used protein precipitation with methanol as the extracting solution, the drying time of the VAMS was 2 hours, and the sonication time was 30 minutes. LLOQ values obtained were 8 ng/mL for doxorubicin and 3 ng/mL for doxorubicinol with the linearity of 0.9904 for doxorubicin and 0.9902 for doxorubicinol.
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Bagdasaryan, Alina A., Vladimir N. Chubarev, Elena A. Smolyarchuk, Vladimir N. Drozdov, Ivan I. Krasnyuk, Junqi Liu, Ruitai Fan, Edmund Tse, Evgenia V. Shikh, and Olga A. Sukocheva. "Pharmacogenetics of Drug Metabolism: The Role of Gene Polymorphism in the Regulation of Doxorubicin Safety and Efficacy." Cancers 14, no. 21 (November 4, 2022): 5436. http://dx.doi.org/10.3390/cancers14215436.

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Breast cancer (BC) is the prevailing malignancy and major cause of cancer-related death in females. Doxorubicin is a part of BC neoadjuvant and adjuvant chemotherapy regimens. The administration of anthracycline derivates, such as doxorubicin, may cause several side effects, including hematological disfunction, gastrointestinal toxicity, hepatotoxicity, nephrotoxicity, and cardiotoxicity. Cardiotoxicity is a major adverse reaction to anthracyclines, and it may vary depending on individual differences in doxorubicin pharmacokinetics. Determination of specific polymorphisms of genes that can alter doxorubicin metabolism was shown to reduce the risk of adverse reactions and improve the safety and efficacy of doxorubicin. Genes which encode cytochrome P450 enzymes (CYP3A4 and CYP2D6), p-glycoproteins (ATP-binding cassette (ABC) family members such as Multi-Drug Resistance 1 (MDR1) protein), and other detoxifying enzymes were shown to control the metabolism and pharmacokinetics of doxorubicin. The effectiveness of doxorubicin is defined by the polymorphism of cytochrome p450 and p-glycoprotein-encoding genes. This study critically discusses the latest data about the role of gene polymorphisms in the regulation of doxorubicin’s anti-BC effects. The correlation of genetic differences with the efficacy and safety of doxorubicin may provide insights for the development of personalized medical treatment for BC patients.
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Dissertations / Theses on the topic "Doxorubicin"

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Mazevet, Marianne. "Etude de la cardiotoxicité induite par les traitements anticancéreux : Rôle d’Epac dans la cardiotoxicité induite par la Doxorubicine." Thesis, Université Paris-Saclay (ComUE), 2015. http://www.theses.fr/2015SACLS190/document.

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La doxorubicine induit un stress oxydant, des dommages à l’ADN conduisant aussi bien à la mort des cellules cancéreuses que des cardiomyocytes. De nos jours, plusieurs hypothèses non reliées à la mort cellulaire et impliquant d’autres mécanismes ou l’altération des signalisations cardiaques telles que la signalisation β-adrénergique ont émergé. Cette thèse a donc pour objectif l’étude du rôle d’Epac, facteur d’échange directement activé par l’AMP cyclique, lui-même produit après stimulation β-adrénergique, dans la cardiotoxicité induite par la doxorubicine. En effet, la doxorubicine induit une cardiomyopathie dilatée 15 semaines après traitement associée à une altération de l’homéostasie calcique. Ces altérations sont corrélées à la modulation temps et dose-dépendantes de la signalisation d’Epac. Cette même altération globale de la signalisation d’Epac a également été observée in vitro après 24h de traitement à la dox. De plus, l’inhibition spécifique d’Epac 1 a permis la prévention des dommages à l’ADN et de façon subséquente de la mort des cardiomyocytes. L’invalidation du gène d’Epac1 chez la souris a également permis la prévention in vivo des altérations de l’homéostasie calcique ainsi que de la fonction cardiaque induite par la dox. Enfin, l’inhibition d’Epac n’interfère pas avec l’efficacité antitumorale de la doxorubicine sur différentes lignées cancéreuses. En conclusion, nous avons identifié Epac comme nouvelle cible thérapeutique de la cardiotoxicité induite par la dox permettant sa prévention sans réduire l’efficacité du traitement anticancéreux
The mechanisms underlying doxorubicin (Dox)-induced cardiotoxicity involve reactive oxygen species generation, DNA intercalation and topoisomerase II (TopII) inhibition which trigger DNA damage, oxidative stress, alteration of calcium homeostasis and lead to cardiomyocyte death. Now, evidences have emerged that Dox may promote cardiotoxicity by alternative mechanisms or by signaling pathways modulation including β-adrenergic signaling unrelated directly to cell death. This study provides in vitro and in vivo evidence of the guanine exchange factor directly activated by Epac role, a guanine exchange factor directly activated by cyclic AMP produced after β-AR stimulation, in cardiotoxicity induced by doxorubicin. Indeed, Dox leads to the development of a dilated cardiomyopathy (DCM) 15 weeks post treatment in mice associated with calcium homeostasis abnormalities. These alterations were associated with time- and dose-dependent alterations of Epac signaling. The same alterations of Epac signaling were observed in vitro after 24h of dox treatment. Furthermore, we first showed that the specific pharmacologic or genetic inhibition of Epac1 but not Epac2 prevents the deleterious effects of Dox in vitro. These cardioprotection were confirmed in vivo in transgenic Knock-out Epac1 mice. Epac 1 inhibition did not interfere with the attempted Dox antitumor efficiency on tumor cell lines. Altogether, these findings identify the cAMP-binding protein, Epac, as a potential therapeutic target of dox-induced cardiotoxicity
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Chitphet, Khanidtha. "Targeted delivery of doxorubicin." Diss., University of Iowa, 2019. https://ir.uiowa.edu/etd/6924.

