Doxorubicin pathways

Thorn, Caroline F.; Oshiro, Connie; Marsh, Sharon; Hernandez‐Boussard, Tina; McLeod, Howard L.; Klein, Teri E.; Altman, Russ B.

doi:10.1097/fpc.0b013e32833ffb56

Cited by 1,308 publications

(599 citation statements)

References 56 publications

(72 reference statements)

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“…Therefore, we associated MDA-MB-231 cells with an under-treatment/baseline resistance breast cancer model. Doxorubicin anti-tumor effects are mediated through two mechanisms: DNA intercalation and inhibition of topoisomerase II DNA repair activity and the generation of free radicals [24], which cause dramatic changes at or near promoters, therefore, impairing transcription [25]. As expected, we have found thousands of genes to be deregulated upon doxorubicin treatment.…”

Section: Discussionsupporting

confidence: 71%

Regulation of stem cells-related signaling pathways in response to doxorubicin treatment in Hs578T triple-negative breast cancer cells

et al. 2015

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Different molecular changes have been previously associated with therapeutic response and recurrent disease, however, the detailed mechanism of action in triple-negative breast cancer subtype remains elusive. In this study, we investigated the cellular and molecular signaling of two claudin-low triple-negative breast cancer cells to doxorubicin and docetaxel treatment. Whole human transcriptomic evaluation was used to identify the subsequent changes in gene expression, while biological effects were measured by means of proliferation and anchorage-independent growth assays. Microarray analysis revealed changes in stem cell-related signaling pathways, suggesting that doxorubicin treatment affects the balance between self-renewal and differentiation. While the treatment reduced the proliferation, aggregation and mammosphere forming ability of stem-like cells derived from Hs578T cell line, stem-like cells derived from MDA-MB-231 cells were not significantly affected. Our results suggest that claudin-low triple-negative breast cancer cells might predominantly alter stem cell-related signaling pathways to promote stem-like cells activity as an innate resistance mechanism to doxorubicin treatment.

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Section: Discussionsupporting

confidence: 71%

Regulation of stem cells-related signaling pathways in response to doxorubicin treatment in Hs578T triple-negative breast cancer cells

et al. 2015

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“…The mechanism of cardio‐toxicity here involves disruption of topoisomerase‐II‐mediated DNA repair and generation of oxygen‐derived free radicals 4, 5, 6, 7. Serial echocardiograms during several years after doxorubicin administration showed stable LVEF.…”

Section: Discussionmentioning

confidence: 98%

Gemcitabine induced cardiomyopathy: a case of multiple hit cardiotoxicity

2016

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Gemcitabine is a commonly used antineoplastic agent used to treat a variety of cancers with rarely reported cardiac side effects. We describe a case of a 67‐year‐old woman with follicular lymphoma who experienced a rarely reported side effect of gemcitabine: cardiomyopathy. This case highlights a multiple hit mechanism of myocyte damage that may occur following the use of multiple cardio‐toxic agents despite their administration in doses not associated with cardiotoxicity.

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“…In this respect, the fact that 4-HC acts as an inhibitor of microsomal mixed function oxidase (16) could explain why the combination treatment of Doxo and 4-HC did not decrease cell viability in comparison with Doxo alone when 4-HC in lower concentrations was administered. Namely, the Doxo bioactivation network is comprised of a system of reduction/oxidation reactions that lead to formation of toxic Doxo metabolites and reactive oxygen species (ROSs) responsible for lipid peroxidation and membrane damage, DNA damage, oxidative stress and trigger apoptotic pathways of cell death (2). Reductive conversion of Doxo is characterized by the oneelectron reduction of the quinone moiety of Doxo, via NADPH and cytochrome P450 reductase, into a semiquinone radical.…”

Section: Alamarblue Vs Mtt Assaymentioning

confidence: 99%

“…However, because of the fear of long-term cardiotoxicity, this drug is included in adjuvant regimens. In addition, resistance to Doxo, occurring as a multifactorial phenomenon, causes an incomplete response requiring combination chemotherapy (2).…”

mentioning

confidence: 99%

Hydrazinyldiene-chroman-2,4-diones in inducing growth arrest and apoptosis in breast cancer cells: Synergism with doxorubicin and correlation with physicochemical properties

et al. 2017

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This study evaluates the effects of previously synthesized hydrazinyldiene-chroman-2,4-diones on cell proliferation and apoptosis, cell cycle distribution and migration capacity of MCF-7 breast cancer cells in synergy with doxorubicin. Physicochemical properties of the synthesized compounds were correlated with their structure and activity. Significant cell viability decrease in comparison with the effect of doxorubicin alone and the reference 4-hydroxycoumarin was observed when combination treatment comprising doxorubicin and the title compounds was applied. Synergistic effect with doxorubicin was also observed in down-regulation of phospho-Thr 308Akt levels, confirming reduced proliferation and increased apoptosis. Combined treatment increased the percentage of cells arrested at the G 2 /M stage. Additive inhibition of cell migration was also observed, pointing to the possibility of reducing the risk of metastases. With their solubility profile and log D 7.4 , all the synthesized compounds follow Lipinski's rule of five for good permeability (absorption) potential.

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Doxorubicin pathways

Cited by 1,308 publications

References 56 publications

Regulation of stem cells-related signaling pathways in response to doxorubicin treatment in Hs578T triple-negative breast cancer cells

Regulation of stem cells-related signaling pathways in response to doxorubicin treatment in Hs578T triple-negative breast cancer cells

Gemcitabine induced cardiomyopathy: a case of multiple hit cardiotoxicity

Hydrazinyldiene-chroman-2,4-diones in inducing growth arrest and apoptosis in breast cancer cells: Synergism with doxorubicin and correlation with physicochemical properties

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