Polymorphisms of ABCC5 and NOS3 genes influence doxorubicin cardiotoxicity in survivors of childhood acute lymphoblastic leukemia

Krajinović, Maja; Elbared, J; Drouin, Simon; Bertout, Laurence; Rezgui, Aziz; Ansari, Marc; Mj, Raboisson; Se, Lipshultz; Lb, Silverman; Se, Sallan; Ds, Neuberg; Jl, Kutok; Laverdière, Caroline; Sinnett, Daniel; Andelfinger, Grégor

doi:10.1038/tpj.2015.63

Cited by 87 publications

(71 citation statements)

References 45 publications

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“…When we limited the results to publications consistent with the revised label for Cardioxane, 13 clinical trials [6][7][8][9][10][11][12][13][14][15][16][17][18] and four meta-analyses or systematic reviews remained [19][20][21][22]. These meta-analyses and systematic…”

Section: Resultsmentioning

confidence: 99%

“…Dexrazoxane is an effective cardioprotectant in children Since the CHMP review, 11 relevant publications have examined the use of dexrazoxane in children [6,7,[9][10][11][12][14][15][16][17][18]. The Children's Oncology Group (COG) P9404 randomized trial evaluated oncologic efficacy, cardioprotective effectiveness and safety following dexrazoxane therapy in 537 children and adolescents with newly diagnosed T-cell acute lymphoblastic leukemia (ALL) or lymphoblastic non-Hodgkin lymphoma (Table 1) [6].…”

Section: Resultsmentioning

confidence: 99%

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Risk–Benefit of Dexrazoxane for Preventing Anthracycline-Related Cardiotoxicity: Re-Evaluating the European Labeling

Tabone²,

et al. 2018

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Dexrazoxane can prevent anthracycline-associated cardiotoxicity. However, in 2011, its use in children was contraindicated by the EMA over concerns of increased risk of infection, myelosuppression and second primary malignancies, and because its efficacy in children had not then been established. We review here the evidence published since 2011, which confirms that dexrazoxane is an effective cardioprotectant in children and adolescents, is not associated with an increased risk of second primary malignancies or excess early or late mortality and does not impair chemotherapy efficacy. Based on this evidence, the contraindication for children and adolescents requiring high doses of anthracyclines and at risk for cardiotoxicity was removed from the European labeling for dexrazoxane.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Risk–Benefit of Dexrazoxane for Preventing Anthracycline-Related Cardiotoxicity: Re-Evaluating the European Labeling

Tabone²,

et al. 2018

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“…The solute carrier family (SLC) is responsible for anthracycline transport into the cell, while ABC (ATP-binding cassette) transporters are involved in energy-dependent anthracycline efflux from the cell. Significant associations have been found between ACT and SNPs in various SLC and ABC genes [33,[43][44][45].…”

Section: Cardiotoxicitymentioning

confidence: 97%

“…Mutant haplotypes of this gene have been associated with increased cardiac iron load, elevated troponin levels, and decreased LV fractional shortening [48,49]. Genes more directly involved in mitigating oxidative stress and subsequent tissue remodeling such as endothelial nitric oxide synthase 3 (NOS3) and hyaluronan synthase 3 (HAS3), have also been found to modify the risk of anthracycline dose-dependent cardiomyopathy risk [33,89].…”

Section: Cardiotoxicitymentioning

confidence: 98%

Pharmacogenetic Predictors of Treatment-Related Toxicity Among Children With Acute Lymphoblastic Leukemia

Maxwell

Cole

2017

Curr Hematol Malig Rep

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Multiple studies have examined the toxicities of the primary chemotherapeutic agents used to treat childhood ALL in relation to host genetic factors. However, few results have been replicated independently, largely due to cohort differences in ancestry, chemotherapy treatment protocols, and definitions of toxicities. To date, there is only one widely accepted clinical guideline for dose modification based on gene status: thiopurine dosing based on TPMT genotype. Based on recent data, it is likely that this guideline will be modified to incorporate other gene variants, such as NUDT15. We highlight genetic variants that have been consistently associated with TRT across treatment groups, as well as those that best illustrate the underlying pathophysiology of TRT. In the coming decade, we expect that survivorship care will routinely specify screening recommendations based on genetics. Furthermore, clinical trials testing protective interventions may modify inclusion criteria based on genetically determined risk of specific TRTs.

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“…Reichwagen et al found that NADPH oxidase gene polymorphisms were associated with anthracyclineinduced cardiotoxicity in patients affected with B-cell lymphoma [75] . Krajinovic et al revealed that ABCC5 and NOS3 gene polymorphisms have been associated with the development of doxorubicin-induced cardiotoxicity in children with acute lymphoblastic leukemia [76] .…”

Section: Doxorubicin-induced Cardiotoxicity Correlation With Apoptosimentioning

confidence: 99%

Molecular Mechanisms of Cardiotoxicity: A Review on Major Side-effect of Doxorubicin

Mobaraki¹,

Faraji²,

Zare³

et al. 2017

pharmaceutical-sciences

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Mobaraki, et al.: Molecular Mechanisms of Doxorubicin-induced CardiotoxicityDoxorubicin is among the most widely used drugs for the treatment of both adult and child cancers. Doxorubicin is the major cause of chemotherapy-induced cardiotoxicity that is dose limiting for the treatment of cancer. Many studies have explored pathophysiology and mechanisms of doxorubicininduced cardiotoxicity. Cellular and animal experiments proposed that doxorubicin-induced cardiotoxicity mechanism is multifactorial. Oxidative stress has been considered as the primary cause of cardiotoxicity. Although there is no effective treatment for doxorubicin-induced cardiotoxicity currently but many investigations are underway to discover preventive treatments whereas no specific treatment has been approved. Studies have shown that reactive oxygen species and topoisomerase 2b are molecular targets for cardioprotection. Therapeutic imaging methods and cardio-biomarkers may be helpful in the improvement of rapid detection of cardiac damage. In this review, effects of doxorubicin on DNA damage, free radical generation, mitochondrial damage, cell death and other parameters have been studied.

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Polymorphisms of ABCC5 and NOS3 genes influence doxorubicin cardiotoxicity in survivors of childhood acute lymphoblastic leukemia

Cited by 87 publications

References 45 publications

Risk–Benefit of Dexrazoxane for Preventing Anthracycline-Related Cardiotoxicity: Re-Evaluating the European Labeling

Risk–Benefit of Dexrazoxane for Preventing Anthracycline-Related Cardiotoxicity: Re-Evaluating the European Labeling

Pharmacogenetic Predictors of Treatment-Related Toxicity Among Children With Acute Lymphoblastic Leukemia

Molecular Mechanisms of Cardiotoxicity: A Review on Major Side-effect of Doxorubicin

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