DNA damage response in patients with pediatric Acute Lymphoid Leukemia during induction therapy

Portich, Júlia Plentz; Santos, R. S. S. dos; Kersting, Nathália; Jorge, Karolina Brochado; Casagrande, Pietro Rebelo; Costa, Gabriela dos Santos; Cionek, Jéssica Maria Gonçalves Dias; Olguins, Danielly Brufatto; Sinigaglia, Marialva; Busatto, Franciele Faccio; Saffi, Jenifer; Maluf, Sharbel Weidner; Loss, Jiseh Fagundes; Brunetto, Algemir Lunardi; Roesler, Rafaël; Farias, Caroline Brunetto de

doi:10.1016/j.leukres.2017.01.013

Cited by 4 publications

(4 citation statements)

References 36 publications

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“…DNA repair is necessary to maintain the integrity and stability of genomic DNA for normal cell survival, otherwise, the frequency of cell death, gene mutations, or evolution to tumor cells would be increased. Thus, evaluating the DNA situation and its response to damage and repair is a promising strategy to prevent/predict treatment for bone regeneration and to ensure that it does not pose a risk for clinical practice [44].…”

Section: Discussionmentioning

confidence: 99%

In Vivo Evaluation of the Genotoxic Effects of Poly (Butylene adipate-co-terephthalate)/Polypyrrole with Nanohydroxyapatite Scaffolds for Bone Regeneration

Elias¹,

Filho

Silva

et al. 2019

Materials

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Here, butylene adipate-co-terephthalate/polypyrrole with nanohydroxyapatite (PBAT/PPy/nHAp) scaffolds were fabricated and characterized. The electrospinning process was carried out using 12 kV, a needle of 23 G, an infusion pump set at 0.3 mL/h, and 10 cm of distance. Afterwards, nHAp was directly electrodeposited onto PBAT/PPy scaffolds using a classical three-electrode apparatus. For in vivo assays (comet assay, acute and chronic micronucleus), 60 male albino Wistar rats with 4 groups were used in each test (n = 5): PBAT/PPy; PBAT/PPy/nHAp; positive control (cyclophosphamide); and the negative control (distilled water). Peripheral blood samples were collected from the animals to perform the comet test after 4 h (for damage) and 24 h (for repair). In the comet test, it was shown that the scaffolds did not induce damage to the % DNA tail and neither for tail length. After the end of 48 h (for acute micronucleus) and 72 h (for chronic micronucleus), bone marrow was collected from each rat to perform the micronucleus test. All of the produced scaffolds did not present genotoxic effects, providing strong evidence for the biological application of PBAT/PPy/nHAp scaffolds.

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Section: Discussionmentioning

confidence: 99%

In Vivo Evaluation of the Genotoxic Effects of Poly (Butylene adipate-co-terephthalate)/Polypyrrole with Nanohydroxyapatite Scaffolds for Bone Regeneration

Elias¹,

Filho

Silva

et al. 2019

Materials

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“…Recently, Portich et al . 14 assessed DNA damage in pediatric patients with acute lymphoid leukemia using the comet assay and found no increase in damage during induction therapy (diagnosis, 15 days, and 35 days), which suggests that this repair pathway may be stimulated in the following scenarios: i) as a tumor response; ii) as a defense from chemotherapy; or iii) both (pathogenesis of the disease and chemotherapy).…”

Section: Discussionmentioning

confidence: 99%

“… 5 The few studies that assessed genomic damage in patients with leukemia used approaches such as the micronucleus (MN) technique, 6 , 7 sister chromatid exchange (SCE), 8-12 or the alkaline comet assay. 13 , 14 The findings of those studies were contradictory. DNA damage in Mexican patients with AML has not been explored.…”

Section: Introductionmentioning

confidence: 99%

DNA damage in acute myeloid leukemia patients of Northern Mexico

et al. 2017

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The purpose of this study was to evaluate DNA damage in the whole genome of peripheral blood leukocytes from patients with acute myeloid leukemia (AML) compared with a control group using DNA breakage detection-fluorescent in situ hybridization (DBD-FISH). Our results suggest that the DNA damage detected in patients with newly diagnosed AML was similar to that observed for the controls; this might be explained by the stimulation of a repair pathway by the pathogenesis itself. These findings indicate that inhibiting the repair pathway could be proposed to enhance the efficacy of chemotherapy.