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Cancer is a group of diseases caused by uncontrolled cellular proliferation and dissemination. After heart disease, cancer is the second most common cause of death in the United States. Main treatment approaches for cancer are surgery, radiotherapy, chemotherapy, and immunotherapy approaches. However, cancer cells have ability to develop resistance to conventional chemotherapy thus lowering the efficacy of those chemotherapeutic agents including doxorubicin (DOX). DOX has been used for the treatment of various cancers. It is usually administered via continuous intravenous infusion. Nevertheless, the use of soluble DOX is often limited by its low therapeutic index. It has been reported that DOX-induced cardiotoxicity is a life-threatening adverse effect and DOX is also a potent vesicant that can cause tissue necrosis following injections. Therefore, this dissertation investigated alternative delivery approaches for DOX including systemic and local delivery systems for enhancing antitumor efficacy while reducing the side effects of free DOX. The first part of this research aimed at developing a formulation capable of actively targeting DOX to tumors. Advances in nanotechnology have provided new ways to delivering DOX into the body and to tumor sites. Among all active targeting ligands developed to date, cRGD peptide (cyclic arginylglycylaspartic acid) occupies a unique position owing to its inherent safety, biocompatibility, and targeting ability. Thus, cRGD was used here to decorate the surface of DOX-loaded PLGA-PEG nanoparticles (NPs) using two independent crosslink reactions, EDC-NHS and thiol-maleimide reactions. The results showed that the different modification reactions yielded NPs of similar size (110-140 nm diameter). All formulations exhibited provided similar burst release phases (of DOX) over the first 12 h followed by sustained release for up to 200 h. For in vivo antitumor activity, C57BL/6J mice carrying melanoma tumors were administered with cRGD-modified DOX-loaded PLGA-PEG NPs (equivalent to 8 μg DOX) by intravenous injection once every other day for up to four doses. Tumor volumes and survival were recorded. The toxicity of this therapy was examined using serum biomarkers including bilirubin, alanine aminotransferase (ALT), and aspartate transaminase (AST). Histopathology of organs (heart, lung, spleen, liver and kidney) was evaluated using hematoxylin and eosin staining (H&E) after euthanizing the treated mice. The results indicated that the cRGD-modified DOX-loaded PLGA-PEG NPs using PLGA-PEG-maleimide polymers (cRGD-DOX-M) demonstrated higher antitumor activity as compared to other groups (p < 0.05). Finally, administration of cRGD-modified DOX-loaded PLGA-PEG NPs had no significant effect on total bilirubin, serum ALT, serum AST levels or animal weight (P > 0.05). There were no signs of tissue damage in any of the tested organs as evaluated by H&E staining. The second part of this dissertation proposed to evaluate the therapeutic effect of combining chemotherapy and immunotherapy in a murine melanoma model. In this study, DOX-loaded PLGA-PEG NPs and anti-programmed death 1 (anti-PD-1) antibodies were chosen as the model of chemotherapy and immunotherapy, respectively. Anti-PD-1 antibodies have shown a great deal of promise in the treatment of melanoma in the clinic. In this study, DOX-loaded PLGA-PEG NPs were administered IV at a dose of 8 µg of DOX/dose per mouse once every other day (total of four injections). Mice in combination treatment groups were also administered with 200 µg of anti-PD-1 solution via intraperitoneal (IP) injection every 3 days for five doses. The combination therapy demonstrated higher antitumor efficacy in vivo as compared to control, soluble DOX, monotherapy of DOX-loaded PLGA-PEG NPs or anti-PD1 solution (p<0.05). Moreover, in vivo safety studies were investigated, and the results suggested that the combination therapy was safe. Lastly, DOX-loaded PLGA-PEG millirods were successfully fabricated by a hot-melt extrusion technique and characterized for in vitro release. It was demonstrated that DOX released from the millirods could be controlled by coating with polylactide (PLA). The locally implanted uncoated DOX- loaded PLGA millirods provided significantly greater antitumor activity against melanoma tumors in mice compared to naïve group and PLA-coated DOX-loaded PLGA millirods. Antitumor activity of the millirods was related to the release profile of DOX from the millirods. PLA-coated DOX-loaded millirods exhibited slower release of DOX compared to uncoated DOX-loaded millirods which probably explains the shorter survival time of mice treated with this formulation. Moreover, skin samples from tumor-free mice were also analyzed. The results demonstrated that uncoated and PLA-coated DOX-loaded millirods could be administered peritumorally without causing local skin necrosis. In conclusion, the novel systemic delivery system and local delivery system of DOX presented here have the potential to be used as alternative approaches for cancer therapy.
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Kalet, Brian T. "Doxorubicin and its formaldehyde conjugates." Connect to online resource, 2008. http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&res_dat=xri:pqdiss&rft_dat=xri:pqdiss:3303814.

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Finn, Nnenna Adimora. "Role of redox systems in doxorubicin metabolism and doxorubicin-mediated cell signaling: a computational analysis." Diss., Georgia Institute of Technology, 2011. http://hdl.handle.net/1853/41149.

