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Articoli di riviste sul tema "Anthracyclines"

1

Sorensen, K., G. Levitt, D. Sebag-Montefiore, C. Bull e I. Sullivan. "Cardiac function in Wilms' tumor survivors." Journal of Clinical Oncology 13, n. 7 (luglio 1995): 1546–56. http://dx.doi.org/10.1200/jco.1995.13.7.1546.

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PURPOSE To study late cardiac function in a single diagnostic group (children with Wilms' tumor) with good long-term survival; to compare patients treated with anthracyclines (doxorubicin) with patients treated without anthracyclines and with a normal child/adolescent group; and to examine the risk factors involved in late cardiac dysfunction. PATIENTS AND METHODS Echocardiographic studies were performed on 97 Wilms' tumor patients treated with anthracyclines (mean cumulative dose, 303 mg/m2) with a mean follow-up time of 7.1 years, on 39 Wilms' tumor patients treated without anthracyclines with a mean follow-up time of 8.9 years, and on 50 normal subjects. Left ventricular (LV) dimensions, end systolic wall stress (a measure of afterload), and load-dependent and -independent measures of contractility were compared between groups. Potential risk factors, including age at diagnosis, follow-up duration, sex, pubertal status, cardiac irradiation, dose-intensity, and cumulative dose of anthracyclines, were studied by multivariate analysis. RESULTS Twenty-five percent of the anthracycline-treated group showed cardiac abnormalities. All but one of these patients had increased LV afterload. Risk factors for increased afterload were anthracycline cumulative dose (P < .05) and anthracycline dose-intensity (P < .02). Wilms' tumor patients treated without anthracyclines had thickened LV walls compared with normal subjects (P < .05). CONCLUSION Total dose and dose-intensity of anthracycline were risk factors for increased LV afterload in long-term Wilms' tumor survivors treated on standard protocols. The increase in afterload accounted for reduced LV shortening, whereas contractility was rarely abnormal. The new finding that Wilms' tumor survivors who do not receive anthracyclines have mild LV hypertrophy may provide some protection against anthracycline-induced cardiotoxic effects.
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Krook, James Edward, Akhil Kumar, Marc L. Fishman, William S. Shimp, Laura Rose Bobolts, Val Fishman, Sharon Davis et al. "Community use of anthracyclines in metastatic breast cancer (MBC)." Journal of Clinical Oncology 31, n. 15_suppl (20 maggio 2013): 1080. http://dx.doi.org/10.1200/jco.2013.31.15_suppl.1080.

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1080 Background: For decades, anthracyclines have been among the most useful treatments for women with MBC. Though recent publications have confirmed an overall decline in the use of anthracyclines in BC, most of that decline was felt to be due to its diminished utilization in the adjuvant management of BC. Current community anthracycline usage pattern in MBC is not known. We investigate and report, herein, how community oncologists in the southeast USA are currently utilizing anthracyclines for MBC. Methods: All chemotherapy treatment requests for HER2+ and HER2- Stage 4 BC were examined, from 2009 through 2012. Chi-Square test was performed for interaction between age and anthracycline utilization, with p-value less than 0.05 considered significant. The proportion of women who had been treated previously in the adjuvant setting with low cumulative doses of anthracyclines, which would have some effect upon subsequent use, was not retrievable. Results: During this span, 420 unique chemotherapy requests were initiated for 247 patients. These included 54 anthracycline requests for 50 MBC patients. The use of anthracyclines for metastatic HER2+ BC was virtually absent (one in 63 requests among 42 patients). The remaining 357 chemotherapy requests were for treatment of 205 HER2- MBC patients. Anthracyclines were employed in 22% of women under 65 years of age and in 25% of those older than 65 (p = 0.77). Approximately 83% (45/54) of anthracycline-requests were for conventional doxorubicin, either alone or in combination with other agents. The rest were for liposomal doxorubicin (6/54) or epirubicin (3/54). Conclusions: Data from the southeast USA identifies that anthracyclines are virtually never used in HER2+ MBC. Even in HER2- MBC, anthracyclines are used in only one out of 4 patients suffering from this disease. The effect of this unheralded alteration in oncology practice must be carefully considered when trends in metastatic breast cancer control are examined. [Table: see text]
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Kumar, Akhil, Marc L. Fishman, William S. Shimp, Laura Rose Bobolts, James Edward Krook, Val Fishman, Sharon Davis et al. "Community use of anthracyclines for adjuvant HER2-positive breast cancer (BC)." Journal of Clinical Oncology 31, n. 15_suppl (20 maggio 2013): e11609-e11609. http://dx.doi.org/10.1200/jco.2013.31.15_suppl.e11609.

