Perspectives on the adaptive response from studies on the response to low                 radiation doses (or to cisplatin) in mammalian cells

Skov, Kirsten A.

doi:10.1191/096032799678840354

Cited by 10 publications

(6 citation statements)

References 28 publications

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“…Radioadaptive responses have been observed in nearly all the species, including Escherichia coli, protozoa, algae, higher plants, and insects (12,35,143,185,192,246,247). The most significant phenomena of LDIR-induced radioprotection include the reduction of the lethal and mutagenic effects caused by subsequent exposure to higher doses (105,154,173,193,204,227), resistance to subsequent radiation-induced genomic instability (96, 105,121,142), and activation of stress-sensitive transcription factors and gene regulators (68,69,202,228). Bhattacharjee and Ito (22) reported that whole-body pre-irradiation of Swiss mice with five repeated exposures to small doses of 1 cGy per day reduces the incidence of thymic lymphoma from 46% to 16% following 2 Gy IR (21).…”

Section: Features Of Ldir-induced Adaptive Responsementioning

confidence: 99%

“…CDK1, cyclin-dependent kinase 1; LDIR, low-dose ionizing radiation; MPI, mitochondrial protein influx; NPI, nuclear protein influx. To see this illustration in color, the reader is referred to the web version of this article at www .liebertpub.com/ars mechanisms activated in response to IR (3,105,154,173,193,204,227). IR induces the expression of a specific cluster of stress responsive genes to repair damaged biomolecules, including DNA, and enhance overall cell survival (7,28,63,68,69,85,120,140,199,202,228).…”

Section: Features Of Ldir-induced Adaptive Responsementioning

confidence: 99%

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Cell Cycle Regulators Guide Mitochondrial Activity in Radiation-Induced Adaptive Response

Alexandrou

2014

Antioxidants & Redox Signaling

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Significance: There are accruing concerns on potential genotoxic agents present in the environment including low-dose ionizing radiation (LDIR) that naturally exists on earth's surface and atmosphere and is frequently used in medical diagnosis and nuclear industry. Although its long-term health risk is being evaluated and remains controversial, LDIR is shown to induce temporary but significant adaptive responses in mammalian cells and animals. The mechanisms guiding the mitochondrial function in LDIR-induced adaptive response represent a unique communication between DNA damage and cellular metabolism. Elucidation of the LDIRregulated mitochondrial activity may reveal new mechanisms adjusting cellular function to cope with hazardous environmental stress. Recent Advances: Key cell cycle regulators, including Cyclin D1/CDK4 and Cyclin B1/ cyclin-dependent kinase 1 (CDK1) complexes, are actively involved in the regulation of mitochondrial functions via phosphorylation of their mitochondrial targets. Accumulating new evidence supports a concept that the Cyclin B1/CDK1 complex acts as a mediator in the cross talk between radiation-induced DNA damage and mitochondrial functions to coordinate cellular responses to low-level genotoxic stresses. Critical Issues: The LDIR-mediated mitochondrial activity via Cyclin B1/CDK1 regulation is an irreplaceable network that is able to harmonize vital cellular functions with adjusted mitochondrial metabolism to enhance cellular homeostasis. Future Directions: Further investigation of the coordinative mechanism that regulates mitochondrial activities in sublethal stress conditions, including LDIR, will reveal new insights of how cells cope with genotoxic injury and will be vital for future targeted therapeutic interventions that reduce environmental injury and cancer risk.

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Section: Features Of Ldir-induced Adaptive Responsementioning

confidence: 99%

Section: Features Of Ldir-induced Adaptive Responsementioning

confidence: 99%

Cell Cycle Regulators Guide Mitochondrial Activity in Radiation-Induced Adaptive Response

Alexandrou

2014

Antioxidants & Redox Signaling

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“…Radioresistance is also linked with the signaling cascades activated during temporary but significant cell cycle arrest (Bebien et al 2003; Fornace et al 1999; Hartwell and Kastan 1994), the degree of DNA damage, the activation of signaling networks; and the activation of pro-survival or pro-apoptotic signaling pathways determines the fate of an irradiated cell (Feinendegen 1999, 2002; Maity et al 1997; Schmidt-Ullrich et al 2000; Stecca and Gerber 1998; Waldman et al 1997; Weichselbaum et al 1994; Wolff 1989, 1998). The induced protection/tolerance of irradiated cells is also evident since pre-exposure to a low or intermediate dose of X- or γ-rays reduces the lethal effects and genomic instability caused by subsequent exposures of higher doses of IR (Kelsey et al 1991; Olivieri et al 1984; Robson et al 2000; Skov 1999; Suzuki et al 1998, 2001). Therefore, a better understanding of the molecular mechanisms underlying the tumor adaptive response is necessary to further increase the efficacy of anti-cancer therapy.…”