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Insensitivity to chemotherapy is an ongoing issue in cancer treatment, one that appears to be highly dependent on patient-specific variations. It has been shown clinically that while a subset of patients will successfully respond to a particular chemotherapeutic regimen, there exists another subset of patients who when exposed to the same course of therapy will remain resistant to treatment or exhibit signs of relapse after treatment has been administered. This discrepancy raises interesting questions regarding the role that patient-specific variations play in controlling the efficacy of chemotherapy treatment regimens. Doxorubicin (Dox) is a common chemotherapeutic agent used in the treatment of a variety of solid tumors and leukemias and resistance to Dox treatment is a major issue in cancer chemotherapy, oftentimes leading to patient relapse. To gain a deeper understanding of the processes that influence Dox resistance, we must first understand the mechanisms that underlie and contribute to Dox's toxicity. To this end, the metabolic reactions that activate Dox have been implicated as major determinants of Dox cytoxicity and as possible factors that control Dox resistance in cancer cells. There are several lines of evidence that redox-dependent metabolism plays a large role in Dox toxicity. The Dox bioactivation network is comprised of a system of reduction/oxidation (redox) reactions that lead to the formation of toxic Dox metabolites and reactive oxygen species (ROS). Moreover, multi-drug resistant acute lymphoblastic leukemia cells derived from relapsed patients have elevated levels of the antioxidant glutathione and show insensitivity to Dox treatment. The redox dependence of Dox bioactivation, the understanding that Dox treatment generates ROS, and the evidence that Dox resistant cells exhibit increased antioxidant capacity, suggest the possibility that redox pathways modulate the efficacy of Dox treatment in cancer cells. The overall objectives of the proposed dissertation, therefore, were to investigate how the redox properties of the Dox bioactivation network influence Dox toxicity in acute lymphoblastic leukemia cells, and to provide evidence that cell-specific variations in the intracellular levels of these redox components influences the degree to which Dox treatment will induce cancer cell death. The significant findings of this study are that the redox reactions involved in Dox metabolism are dual-natured, containing a toxicity-generating module characterized by nicotinamide adenine dinucleotide phosphate (NADPH)-dependent Dox reductive conversion, as well as an ROS signal-generating module characterized by NADPH- and oxygen-dependent Dox redox cycling. The balance between the coupled redox reactions that comprise the toxicity- and ROS signal-generating modules of Dox bioactivation determines the sensitivity-phenotype of leukemia cells and phenotypic changes in the Dox-sensitivity of leukemia cells can be induced by the successful modulation of the Dox bioactivation network through the pharmacological inhibition of NADPH in a concentration- and cell type-dependent manner. This study highlights the importance of the intracellular redox network in controlling chemotherapy-induced ROS. The unequal distribution in antioxidant burden across the various intracellular antioxidant enzymes suggests a significant role for NADPH supply, as controlled by the enzyme glucose-6-phosphate dehydrogenase (G6PD), to the intracellular ROS buffering capacity of cells during instances of oxidative stress. Changes in G6PD activity were shown to promote protein-S-glutathionylation during oxidative stress conditions, thereby implicating G6PD in the modulation of redox-sensitive signal transduction pathways. The intracellular glutathione redox balance, a measure of the intracellular redox environment, can effectively regulate Dox-induced NF-κB signal transduction in leukemia cells. The systematic modulation of intracellular glutathione redox balance in leukemia cells by N-acetylcysteine (NAC) revealed an important role for protein S-glutathionylation mechanisms in the control of NF-κB signal transduction induced by Dox treatment. These findings identify the glutathione redox network as a potential therapeutic target for the systematic modulation of Dox sensitivity in cancer cells and elucidate the complex role that antioxidants such as NAC can play in modulating the effectiveness of Dox chemotherapy treatment regimens. Lastly, this study highlights the need for and the capacity of computational models to accurately describe the complex redox-reactions that contribute to Dox metabolism in leukemia cells. This study is groundbreaking in its use of computational modeling to analyze reversible electron transfer events between proteins using mass-action kinetics. The models developed in this study can accurately explain cytosolic doxorubicin bioactivation, intracellular hydrogen peroxide clearance, and kinase-specific S-glutathionylation, thereby showing that the use of comprehensive and/or relatively simple computational models can provide semi-quantitative predictions about the behavior of redox systems in mammalian cells as they relate to Dox-induced toxicity and Dox-induced cell signaling.
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Stallard, Sheila. "Aspects of doxorubicin resistance in breast cancer." Thesis, University of Aberdeen, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.245194.