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e11609 Background: Anthracyclines remain among the most active agents for the treatment of BC. NSABP B-31, NCCTG N9831 and HERA, each employing anthracyclines followed by trastuzumab in adjuvant HER2+ BC, demonstrated significant reduction in the risk of recurrence and improvement in survival. A fourth study, BCIRG-006, compared a non-anthracycline containing regimen, TCH, to an anthracycline based regimen, AC-TH. Both arms had similar overall survival, but there was a higher incidence of cardiac events in patients who received anthracycline. HER2-analyses in randomized adjuvant trials, in the pre-trastuzumab era, comparing anthracycline with non-anthracycline chemotherapy regimens, show that HER2+ BC derives greater benefit from anthracycline use. TOP2A coamplification, which occurs in 35% of HER2-positive patients, has shown a direct association with anthracycline benefit in several studies. We investigate and report, herein, the ways in which community oncologists are currently treating these patients. Methods: All treatment requests for adjuvant trastuzumab were examined, from 2009 through 2012. Chi-square analysis at 0.05α was used to test for interaction of age group to type of treatment. Results: During this span, oncologists requested adjuvant trastuzumab for 121 patients. In 10% (12/121) of patients, adjuvant trastuzumab alone, without chemotherapy and with or without hormonal therapy, was requested. Among patients who also received adjuvant chemotherapy (109), 35% (38/109), received anthracyclines. There was no relationship of anthracycline-usage with BC stage (data not shown) or patient age (Chi Sq p = 0.73). Adjuvant trastuzumab, without chemotherapy, was requested more often for the elderly (20% versus 4%; Chi Sq p = 0.003). Conclusions: Anthracyclines are utilized in adjuvant HER2+ BC in only about a third of patients, regardless of BC stage or patient age. The availability of a reliable, inexpensive, and convenient test to predict which patients are most likely to benefit from anthracyclines, over other options, would be useful. [Table: see text]
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Neppelenbroek, Suzanne I. M., Yvonne M. Geurts, Berthe M. P. Aleman, Cecile P. M. Janus, Saskia E. Rademakers, Roel J. de Weijer, Richard W. M. Van Der Maazen et al. "Anthracycline exposure and breast cancer risk in female Hodgkin lymphoma survivors." Journal of Clinical Oncology 39, n. 15_suppl (20 maggio 2021): 12074. http://dx.doi.org/10.1200/jco.2021.39.15_suppl.12074.