Section: Tumor Adaptive Response Csc-mediated Tumor Cell Repopulationmentioning

confidence: 99%

Breast cancer adaptive resistance: HER2 and cancer stem cell repopulation in a heterogeneous tumor society

Duru

Candas

Jiang

et al. 2013

J Cancer Res Clin Oncol

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PurposeThe lethal effects of cancer are associated with the enhanced tumor aggressiveness in recurrent and metastatic lesions that show resistant phenotype to anti-cancer therapy, a major barrier to improving overall survival of cancer patients. The presence of heterogeneous populations of cancer cells within a specific tumor including the tumor-initiating cells or so-called cancer stem cells (CSCs) has linked the acquired resistance (AR, or adaptive resistance). Herein, we discuss the CSC-mediated tumor repopulation in AR of breast cancer in this review.MethodsWe emphasize a dynamic feature of gene induction in tumor cells that undergo long-term treatment, and describe a specific HER2-NF-κB-HER2 pro-survival pathway that can be initiated in breast CSCs upon radiation therapy.ResultsElucidation of HER2-induced pro-survival networks, specifically the force driving tumor repopulation due to radioresistant CSCs during anticancer therapies, will have a significant impact on the generation of new diagnostic and therapeutic targets to control of recurrent and metastatic breast tumors.

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“…Different doses of IR are shown to induce an adaptive resistance that is defined to be the reduced cell sensitivity to a higher challenging dose of a stressor when a smaller inducing dose had been applied a few hours earlier [9]. This adaptive radioresistance is evidenced by the fact that pre-exposure to a low or mediate dose of IR (e.g., diagnosis X-ray) reduces the radiation toxicity and decreases the genomic instability caused by a subsequent high dose IR [77,[85][86][87][88][89][90]. To further increase the efficacy of radiotherapy, the molecules responsible for tumor resistance to a therapeutic dose range of IR needs to be elucidated.…”

Section: Nf-κb In Adaptive Radioresistancementioning

confidence: 99%

ATM-NF-κB Connection as a Target for Tumor Radiosensitization

Ahmed

2007

CCDT

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Ionizing radiation (IR) plays a key role in both areas of carcinogenesis and anticancer radiotherapy. The ATM (ataxia-telangiectasia mutated) protein, a sensor to IR and other DNA-damaging agents, activates a wide variety of effectors involved in multiple signaling pathways, cell cycle checkpoints, DNA repair and apoptosis. Accumulated evidence also indicates that the transcription factor NF-kappaB (nuclear factor-kappaB) plays a critical role in cellular protection against a variety of genotoxic agents including IR, and inhibition of NF-kappaB leads to radiosensitization in radioresistant cancer cells. NF-kappaB was found to be defective in cells from patients with A-T (ataxia-telangiectasia) who are highly sensitive to DNA damage induced by IR and UV lights. Cells derived from A-T individuals are hypersensitive to killing by IR. Both ATM and NF-kappaB deficiencies result in increased sensitivity to DNA double strand breaks. Therefore, identification of the molecular linkage between the kinase ATM and NF-kappaB signaling in tumor response to therapeutic IR will lead to a better understanding of cellular response to IR, and will promise novel molecular targets for therapy-associated tumor resistance. This review article focuses on recent findings related to the relationship between ATM and NF-kappaB in response to IR. Also, the association of ATM with the NF-kappaB subunit p65 in adaptive radiation response, recently observed in our lab, is also discussed.

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Perspectives on the adaptive response from studies on the response to low radiation doses (or to cisplatin) in mammalian cells

Cited by 10 publications

References 28 publications

Cell Cycle Regulators Guide Mitochondrial Activity in Radiation-Induced Adaptive Response

Cell Cycle Regulators Guide Mitochondrial Activity in Radiation-Induced Adaptive Response

Breast cancer adaptive resistance: HER2 and cancer stem cell repopulation in a heterogeneous tumor society

ATM-NF-κB Connection as a Target for Tumor Radiosensitization

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Perspectives on the adaptive response from studies on the response to low radiation doses (or to cisplatin) in mammalian cells

Cited by 10 publications

References 28 publications

Cell Cycle Regulators Guide Mitochondrial Activity in Radiation-Induced Adaptive Response

Cell Cycle Regulators Guide Mitochondrial Activity in Radiation-Induced Adaptive Response

Breast cancer adaptive resistance: HER2 and cancer stem cell repopulation in a heterogeneous tumor society

ATM-NF-&#954;B Connection as a Target for Tumor Radiosensitization

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ATM-NF-κB Connection as a Target for Tumor Radiosensitization