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Less than half of all breast cancer patients respond to the anthracycline agents Epirubicin and Doxorubicin, the most effective agents available. Of those that do respond initially many eventually fail to do so. In this thesis some of the possible reasons for this failure are explored and ways of improving responses are also discussed. Doxorubicin uptake to breast cancers is examined in patients undergoing mastectomy who are given a dose pre-operatively. A range of uptakes is seen, but all tumours contained measurable levels of Doxorubicin. Intra-tumoural distribution is assessed using the auto fluorescent properties of Doxorubicin. There was variability of distribution but no gross penetration barriers were observed. To assess the range of 'inherent' variation in the sensitivity of breast cancers individual tumour cells and cells from distant normal breast were cultured in vitro from fresh specimens. Successful cultures were achieved in thirty four out of seventy three tumour samples (46%). Sixteen out of fifty for normal breast samples grew in vitro (29.6%). Chemosensitivity to Doxorubicin was measured using a short term clonogenic assay. There was a wide range in tumour sensitivities (1 x 10-7M to 6 x 10-9M) and also a marked interpatient variation in cells from normal breast (4 x 10-8M - 7 x 10-9M). In vitro sensitivities are correlated with the expression of the MDR-1 gene and gst π gene and long term clinical follow up was carried out to assess eventual responses to chemotherapy drugs and survival. The ability of a range of resistance modifying agents to overcome resistance to Doxorubicin was measured using the cell line MCF-AdrRes , and Quinidine was found to be the most effective resistance modifier.
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Sawangkoon, Suwanakiet. "Potential for carvedilol to modify doxorubicin cardiotoxicity /." The Ohio State University, 2002. http://rave.ohiolink.edu/etdc/view?acc_num=osu1486402544590225.

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Pereira, Gonçalo de Castro. "Mitochondrial Physiology During Doxorubicin-induced Selective Cardiotoxicity." Doctoral thesis, [do autor], 2012. http://hdl.handle.net/10316/21408.

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Ferreira, André. "Exercise and Doxorubicin effects on testes function." Master's thesis, Universidade de Aveiro, 2012. http://hdl.handle.net/10773/10414.

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Mestrado em Biomedicina Molecular
A Doxorubicina (DOX) é um agente antineoplásico de grande eficácia utilizado no tratamento de vários tipos de tumores. No entanto, a sua utilização clínica é limitada devido à sua toxicidade em vários órgãos, com destaque para o coração. Outros órgãos afectados por este fármaco incluem fígado, cérebro, rins e testículos. Algumas estratégias farmacológicas e não farmacológicas têm sido desenvolvidas de forma a contrariar os seus efeitos secundários tóxicos, incluindo suplementação com antioxidantes e, mais recentemente, exercício físico. Assim, o objectivo do presente estudo é avaliar o efeito da actividade física na funcionalidade testicular, bem como no stress oxidativo e apoptose, sugeridos para a acção tóxica da DOX. Trinta e seis ratos macho Sprag-Dawley foram divididos em 6 grupos: salino sedentário (SAL+SED), sedentáros tratados com doses sub-crónicas de DOX – injecções de 2mg.Kg-1 durante sete semanas (DOX+SED), salinos treinados na passadeira durante 12 semanas (SAL+TM), treinados tratados com DOX (DOX+TM), salinos realizando exercício voluntário em roda livre (SAL+FW) e tratados realizando exercício voluntário em roda livre (DOX+FW). Vinte e quatro horas depois da última sessão de exercício, os animais foram sacrificados, os espermatozóides foram obtidos e tratados para estudos de contagem e de motilidade. Os testículos foram recolhidos para posterior análise de marcadores de stress oxidativo (actividade da aconitase, concentrações de substâncias reactivas de ácido tiobarbiturico, malondialdeido (MDA) e de grupos sulfidril (-SH) e sinalização apoptotica (actividades das caspases 3,8 e 9). O tratamento com DOX induziu uma diminuição significativa na contagem e motilidade dos espermatozóides, independentemente da actividade física. Apesar de existir uma tendência para um aumento de MDA e diminuição de –SH com o tratamento com DOX, não foi detectado qualquer efeito significativo nos marcadores de stress oxidativo e apoptose. Não foi observado qualquer efeito do exercício nestes parâmetros. Concluindo, o exercício físico não influenciou o impacto que a DOX teve na funcionalidade testicular. Surpreendentemente, nem a DOX nem o exercício modularam o ambiente redox e a sinalização apoptótica nos testículos, considerando os marcadores analisados.
The anthracycline Doxorubicin (DOX) is a widely used antineoplastic agent against several tumors with high efficacy. However, the clinical use of this drug is limited by its dose-related toxicity in several organs with particular emphasis on the heart. Other organs affected by DOX include liver, brain, kidney and testes. Several pharmacological and non-pharmacological strategies have been designed to antagonize the toxic side effects of DOX, including antioxidant supplementation and, recently, physical exercise. Therefore, the aim of the present study is to analyze the effect of physical exercise in testes function as well as oxidative damage and apoptosis, suggested mechanisms by which DOX exerts its toxic effects. Thirty-six Sprag Dawley male rats were randomly divided into 6 groups as follows: Saline Sedentary (SAL+SED), Sedentary sub-chronically treated with DOX – 2mg.Kg-1 injections for 7 weeks (DOX+SED), Saline endurance treadmill trained for 12 weeks (SAL+TM), trained receiving DOX (DOX+TM), saline voluntary exercised in a free-wheel (SAL+FW) and voluntary exercised receiving DOX (DOX+FW). Twenty-four hours after the last exercise bout, animals were sacrificed; sperm was obtained and treated for counting and motility studies. Testes were harvested for tissues analysis of markers of oxidative stress and damage (aconitase activity, thiobarbituric acid reactive substances, as MDA, and sulfhydryl –SH groups content) and apoptotic signaling (caspases 3,8 and 9 activities). DOX treatment induced significant decrease in sperm count and motility, irrespective of exercise training status. Despite a tendency for MDA increase and –SH decrease with DOX treatment, no significant effect was detected in either markers of oxidative damage or apoptosis. No exercise effect was observed as well. In summary, chronic physical exercise did not influence DOX-induced testes dysfunction. Surprisingly, neither DOX nor exercise modulated testes redox environment and apoptotic signaling, at least seen by the measured markers.
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Jang, Youngmok C. "Effect of doxorubicin-induced apoptosis on gender." [Gainesville, Fla.] : University of Florida, 2003. http://purl.fcla.edu/fcla/etd/UFE0001092.