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12074 Background: Female Hodgkin lymphoma (HL) survivors treated with chest radiotherapy (RT) at a young age have a strongly increased risk of breast cancer (BC). Recently concern has been raised that anthracyclines may also increase BC risk, based on studies in childhood cancer survivors with/without a history of chest RT. So far, the association between anthracyclines and BC risk has not been examined in cancer survivors treated at adolescent/adult ages. Now that RT dose and volumes are decreasing, the potential contribution of anthracyclines to BC risk is an important issue. Methods: We assessed BC risk in a cohort of 2314 female 5-year HL survivors, treated at ages 15-50 years and diagnosed between 1965 and 2008 in 20 Dutch hospitals. Treatment factors were time-dependently included in the analysis, focusing on the effect of anthracycline exposure on BC risk. Results: After a median follow-up of 18.8 years, 258 women developed invasive BC or ductal carcinoma in situ as a subsequent malignancy. The 30-year cumulative incidence was 15.0% (95% Confidence Interval (CI) 12.8-17.4%). Mantle field RT (or other RT involving both axillae) was associated with increased risk of BC (Hazard ratio (HR) 1.9; 95% CI 1.2-2.8) compared to no supradiaphragmatic RT or RT to the neck only (Table 1). Gonadotoxic treatment (>4.2 g/m2 procarbazine or pelvic RT) significantly decreased this risk. In a multivariable analysis, anthracycline exposure was associated with increased BC risk (HR 1.8; 95% CI 1.3-2.5) in patients who received a cumulative dose of >200 mg/m2. Among patients exposed to gonadotoxic treatment, the HR of BC associated with >200mg/m2 anthracyclines was 3.8 (95% CI 2.0-7.2), with a trend for higher risk with higher anthracycline dose (HR 1.58 per 100mg/m2 anthracycline, p<0.001). Conclusions: Our results suggest an association of anthracyclines with BC risk in HL survivors. Also when accounting for the protective effect of gonadotoxic treatment on RT-associated BC risk, anthracyclines significantly contributed to a higher BC risk.[Table: see text]
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Blanco, Javier G., Can-Lan Sun, Wendy Landier, Lu Chen, Diego Esparza-Duran, Wendy Leisenring, Allison Mays et al. "Anthracycline-Related Cardiomyopathy After Childhood Cancer: Role of Polymorphisms in Carbonyl Reductase Genes—A Report From the Children's Oncology Group". Journal of Clinical Oncology 30, n. 13 (1 maggio 2012): 1415–21. http://dx.doi.org/10.1200/jco.2011.34.8987.

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Purpose Carbonyl reductases (CBRs) catalyze reduction of anthracyclines to cardiotoxic alcohol metabolites. Polymorphisms in CBR1 and CBR3 influence synthesis of these metabolites. We examined whether single nucleotide polymorphisms in CBR1 (CBR1 1096G>A) and/or CBR3 (CBR3 V244M) modified the dose-dependent risk of anthracycline-related cardiomyopathy in childhood cancer survivors. Patients and Methods One hundred seventy survivors with cardiomyopathy (patient cases) were compared with 317 survivors with no cardiomyopathy (controls; matched on cancer diagnosis, year of diagnosis, length of follow-up, and race/ethnicity) using conditional logistic regression techniques. Results A dose-dependent association was observed between cumulative anthracycline exposure and cardiomyopathy risk (0 mg/m2: reference; 1 to 100 mg/m2: odds ratio [OR], 1.65; 101 to 150 mg/m2: OR, 3.85; 151 to 200 mg/m2: OR, 3.69; 201 to 250 mg/m2: OR, 7.23; 251 to 300 mg/m2: OR, 23.47; > 300 mg/m2: OR, 27.59; Ptrend < .001). Among individuals carrying the variant A allele (CBR1:GA/AA and/or CBR3:GA/AA), exposure to low- to moderate-dose anthracyclines (1 to 250 mg/m2) did not increase the risk of cardiomyopathy. Among individuals with CBR3 V244M homozygous G genotypes (CBR3:GG), exposure to low- to moderate-dose anthracyclines increased cardiomyopathy risk when compared with individuals with CBR3:GA/AA genotypes unexposed to anthracyclines (OR, 5.48; P = .003), as well as exposed to low- to moderate-dose anthracyclines (OR, 3.30; P = .006). High-dose anthracyclines (> 250 mg/m2) were associated with increased cardiomyopathy risk, irrespective of CBR genotype status. Conclusion This study demonstrates increased anthracycline-related cardiomyopathy risk at doses as low as 101 to 150 mg/m2. Homozygosis for G allele in CBR3 contributes to increased cardiomyopathy risk associated with low- to moderate-dose anthracyclines, such that there seems to be no safe dose for patients homozygous for the CBR3 V244M G allele. These results suggest a need for targeted intervention for those at increased risk of cardiomyopathy.
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Rybczyńska-Tkaczyk, Kamila. "Enhanced Efficiency of the Removal of Cytostatic Anthracycline Drugs Using Immobilized Mycelium of Bjerkandera adusta CCBAS 930". Molecules 26, n. 22 (12 novembre 2021): 6842. http://dx.doi.org/10.3390/molecules26226842.

