Oxidized extracellular DNA as a stress signal that may modify response to anticancer therapy

Glebova, K. V.; Вейко, Н. Н.; Kostyuk, Svetlana V.; Ижевская, В. Л.; Baranova, Ancha

doi:10.1016/j.canlet.2013.09.005

Cited by 53 publications

(38 citation statements)

References 125 publications

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“…Scavenging ROS inhibiting bystander effect effectively has been reported in many previous studies [1, 2, 28]. Lower production of ROS after irradiation in mitochondrial DNA lacking ρ 0 cells compared with the normal cells is considered as one main reason by which ρ 0 cells irradiation doesn't induce a bystander effect [7–9].…”

Section: Discussionmentioning

confidence: 89%

Akt/mTOR mediated induction of bystander effect signaling in a nucleus independent manner in irradiated human lung adenocarcinoma epithelial cells

Wang

Prise

et al. 2017

Oncotarget

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Cytoplasm is an important target for the radiation-induced bystander effect (RIBE). In the present work, the critical role of protein kinase B (Akt)/mammalian target of rapamycin (mTOR) pathway in the generation of RIBE signaling after X-ray irradiation and the rapid phosphorylation of Akt and mTOR was observed in the cytoplasm of irradiated human lung adenocarcinoma epithelial (A549) cells. Targeting A549 cytoplasts with individual protons from a microbeam showed that RIBE signal(s) mediated by the Akt/mTOR pathway were generated even in the absence of a cell nucleus. These results provide a new insight into the mechanisms driving the cytoplasmic response to irradiation and their impact on the production of RIBE signal(s).

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Section: Discussionmentioning

confidence: 89%

Akt/mTOR mediated induction of bystander effect signaling in a nucleus independent manner in irradiated human lung adenocarcinoma epithelial cells

Wang

Prise

et al. 2017

Oncotarget

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“…However, ccfDNA in our study was taken not only 1–2 days after the treatment initiation but also more than a month in a treatment. The possible explanation can be then based on the fact that the majority of ccfDNA is of non-cancerous origin and originates from apoptotic and stressed cells [6]. Chemotherapy and radiotherapy can stress normal cells and increase non-cancerous ccfDNA release.…”

Section: Discussionmentioning

confidence: 99%

Detection of copy number alterations in cell-free tumor DNA from plasma

2017

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BackgroundSomatic copy number alterations (SCNAs) occurring in tumors can provide information about tumor classification, patient's outcome or treatment targets. Liquid biopsies, incl. plasma samples containing circulating cell-free tumor DNA (ccfDNA) can be used to assess SCNAs for clinical purposes, however specify and reliability of methods have to be tested.MethodsSNP microarrays (Affymetrix) were used to generate whole-genome copy number profiles from plasma ccfDNA (OncoScan) and paired tumor biopsies (CytoScan) from ten patients with metastatic cancers. Numerical, segmental and focal SCNAs were assessed using ASCAT/TuScan and SNP-FASST2.ResultsAberrations in ccfDNA in 4 patients resembled numerical (76%) and segmental (80%) aberrations in tDNA. Three patients represented low correlation due to postponed sampling time, ccfDNA quality and possible treatment interference. Breakpoints of high-amplitude amplification were assessed with high accuracy and relative breakpoints difference of only 7% (0.02–37%). Similarly, biallelic losses were reliably detected. Array was 100% successful in detection of SCNAs on clinically relevant genes compared to SCNAs in tumor biopsies. Tracking of SCNAs changes during the treatment course of one patient also indicated that apoptosis/necrosis of non-cancerous cells presumably induced by treatment can influence ccfDNA composition and introduce false-negative findings into the analysis of liquid biopsies.ConclusionsGenomic alterations detected in ccfDNA from liquid biopsies by comprehensive SNP array are reliable source for information for stratification of patients for targeted treatment.General significanceClinically relevant SCNAs can be detected in ccfDNA with high resolution and can therefore serve as an alternative to tumor biopsy in defining treatment targets.

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“…A correct genomic content packaging of a cell committed to die would minimize the spreading of harmful genes, such as oncogenes or viral DNA. In this context, extracellular DNA from dead cells can activate intracellular pathways in living "receptor" cells, leading to disparate consequences that range from cytotoxicity to cellular transformation (46,47). Therefore, knowing how chromatin collapse and nuclear disassembly are regulated during caspase-dependent apoptosis could be instrumental for understanding the intimate mechanism that governs an accurate and silent non-harmful cell death.…”

Section: Discussionmentioning

confidence: 99%

Caspase-activated DNase Is Necessary and Sufficient for Oligonucleosomal DNA Breakdown, but Not for Chromatin Disassembly during Caspase-dependent Apoptosis of LN-18 Glioblastoma Cells

Sánchez-Osuna¹,

Garcia-Belinchón²,

Iglesias-Guimarais³

et al. 2014

Journal of Biological Chemistry

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Background: DFF40/CAD mediates nuclear fragmentation and oligonucleosomal DNA degradation during apoptosis. Results: DFF40/CAD overexpression allows apoptotic-defective LN-18 cells to display internucleosomal DNA degradation but not chromatin disassembly upon cytotoxic insult. Conclusion: DFF40/CAD can induce DNA laddering in the absence of apoptotic chromatin disassembly. Significance: Dissecting DFF40/CAD regulation may shed light on some of the apparent non-desirable tumor responses in currently used anti-cancer therapies.

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Oxidized extracellular DNA as a stress signal that may modify response to anticancer therapy

Cited by 53 publications

References 125 publications

Akt/mTOR mediated induction of bystander effect signaling in a nucleus independent manner in irradiated human lung adenocarcinoma epithelial cells

Akt/mTOR mediated induction of bystander effect signaling in a nucleus independent manner in irradiated human lung adenocarcinoma epithelial cells

Detection of copy number alterations in cell-free tumor DNA from plasma

Caspase-activated DNase Is Necessary and Sufficient for Oligonucleosomal DNA Breakdown, but Not for Chromatin Disassembly during Caspase-dependent Apoptosis of LN-18 Glioblastoma Cells

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