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Bengaied, Dorsaf. "Nanoparticules de resveratrol/PLAGA pour réduire la toxicité notamment hépatique de la doxorubicine." Electronic Thesis or Diss., Sorbonne Paris Cité, 2018. http://www.theses.fr/2018USPCB012.

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La doxorubicine (DOX) a été utilisée dans le traitement de divers cancers, mais son administration est limitée par une toxicité dose-dépendante. Ses effets cytotoxiques sur les cellules ont montré des cardiotoxicités, d'hépatotoxicité, d'insufisance rénale. L'utilisation des antioxydants ont été explorés pour leurs propriétés de prévention du cancer et et de la toxicité induite par DOX. Le resvératrol (RSV) est un constituant polyphénolique de plusieurs aliments principalement de raisin et de vin. Récemment, son potentiel anticancéreux a été largement exploré, révélant son effet anti-prolifératif sur différentes lignées de cellules cancéreuses, in vitro et in vivo. Le RSV est également connu pour avoir des effets modulateurs sur l'apoptose, la migration et la croissance des cellules via diverses voies de signalisation. Bien que le RSV possède une grande valeur médicinale, ses applications en tant que médicament thérapeutique sont limitées. Des problèmes tels qu'une biodisponibilité orale faible et une solubilité aqueuse médiocre font du RSV un candidat peu fiable à des fins thérapeutiques. De plus, la digestion gastro-intestinale rapide du VRS constitue également un obstacle majeur à sa traduction clinique. Par conséquent, pour surmonter ces inconvénients, nous avons fabriqué des nanoparticules de PLGA/RSV, PLGA/DOX et PLGA/RSV/DOX. Les nanoparticules de RSV ont montré des résultats prometteurs dans son absorption par le système épithélial ainsi que la livraison améliorée au site cible et de réduire l'hépatotoxicité induite par la doxorubicine
Doxorubicin (DOX) has been used in the treatment of variety of cancers but its administration is limited by a dose-dependent toxicity. Its cytotoxic effects on malignant cells, have shown an increase in the risk of cardiotoxicity, hepatoxicity, renal insufisance. Antioxydants have been explored for both their cancer preventive properties and chemodulatory of DOX toxicity. Resveratrol (RSV) is a polyphenolic constituent of several dietary mainly of grapes and wine origin recently its anti-cancer potential has been extensively explored, revealing its anti-proliferative effect on different cancer cell lines, both in vitro and in vivo. RSV is also known to have modulatory effects on cell apoptosis, migration and growth via various signaling pathways. Though, RSV possesses great medicinal value, its applications as a therapeutic drug are limited. Problems like low oral bioavailability and poor aqueous solubility make RSV an unreliable candidate for therapeutic purposes. Additionally, the rapid gastrointestinal digestion of RSV is also a major barrier for its clinical translation. Hence, to overcome these disadvantages RSV-based nanodelivery systems have been considered in recent times.we used nanodelivery systems of RSV, DOX and DOX/RSV have shown promising results in its uptake by the epithelial system as well as enhanced delivery to the target site and reduce the hepatotoxicity induced by doxorubicin
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Books on the topic "Doxorubicin"

1

Ramji, Shairoj. Bioactivation of doxorubicin by human NADPH-cytochrome P450 reductase. Ottawa: National Library of Canada, 1998.

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Bengoa-Becerra, Cristina. Prospective comparison of adriamycin, vinblastine, and mitomycin C (AVM) versus adriamycin alone in the treatment of metastatic breast cancer. [New Haven: s.n.], 1988.

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Möhrer, Birgit. Aufnahme der I-123-markierten Anthrazykline Doxorubicin und Iododoxorubicin in kultivierte Mammacarzinomzellen. [s.l.]: [s.n.], 1997.

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Kampe-Juzak, Eva Christina. Liposomales Doxorubicin versus Bleomycin-Vincristin: Vergleich der Effektivität beim HIV-assoziierten Kaposi Sarkom. [s.l.]: [s.n.], 1999.

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Eng, Jamei R. Pharmacogenomics of paclitaxel and doxorubicin resistance in human MCF-7 breast cancer cell lines. Sudbury, Ont: Laurentian University, 2004.

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C, Forbes, National Co-ordinating Centre for HTA (Great Britain), and Health Technology Assessment Programme, eds. A Systematic review and economic evaluation of pegylated liposomal doxorubicin hydrochloride for ovarian cancer. Southampton: NCCHTA, 2002.

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C, Forbes, National Co-ordinating Centre for HTA (Great Britain), and Health Technology Assessment Programme, eds. A systematic review and economic evaluation of pegylated liposomal doxorubicin hydrochloride for ovarian cancer. Alton: Core Research on behalf of the NCCHTA, 2002.

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Traunecker, Heidi. The biology of drug resistance in human sarcoma cells following a brief exposure to doxorubicin. Birmingham: University of Birmingham, 1999.