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“… 7 In platinum drug sensitive cells, the prolonged DNA damage repair process leads to P53-dependent and independent apoptosis, while those cells with hyper-activated NER machinery or overexpressed NER proteins often show resistance to platinum drug-induced cytotoxity. 8 – 12 …”

Section: Introductionmentioning

confidence: 99%

NEAT1_2—SFPQ axis mediates cisplatin resistance in liver cancer cells in vitro

Yi¹,

Chen

Guo³

et al. 2018

OTT

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BackgroundLiver cancer is a type of malignant tumor with high morbidity and mortality in People’s Republic of China. Its occurrence and development involve the variation and expression changes of multiple genes, and the pathogenesis and related regulatory networks are complex.PurposeIn the present research, we investigate the involvement of NEAT1_2 and SFPQ in cisplatin resistance in liver cancer. The effects of LncRNA NEAT1 and SFPQ expression on the chemotherapeutic resistance of liver cancer cells were analyzed.MethodsThe expression level of NEAT1_2 and SFPQ mRNA in tissue specimens or cell lines were examined by RT-qPCR and western blotting. CCK-8 assay was performed to evaluate cell viability. Cell proliferation was performed using the EdU cell proliferation assay.ResultsOur data showed that increase NEAT1_2 and SFPQ expressions in liver cancer specimens were associated with the development of cisplatin resistance; high SFPQ expression level impaired patients’ survival from liver cancer. Gain-and loss-of function assay using NEAT1_2 knock-in and knock-out cells constructed using CRISPER/Cas9 system revealed that NEAT1_2 is essential for liver cancer cell survival and mediates cisplatin resistance in liver cancer cells at least partially through SFPQ. Artificial change in NEAT1_2 expression level didn’t significantly influence SFPQ transcription or translation level.ConclusionOur data revealed NEAT1_2—SFPQ axis as a novel cisplatin resistance mechanism in liver cancer cells in vitro.

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DNA damage response in patients with pediatric Acute Lymphoid Leukemia during induction therapy

Cited by 4 publications

References 36 publications

In Vivo Evaluation of the Genotoxic Effects of Poly (Butylene adipate-co-terephthalate)/Polypyrrole with Nanohydroxyapatite Scaffolds for Bone Regeneration

In Vivo Evaluation of the Genotoxic Effects of Poly (Butylene adipate-co-terephthalate)/Polypyrrole with Nanohydroxyapatite Scaffolds for Bone Regeneration

DNA damage in acute myeloid leukemia patients of Northern Mexico

NEAT1_2—SFPQ axis mediates cisplatin resistance in liver cancer cells in vitro

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DNA damage response in patients with pediatric Acute Lymphoid Leukemia during induction therapy

Cited by 4 publications

References 36 publications

In Vivo Evaluation of the Genotoxic Effects of Poly (Butylene adipate-co-terephthalate)/Polypyrrole with Nanohydroxyapatite Scaffolds for Bone Regeneration

In Vivo Evaluation of the Genotoxic Effects of Poly (Butylene adipate-co-terephthalate)/Polypyrrole with Nanohydroxyapatite Scaffolds for Bone Regeneration

DNA damage in acute myeloid leukemia patients of Northern Mexico

NEAT1_2&mdash;SFPQ axis mediates cisplatin resistance in liver cancer cells in vitro

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NEAT1_2—SFPQ axis mediates cisplatin resistance in liver cancer cells in vitro