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The aim of this study was to evaluate the bioremoval of anthracycline antibiotics (daunomycin-DNR, doxorubicin–DOX, and mitoxantrone-MTX) by immobilized mycelium of B. adusta CCBAS 930. The activity of oxidoreductases: versatile peroxidases (VP), superoxide dismutase (SOD), catalase (CAT), and glucose oxidase (GOX), and the levels of phenolic compounds (PhC) and free radicals (SOR) were determined during the biotransformation of anthracyclines by B. adusta strain CCBAS 930. Moreover, the phytotoxicity (Lepidium sativum L.), biotoxicity (MARA assay), and genotoxicity of anthracyclines were evaluated after biological treatment. After 120 h, more than 90% of anthracyclines were removed by the immobilized mycelium of B. adusta CCBAS 930. The effective biotransformation of anthracyclines was correlated with detoxification and reduced genotoxicity.
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Torkkell, Sirke, Tero Kunnari, Kaisa Palmu, Juha Hakala, Pekka Mäntsälä e Kristiina Ylihonko. "Identification of a Cyclase Gene Dictating the C-9 Stereochemistry of Anthracyclines from Streptomyces nogalater". Antimicrobial Agents and Chemotherapy 44, n. 2 (1 febbraio 2000): 396–99. http://dx.doi.org/10.1128/aac.44.2.396-399.2000.

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ABSTRACT Nogalamycin is an anthracycline antibiotic produced byStreptomyces nogalater. Its aglycone has a unique stereochemistry (7S, 9S, 10R) compared to that of most other anthracyclines (7S, 9R, 10R). The gene snoaL, encoding a nogalonic acid methyl ester cyclase for nogalamycin, was used to generate nogalamycinone, demonstrating that the single cyclase dictates the C-9 stereochemistry of anthracyclines.
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Krell, J., C. Harper-Wynne, D. Miles, V. Misra, S. Cleator, D. Krell e C. Palmieri. "What is the evidence for rechallenging with anthracyclines or taxanes in metastatic breast cancer? A review of the data". Journal of Clinical Oncology 27, n. 15_suppl (20 maggio 2009): 1072. http://dx.doi.org/10.1200/jco.2009.27.15_suppl.1072.

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1072 Background: Anthracyclines and taxanes are widely used in the adjuvant setting for high risk, early stage breast cancer. This raises the issue of what is the optimal therapy for those patients who relapse, and what the potential role, if any, there is for rechallenge with these agents. The current evidence base for rechallenging with anthracyclines/anthracediones and taxanes in metastatic breast cancer (MBC) is examined in this study. Methods: Medline/Pubmed database searches were performed upto October 2008 to identify studies in which patients (pts) were rechallenged with anthracyclines/anthracediones or taxanes in MBC. Results: The efficacy data, as well as the safety data relating to neurotoxicity and cardiotoxicity from these studies, are summarized in the Table. Twenty-seven studies were identified (20=anthracycline/anthracedione, 7= taxane) of which only two were prospective studies. Both were small (n= 74 & 51) and related to anthracycline rechallenging. Conclusions: Evidence exists to support rechallenging with anthracyclines and taxanes. However, there are few prospective data on reexposure to taxanes and no data comparing anthracyclines versus taxanes following adjuvant exposure to both agents, supporting the need for clinical trials in this area. Such trials should ideally incorporate a cross-over design at treatment failure, which would shed light on the optimal sequence in which these agents should be administered. [Table: see text] No significant financial relationships to disclose.
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Chen, Wei-Wu, Twan Ying Chang, Shu-Min Huang, Ching-Hung Lin, Chiun Hsu, Ann-Lii Cheng e Yen-Shen Lu. "The first two lines of chemotherapy for anthracycline-naïve metastatic breast cancer: A comparative study of efficacy between anthracyclines and nonanthracyclines." Journal of Clinical Oncology 30, n. 15_suppl (20 maggio 2012): 1061. http://dx.doi.org/10.1200/jco.2012.30.15_suppl.1061.