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German-Italian, Oncological Symposium (3rd 1984 Venice Italy). Progress in hormono- and chemotherapy. Freiburg: Kehrer, 1985.

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Beaumont, Peter Orton. Role of glutathione S-transferases in the resistance of human colon cancer cell lines to doxorubicin. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1999.

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Book chapters on the topic "Doxorubicin"

1

Mader, Ines, Patrizia Fürst-Weger, Robert M. Mader, Elisabeth I. Semenitz, Robert Terkola, and Sabine M. Wassertheurer. "Doxorubicin." In Paravasation von Zytostatika, 131–43. Vienna: Springer Vienna, 2002. http://dx.doi.org/10.1007/978-3-7091-3799-4_22.

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Mader, Ines, Patrizia Fürst-Weger, Robert Mader, Elisabeth Nogler-Semenitz, and Sabine Wassertheurer. "Doxorubicin." In Extravasation of Cytotoxic Agents, 195–212. Vienna: Springer Vienna, 2010. http://dx.doi.org/10.1007/978-3-211-88893-3_29.

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Mader, Ines, Patrizia E. Fürst-Weger, Robert M. Mader, Elisabeth I. Semenitz, Robert Terkola, and Sabine M. Wassertheurer. "Doxorubicin." In Extravasation of Cytotoxic Agents, 120–30. Vienna: Springer Vienna, 2003. http://dx.doi.org/10.1007/978-3-7091-3710-9_22.

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Mader, Ines, Patrizia Fürst-Weger, Robert Mader, Elisabeth Nogler-Semenitz, and Sabine Wassertheurer. "Doxorubicin liposomal, Doxorubicin pegylated liposomal." In Extravasation of Cytotoxic Agents, 213–17. Vienna: Springer Vienna, 2010. http://dx.doi.org/10.1007/978-3-211-88893-3_30.

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Mader, Ines, Patrizia Fürst-Weger, Robert M. Mader, Elisabeth I. Semenitz, Robert Terkola, and Sabine M. Wassertheurer. "Doxorubicin liposomal." In Paravasation von Zytostatika, 144–47. Vienna: Springer Vienna, 2002. http://dx.doi.org/10.1007/978-3-7091-3799-4_23.

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Guerrieri, Patrizia, Paolo Montemaggi, Volker Budach, Carmen Stromberger, Volker Budach, Volker Budach, Anthony E. Dragun, et al. "Liposomal Doxorubicin." In Encyclopedia of Radiation Oncology, 450. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-540-85516-3_326.

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Kapoor, Amar S. "Doxorubicin Cardiotoxicity." In Cancer and the Heart, 227–31. New York, NY: Springer New York, 1986. http://dx.doi.org/10.1007/978-1-4612-4898-9_21.

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Mader, Ines, Patrizia E. Fürst-Weger, Robert M. Mader, Elisabeth I. Semenitz, Robert Terkola, and Sabine M. Wassertheurer. "Doxorubicin liposomal." In Extravasation of Cytotoxic Agents, 131–33. Vienna: Springer Vienna, 2003. http://dx.doi.org/10.1007/978-3-7091-3710-9_23.

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Rossini, L., E. Monti, D. Cova, and F. Piccinini. "Determination of Doxorubicin and Doxorubicin-3-ol in Rat Heart." In Archives of Toxicology, 474–78. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-71248-7_102.

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Kratz, Felix. "Acid-Sensitive Prodrugs of Doxorubicin." In Topics in Current Chemistry, 73–97. Berlin, Heidelberg: Springer Berlin Heidelberg, 2007. http://dx.doi.org/10.1007/128_2007_5.

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Conference papers on the topic "Doxorubicin"

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Tsvetkov, Ivan, Natalia Zolotova, Anna Kosyreva, Dzhuliia Dzhalilova, Liliya Mikhailova, Vera Kudelkina, Artem Shelkov, Olga Makarova, Valeriy Chernikov, and Victoria Razzhivina. "Morphological Value of Nephrotoxic Effects of Doxorubicin and PLGA-Doxorubicin." In ECMS 2021. Basel Switzerland: MDPI, 2021. http://dx.doi.org/10.3390/ecms2021-10834.

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Bajic, Dragana, Vladislav Pajovic, Marija Matic, Marko Vasic, Olivera Sarenac, and Nina Japundzic-Zigon. "Phenomapping Doxorubicin-induced Cardiomyopathy." In 2020 11th Conference of the European Study Group on Cardiovascular Oscillations (ESGCO). IEEE, 2020. http://dx.doi.org/10.1109/esgco49734.2020.9158036.

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Lichtenfels, Martina, Camila Alves da Silva, Alessandra Borba Anton de Souza, Heloisa Rezende, Luiza Kobe, Isabela Miranda, Antônio Luiz Frasson, and Caroline Brunetto de Farias. "VALIDATION OF A NOVEL IN VITRO BREAST CANCER CHEMORESISTANCE PLATFORM IN NEOADJUVANT SETTING." In Brazilian Breast Cancer Symposium 2022. Mastology, 2022. http://dx.doi.org/10.29289/259453942022v32s2013.

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Objective: The aim of this study was to validate a novel in vitro chemoresistance platform for two drugs commonly used in the neoadjuvant setting for breast cancer (BC). Methods: Three BC cell lines (MCF-7 (luminal); SKBR3 (HER2+); and MDA-MB-231 (triple-negative) were used to confirm the efficacy of the platform. Patients with invasive BC and partial response to neoadjuvant chemotherapy were included in this initial report. Fresh tumor samples were collected during surgery and dissociated to obtain the tumor cells. The tumor cells were cultured in the chemoresistance platform with doxorubicin and paclitaxel and after 72-h cell viability was evaluated. The test result is defined based on cell viability as low (60%) resistance. Results: The three BC cell lines presented low resistance to doxorubicin, MCF-7 and SKBR3 cells also presented low resistance to paclitaxel, whereas MDA-MB-231 has intermediate resistance. Samples from 10 BC patients with partial response to neoadjuvant chemotherapy were tested in the novel chemoresistance platform. All the patients received doxorubicin and paclitaxel as part of the treatment. The overall rate of assay success was 100%. Regarding molecular subtypes, 40% were Luminal, 20% Luminal HER2, 10% HER2, and 30% triple-negative. The 10 samples presented 100% high resistance to paclitaxel. High resistance to doxorubicin was observed in 70% of the samples, intermediate in 10%, and low in 20%. The chemoresistance platform demonstrated that samples already treated with paclitaxel and doxorubicin in a neoadjuvant setting presented more high resistance to the drugs compared to the BC cell lines. Conclusion: This preliminary result demonstrated more high resistance in tumors previously treated with doxorubicin and paclitaxel compared to BC cell lines without previous treatment and highlighted the success of the in vitro chemoresistance platform to test tumor samples after neoadjuvant treatment.
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Popova, V. K., and E. V. Dmitrienko. "MAGNETIC NANOHYBRIDS OF MIXED IRON OXIDE AND CALCIUM CARBONATE FOR TARGETED DOXORUBICIN DELIVERY." In X Международная конференция молодых ученых: биоинформатиков, биотехнологов, биофизиков, вирусологов и молекулярных биологов — 2023. Novosibirsk State University, 2023. http://dx.doi.org/10.25205/978-5-4437-1526-1-114.

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This work is aimed at obtaining and studying the properties of calcium carbonate nanoparticles (NPs) and their composites with mixed iron oxide less than 200 nm in size. High binding efficiency of NPs with doxorubicin and nucleic acids, as well as pH-dependent degradation profile of drug interaction were demonstrated. The PMs have no toxic effect, and their doxorubicin-bound version is not inferior in efficacy to the individual drug.
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Lichtenfels, Martina, Vivian Fontana, Francine Hickmann Nyland, Bianca Silva Marques, Mário Casales Schorr, Júlia Caroline Marcolin, Caroline Brunetto de Farias, and José Luiz Pedrini. "What happens in residual disease after neoadjuvant chemotherapy? Efficacy of a novel in vitro breast cancer chemoresistance platform to demonstrate high resistance to drugs." In Brazilian Breast Cancer Symposium 2023. Mastology, 2023. http://dx.doi.org/10.29289/259453942023v33s1010.

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Objective: Our preliminary study aimed to validate the efficacy of a novel in vitro chemoresistance platform to demonstrate tumor resistance in residual disease after neoadjuvant treatment for breast cancer. Methodology: Patients with invasive BC who presented residual disease after neoadjuvant chemotherapy (NACT) were included. Fresh tumor samples were collected during surgery and dissociated to obtain the tumor cells. The tumor cells were cultured in the chemoresistance platform with doxorubicin, epirubicin, paclitaxel, docetaxel, and cyclophosphamide, and after 72 h, cell viability was evaluated. The test result is defined based on cell viability as low (60%) resistance. Results: Samples from 20 patients with residual disease after NACT were tested in the chemoresistance platform. Regarding molecular subtypes: 9 tumors were triple-negative (45%), 6 luminal (30%), 4 LuminalHER2 (20%), and 1 HER2 (5%). A total of 16 (80%) patients responded partially to NACT, and 4 (20%) presented disease progression. Most (80%) of the patients used ACT (doxorubicin + cyclophosphamide + paclitaxel) chemotherapy regimen, 10% only paclitaxel, and 10% doxorubicin plus cyclophosphamide. The chemoresistance platform demonstrated that tumors treated with doxorubicin, paclitaxel, and cyclophosphamide in neoadjuvant setting presented high rates of resistance to the drugs (94.7% showed high resistance to paclitaxel, 58% to doxorubicin, and 52.6% to cyclophosphamide). In addition, we investigate if the tumor becomes more resistant to drugs from the same class (taxanes and adriamycin) of the treatment already used by the patients and evidenced 93.7% of high resistance to docetaxel and 50% to epirubicin. Conclusion: This preliminary finding highlighted the efficacy of the in vitro chemoresistance platform to demonstrate the acquisition of resistance during NACT and suggested a role of acquired resistance in the worse prognosis of patients with residual disease after NACT.
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Soares, Leonardo Ribeiro, Nathállia Alamino Silva, Pedro Vinicyus Novais e. Souza, Alexandre Roriz Blumenschein, and Nayara Alves Freitas Lemos. "Multidisciplinary treatment after doxorubicin extravasation: Improvement of range of motion in the elbow joint." In Brazilian Breast Cancer Symposium 2023. Mastology, 2023. http://dx.doi.org/10.29289/259453942023v33s1060.