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1061 Background: For anthracycline-naïve metastatic breast cancer (AN-MBC) patients, past evidence indicated that anthracyclines are beneficial in the first-two lines of palliative chemotherapy but with considerable toxicities. However, with the provision of newer chemotherapies, comparative studies addressing the efficacy between anthracyclines and non-anthracyclines in the first-two lines of palliative chemotherapy for AN-MBC were lacking. Methods: We collectedclinicopathological characteristics of AN-MBC patients who had received palliative chemotherapy in National Taiwan University Hospital between 2001 and 2006. Patients were classified as anthracycline or non-anthracycline group according to the first-two lines of chemotherapy. Kaplan-Meier method and log-rank test were used for the estimation and comparison of both overall survival (OS) and time to treatment failure of the first-two lines (TTF2).Cox proportional hazard model was used for OS and TTF2. Best composite response rate (BCRR) were compared with logistic regression test. Results: A total of 109 (43.1%) patients in the anthracycline group and 144 (56.9%) patients in non-anthracycline group were analyzed. Between these two groups, the distributions of clinicopathological variables were generally similar and their median OS (33.3 vs 34.2 months, p = 0.179), TTF2 (13.3 vs 12.7 months, p = 0.104), and BCRR (59.5 vs 61.1%, p = 0.81) were not significantly different. Subgroup analysis showed that patients in the anthracycline group had a trend toward better OS in the estrogen receptor (ER) negative/ human epidermal growth factor receptor type II (HER2) positive subtype (median OS 58.0 vs 31.2 months, p = 0.081). In multivariate analysis, patients in the anthracycline group had a trend toward better OS (HR 0.72, 95% CI 0.52 - 1.00, p = 0.052). However, the exclusion of ER-/Her2+ subtype attenuated the impact of early anthracycline treatment on OS (HR 0.82, 95% CI 0.56 - 1.18, p = 0.28). Conclusions: Our study demonstrated that anthracyclines may not be mandatory in the first-two lines of palliative chemotherapy for AN-MBC but may be more beneficial to ER-/Her2+ subtype patients.
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Gianni, Luca, Larry Norton, Norman Wolmark, Thomas M. Suter, Gianni Bonadonna e Gabriel N. Hortobagyi. "Role of Anthracyclines in the Treatment of Early Breast Cancer". Journal of Clinical Oncology 27, n. 28 (1 ottobre 2009): 4798–808. http://dx.doi.org/10.1200/jco.2008.21.4791.

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Purpose To review data relating to anthracyclines in the adjuvant treatment of early breast cancer. Design This is a report from a seminar in which the future of anthracyclines in the adjuvant treatment of breast cancer was considered. In particular, the question of whether anthracyclines should now be discarded and replaced by taxanes was addressed. Results Accumulating data from large randomized trials indicate that genetic markers may have a role in predicting sensitivity to cytotoxic drugs. However, no reliable, validated test is available for predicting sensitivity to anthracyclines in particular. Topoisomerase IIα amplification and/or deletion, especially in conjunction with human epidermal growth factor receptor-2 amplification, has been proposed to fulfill this role but more data are needed. Currently, only one published trial has shown that a taxane-based regimen may be superior to an anthracycline-based regimen, but several trials indicate that combinations including both anthracyclines and taxanes may be better still. Further studies aimed at optimizing anthracyclines and taxanes in combination, and integrating biologic agents, seem to be the way forward. There is no validated test that can determine whether anthracyclines can be of greater benefit than other agents for individual patients. Conclusion Anthracyclines have been extensively tested in clinical trials spanning several decades; currently, there are insufficient data to recommend replacing them in the adjuvant treatment of breast cancer.
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Tesi sul tema "Anthracyclines"

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Nedonchelle, Agnès. "Synthèse énantiospécifique et activité de nouvelles anthracyclines". Paris 5, 1988. http://www.theses.fr/1988PA05P603.

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Huguen, Thierry. "Analyse par chimiluminescence : application au dosage des anthracyclines". Paris 5, 1991. http://www.theses.fr/1991PA05P010.

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HEMAMOU, MOHCINE. "Analyse chromatographique des anthracyclines". Amiens, 1988. http://www.theses.fr/1988AMIEM080.