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Introduction: Chemotherapy extravasation is an infrequent complication with challenging consequences for the patient and the care team. Doxorubicin is a chemotherapeutic used in the treatment of breast cancer, being classified as a DNAbinding vesicant agent, and its spillage into the interstitial space can lead to severe tissue damage. The acute condition includes pain, hyperemia, edema, ulceration, and necrosis in the region, evolving with fibrosis, restriction of range of motion (ROM), and other chronic sequelae. Objective: The objective of this study was to describe the multidisciplinary treatment of a case of Doxorubicin extravasation with ROM restriction in the elbow joint. Report: A female, 29 years old, with invasive ductal carcinoma, cT2N1M0, with luminal phenotype B. Neoadjuvant chemotherapy was initiated with AC scheme (Doxorubicin + Cyclophosphamide). There was a suspicion of extravasation in the peripheral access (cubital fossa) during the application of Doxorubicin in the first cycle. Topical treatment with corticosteroids was started, but the patient developed burning sensation, edema, and local hyperemia. In the following days, oral corticosteroids, antibiotics, and dimethylsulfoxide (DMSO) were added, followed by physiotherapy. Despite partial improvement, the patient evolved with skin hyperpigmentation, tissue fibrosis, restriction of elbow extension movement, and arm retraction at 90º, making it difficult to perform domestic and daily activities. After oncological surgical treatment, zetaplasty was performed on the affected arm, with an increase in ROM of about 20º. Subsequently, with the intensification of physiotherapy and pilates sessions, the patient achieved a global improvement of 30º and returned to most daily activities. Thus, we describe a case of Doxorubicin extravasation with chronic sequelae, which was managed by a multidisciplinary team. In this context, physiotherapy played a key role in improving the patient’s ROM and returning to daily activities.
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Ryu, Jung Su, and Drazen Raucher. "Abstract 5129: Cell-penetrating doxorubicin released from Elastin-like polypeptide kills doxorubicin-resistant cancer cells." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-5129.

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Goukassian, David, Sharath Sasi, Juyong Lee, Daniela Budiu, Christopher Lawson, Michael Maysky, Lynn Hlatky, Joseph Carrozza, James P. Morgan, and Xinhua Yan. "Abstract 1209: Concurrent administration of doxorubicin and lapatinib worsens doxorubicin-induced cardiac dysfunction in mice." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-1209.

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Lafeuille, M., R. McKenzie, N. Yameogo, M. Senbetta, F. Vekeman, C. Piech, and P. Lefebvre. "Evaluation of Cardiac Comorbidities in Patients with Metastatic Breast Cancer Receiving Doxorubicin-Based and Non-Doxorubicin-Based Chemotherapy." In Abstracts: Thirty-Second Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 10‐13, 2009; San Antonio, TX. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.sabcs-09-2078.

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Mete, Derya, Nesrin Horzum, and Gülşah Şanlı Mohamed. "Controlled Release of Doxorubicin from Electrospun Gelatin Nanofibers." In The World Congress on Recent Advances in Nanotechnology. Avestia Publishing, 2016. http://dx.doi.org/10.11159/nddte16.126.

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Reports on the topic "Doxorubicin"

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Sridhar, Rajagopalan. Chemomodulation of Doxorubicin Pharmacodynamics. Fort Belvoir, VA: Defense Technical Information Center, October 1999. http://dx.doi.org/10.21236/ada384287.

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

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Abstract:
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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Morris, Marilyn E. Organic Isothiocyanates: Dietary Modulators of Doxorubicin Resistance in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, June 2004. http://dx.doi.org/10.21236/ada427922.

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Sahin, Aysegul A. Treatment of Metastatic Breast Carcinoma Refractory to Doxorubicin with Liposomal-Annamycin. Fort Belvoir, VA: Defense Technical Information Center, October 2001. http://dx.doi.org/10.21236/ada411291.

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Sahin, Aysegul A. Treatment of Metastatic Breast Carcinoma Refactory to Doxorubicin with Liposomal-Annamycin. Fort Belvoir, VA: Defense Technical Information Center, October 1999. http://dx.doi.org/10.21236/ada391551.

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Sahin, Aysegul A. Treatment of Metastatic Breast Carcinoma Refractory to Doxorubicin with Liposomal-Annamycin. Fort Belvoir, VA: Defense Technical Information Center, October 2000. http://dx.doi.org/10.21236/ada393780.

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Sachdeva, Mandip S. Reversal of Doxorubicin Resistance in Human Breast Adenocarcinoma (MCF-7) Cells by Liposomal Monensin. Fort Belvoir, VA: Defense Technical Information Center, June 2005. http://dx.doi.org/10.21236/ada443420.

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Sachdeva, Mandip S., and Krishna Agrawal. Reversal of Doxorubicin Resistance in Human Breast Adenocarcinoma (MCF-7) Cells by Liposomal Monensin. Fort Belvoir, VA: Defense Technical Information Center, May 2002. http://dx.doi.org/10.21236/ada405579.

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Gabrielson, Kathleen L. Akt Rescue in Cardiomyocytes but not Breast Cancer Cells after Doxorubicin and Anti-erbB2 Treatment. Fort Belvoir, VA: Defense Technical Information Center, April 2005. http://dx.doi.org/10.21236/ada435439.

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Koch, Tad H. Mechanisms for Breast Cancer Cell Resistance to Doxorubicin and Solutions to Resistance and Side Effects. Fort Belvoir, VA: Defense Technical Information Center, October 2000. http://dx.doi.org/10.21236/ada393325.

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