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Kulkarni, A. D. "Synthesis of analogues of anthracyclines". Thesis(Ph.D.), CSIR-National Chemical Laboratory, Pune, 1986. http://dspace.ncl.res.in:8080/xmlui/handle/20.500.12252/3250.

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François, Anne. "Toxicité comparative des anthracyclines et des anthracène-diones". Paris 5, 1993. http://www.theses.fr/1993PA05P001.

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Young, Charlene Rebecca. "Rational drug design : an information driven approach to the design of an anthracycline analog /". [Boise, Idaho] : Boise State University, 2009. http://scholarworks.boisestate.edu/td/10/.

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Gallois, Laurence. "Interaction des anthracyclines avec des membranes". Paris 13, 1996. http://www.theses.fr/1996PA132031.

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L'interaction des anthracyclines avec des membranes est une étape importante dans la compréhension du mécanisme d'entrée et d'action de ces médicaments dans la cellule. Les anthracyclines sont des molécules amphiphiles qui peuvent interagir à la fois de manière électrostatique et de manière hydrophobe. Nous avons subdivisé notre étude en deux parties: la première en utilisant un modèle membranaire extrêmement simplifié, les liposomes, et la seconde en utilisant des membranes naturelles de cellules k562 sensibles et résistantes à la doxorubicine. L'étude de l'interaction des anthracyclines avec des liposomes a été réalisée par deux techniques différentes: I) par dichroïsme circulaire à faible rapport de phospholipide par anthracycline et à forte concentration d'anthracycline et II) par microspectrofluorimétrie à rapport plus élevé de phospholipide par anthracycline et a faible concentration d'anthracycline. L'interaction électrostatique intervient au niveau de la liaison des molécules chargées à la membrane, mais elle est masquée par l'interaction hydrophobe: elle est détectable dans le cas de certaines anthracyclines très peu lipophiles et à faible rapport de phospholipide par anthracycline. Les anthracyclines sont localisées dans les tètes polaires phospholipidiques plus ou moins profondément. Lorsque nous remplaçons les liposomes par des membranes naturelles, nous constatons un comportement différent. Il peut être du à un changement de fluidité attribuée à la présence d'autres composants membranaires, principalement des protéines, ou à des interactions avec des protéines
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Harper, Mark F. "Studies on heterocyclic compounds related to anthracyclines". Thesis, Heriot-Watt University, 1985. http://hdl.handle.net/10399/1613.

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Nicholson, J. R. "Redox inactive ring C - aglycones of anthracyclines". Thesis, Teesside University, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.383678.

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NOBILI, PIERI NATHALIE. "Les anthracyclines : administration intraveineuse en perfusion continue". Aix-Marseille 2, 1994. http://www.theses.fr/1994AIX20116.

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Libri sul tema "Anthracyclines"

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Maran, Carmen. Discovery and development of anthracycline antitumor antibiotics. Timisoara: Universitatea din Timișoara, Departementul de Chimie, 1994.

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Karsten, Krohn, a cura di. Anthracycline chemistry and biology. Berlin: Springer, 2008.

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1948-, Priebe Waldemar, e American Chemical Society. Division of Carbohydrate Chemistry., a cura di. Anthracycline antibiotics: New analogues, methods of delivery, and mechanisms of action. Washington, DC: American Chemical Society, 1995.

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William, Lown J., a cura di. Anthracycline and anthracenedione-based anticancer agents. Amsterdam: Elsevier, 1988.

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M, Nepomni͡a︡shchikh L., Semenov D. E e T͡S︡ellarius I͡U︡ G, a cura di. Morfologii͡a︡ plasticheskoĭ nedostatochnosti myshechnykh kletok serdt͡s︡a. Novosibirsk: Izd-vo "Nauka," Sibirskoe otd-nie, 1985.

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Priebe, Waldemar, a cura di. Anthracycline Antibiotics. Washington, DC: American Chemical Society, 1994. http://dx.doi.org/10.1021/bk-1995-0574.

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M, Muggia Franco, Green Michael D. 1949- e Speyer James L, a cura di. Cancer treatment and the heart. Baltimore: Johns Hopkins University Press, 1992.

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Krohn, Karsten, a cura di. Anthracycline Chemistry and Biology II. Berlin, Heidelberg: Springer Berlin Heidelberg, 2008. http://dx.doi.org/10.1007/978-3-540-75813-6.

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Krohn, Karsten, a cura di. Anthracycline Chemistry and Biology I. Berlin, Heidelberg: Springer Berlin Heidelberg, 2008. http://dx.doi.org/10.1007/978-3-540-75815-0.

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Timothy, Bricker J., Green Daniel M e D'Angio Giulio J. 1922-, a cura di. Cardiac toxicity after treatment for childhood cancer. New York: Wiley-Liss, 1993.

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Capitoli di libri sul tema "Anthracyclines"

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Schwab, Manfred. "Anthracyclines". In Encyclopedia of Cancer, 1. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-27841-9_6646-2.

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Legha, Sewa S., Gabriel N. Hortobagyi e Robert S. Benjamin. "Anthracyclines". In Cancer Chemotherapy by Infusion, 130–44. Dordrecht: Springer Netherlands, 1987. http://dx.doi.org/10.1007/978-94-009-3193-0_10.

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Sweatman, Trevor W., e Mervyn Israel. "Anthracyclines". In Cancer Therapeutics, 113–36. Totowa, NJ: Humana Press, 1997. http://dx.doi.org/10.1007/978-1-59259-717-8_5.

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

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Giannini, Giuseppe, e Domenico Alloatti. "Fluorinated Anthracyclines". In Anthracycline Chemistry and Biology I, 215–48. Berlin, Heidelberg: Springer Berlin Heidelberg, 2007. http://dx.doi.org/10.1007/128_2007_9.

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de Vries, E. G. E., J. G. Zijlstra e N. H. Mulder. "Morpholinyl anthracyclines : option for reversal of anthracycline resistance ?" In Proceedings of the 3rd International Congress on Neo-Adjuvant Chemotherapy, 403–4. Paris: Springer Paris, 1991. http://dx.doi.org/10.1007/978-2-8178-0782-9_97.

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Post, C., F. Tagliavini, R. A. McArthur, F. Della Vedova, M. Gerna, T. Bandiera, M. Varasi, A. Molinari e J. Lansen. "Anthracyclines and Amyloidosis". In Advances in Behavioral Biology, 197–204. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4615-5337-3_29.

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Laatsch, Hartmut, e Serge Fotso. "Naturally Occurring Anthracyclines". In Anthracycline Chemistry and Biology I, 3–74. Berlin, Heidelberg: Springer Berlin Heidelberg, 2008. http://dx.doi.org/10.1007/128_2008_5.

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Orlowski, Robert Z. "Anthracyclines and Bortezomib". In Proteasome Inhibitors in Cancer Therapy, 171–80. Totowa, NJ: Humana Press, 2004. http://dx.doi.org/10.1007/978-1-59259-794-9_14.

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Mordente, Alvaro, Elisabetta Meucci, Andrea Silvestrini, Giuseppe Ettore Martorana e Bruno Giardina. "Anthracyclines and Mitochondria". In Advances in Experimental Medicine and Biology, 385–419. Dordrecht: Springer Netherlands, 2011. http://dx.doi.org/10.1007/978-94-007-2869-1_18.

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Atti di convegni sul tema "Anthracyclines"

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McGoron, Anthony J., e Alicia Fernandez-Fernandez. "Development of a Multiple Indicator Dilution Technique Using Fluorescent Dyes to Measure Cardiac Capillary Permeability". In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-192955.

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Abstract (sommario):
Anthracyclines are widely-used drugs for the treatment of cancer. Although these drugs are effective in reducing or containing tumor progress, their long-term use is limited by toxicity effects. A special area of concern is related to the toxic effects that these drugs have on the myocardial tissue, including interstitial edema, fibrosis, degeneration of myocardial cells, and cardiac dilatation, among others. The end result is an overall impairment in cardiac function that limits the use of these agents [1,2]. This damage in heart function can be life-threatening, and it causes special concern in patients with prior cardiac dysfunction, as well as in children [2]. As a result of these disadvantages, there is a trend in current research to develop anthracycline derivatives or modified formulations with reduced cardiotoxic effects, as well as to learn more of the mechanisms that mediate this cardiac toxicity. Our long-term goal is to measure changes in capillary endothelium permeability in the heart after administration of anthracyclines which may contribute to the overall deterioration in function observed after chronic treatment with this medication. The goal of this project was to develop a sensitive, non-radioactive technique to measure capillary permeability in experimental animal models. This technique could then be applied in future studies of anthracycline cardiotoxicity.
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Lin, Cindy, Sarah E. Herlihy, Marina Li, Hui Deng, Luca Bernabei, Dmitry I. Gabrilovich, Dan T. Vogl e Yulia Nefedova. "Abstract 2103: NETs promote tumor resistance to anthracyclines". In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-2103.

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Lin, Cindy, Sarah E. Herlihy, Marina Li, Hui Deng, Luca Bernabei, Dmitry I. Gabrilovich, Dan T. Vogl e Yulia Nefedova. "Abstract 2103: NETs promote tumor resistance to anthracyclines". In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-2103.

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Tent, Michiel. "Statins associated with reduced heart dysfunction from anthracyclines". In ACC 2023 Scientific Session, a cura di Marc Bonaca. Baarn, the Netherlands: Medicom Medical Publishers, 2023. http://dx.doi.org/10.55788/6423cd7f.

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Suzuki, Yuichiro J., e Ludmila Jelinkova. "Effects Of Anthracyclines On Rats With Pulmonary Hypertension". In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a3411.

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Munro, A., D. Cameron, J. Thomas, C. Twelves e J. Bartlett. "BUBR1 and MAD2: Novel Markers for Predicting Benefit from Adjuvant Anthracyclines?" 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-09-2124.

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Bartlett, JM, C. Desmedt, A. Munro, FP O'Malley, D. Larsimont, A. di Leo, DA Cameron et al. "Chromosome 17 polysomy: a unifying hypothesis underlying benefit from adjuvant anthracyclines?." In CTRC-AACR San Antonio Breast Cancer Symposium: 2008 Abstracts. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.sabcs-6059.

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Davison, Craig, Olivier P. Chevallier, Catherine Knowlson, Melanie McKechnie, Robbie Carson, Jaime Esteve, Richard Wilson, Robert D. Ladner e Melissa J. LaBonte (Wilson). "Abstract 3836: Imbalanced nucleotide metabolism sensitizes breast cancer cells to anthracyclines". In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-3836.

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Colasanti, Alberto, Annamaria Kisslinger, Raffaele Liuzzi, Michele Mastrocinque, Maria Quarto, Patrizia Riccio, Giuseppe Roberti e Fulvia Villani. "Quantitative analysis of anthracyclines kinetics in cells varying in drug responsiveness". In BiOS Europe '96, a cura di Stanley B. Brown, Benjamin Ehrenberg e Johan Moan. SPIE, 1996. http://dx.doi.org/10.1117/12.260777.

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Karim, Hazhar, Alex Bogason e Sigurd Vitols. "Abstract 1705: Comparison of uptake mechanisms for different anthracyclines in leukemic cells". 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.am2011-1705.

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Rapporti di organizzazioni sul tema "Anthracyclines"

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Ding, Boni. Influence of different order of taxanes and anthracyclines on the neoadjuvant chemotherapy for breast cancer: a Systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review Protocols, aprile 2020. http://dx.doi.org/10.37766/inplasy2020.4.0134.

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Jones, Lee W. Examining the Effects of Exercise Training on Tumor Response to Anthracycline-Based Chemotherapy. Fort Belvoir, VA: Defense Technical Information Center, agosto 2004. http://dx.doi.org/10.21236/ada432983.

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Chen, Yanjun, Junteng Zheng, Ye Luo, Huihua Yang e Zhiming Yuan. Enalapril and carvedilol for prevention anthracycline-induced cardiotoxicity:a systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, giugno 2020. http://dx.doi.org/10.37766/inplasy2020.6.0005.

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