Chapter 8: Perspectives for the use of biological indicators for the assessment of radiation induced responses and impairments: Biologic indicators of exposure: Are markers associated with oncogenesis useful as biologic markers of effect?

Stem Cells ◽  
1995 ◽  
Vol 13 (S1) ◽  
pp. 326-338 ◽  
Author(s):  
Benedikt L. Ziegler ◽  
Melanie Weiss ◽  
Stefan Thoma ◽  
Christa Lamping ◽  
Theodor M. Fliedner
Keyword(s):  
Biological Indicators ◽  
Induced Responses ◽  
Biologic Markers ◽  
Radiation Induced

scholarly journals New biological indicators to evaluate and monitor radiation-induced damage: an accident case report.

2008 ◽  
Vol 43 (5) ◽  
Author(s):  
J.-M. Bertho ◽  
L. Roy ◽  
M. Souidi ◽  
Y. Gueguen ◽  
J.-J. Lataillade ◽  
...  
Keyword(s):  
Case Report ◽  
Biological Indicators ◽  
Radiation Induced ◽  
Accident Case

scholarly journals Ionizing Radiation-Induced Responses in Human Cells with Differing TP53 Status

2013 ◽  
Vol 14 (11) ◽  
pp. 22409-22435 ◽  
Author(s):  
Razmik Mirzayans ◽  
Bonnie Andrais ◽  
April Scott ◽  
Ying Wang ◽  
David Murray
Keyword(s):  
Ionizing Radiation ◽  
Human Cells ◽  
Induced Responses ◽  
Radiation Induced ◽  
Tp53 Status

Low-dose radiation-induced responses: Focusing on epigenetic regulation

2010 ◽  
Vol 86 (7) ◽  
pp. 517-528 ◽  
Author(s):  
Shumei Ma ◽  
Xin Liu ◽  
Benzheng Jiao ◽  
Yu Yang ◽  
Xiaodong Liu
Keyword(s):  
Epigenetic Regulation ◽  
Low Dose ◽  
Induced Responses ◽  
Low Dose Radiation ◽  
Radiation Induced ◽  
Dose Radiation

scholarly journals Role of ATP as a Key Signaling Molecule Mediating Radiation-Induced Biological Effects

Dose-Response ◽  
2017 ◽  
Vol 15 (1) ◽  
pp. 155932581769063 ◽  
Author(s):  
Shuji Kojima ◽  
Yasuhiro Ohshima ◽  
Hiroko Nakatsukasa ◽  
Mitsutoshi Tsukimoto
Keyword(s):  
Immune Responses ◽  
Biological Effects ◽  
The Body ◽  
Cytotoxic Agents ◽  
Induced Responses ◽  
Adaptive Responses ◽  
Γ Irradiation ◽  
Protective Mechanisms ◽  
Signaling Molecule ◽  
Radiation Induced

Adenosine triphosphate (ATP) serves as a signaling molecule for adaptive responses to a variety of cytotoxic agents and plays an important role in mediating the radiation stress-induced responses that serve to mitigate or repair the injurious effects of γ radiation on the body. Indeed, low doses of radiation may have a net beneficial effect by activating a variety of protective mechanisms, including antitumor immune responses. On the other hand, ATP signaling may be involved in the radiation resistance of cancer cells. Here, focusing on our previous work, we review the evidence that low-dose γ irradiation (0.25-0.5 Gy) induces release of extracellular ATP, and that the released ATP mediates multiple radiation-induced responses, including increased intracellular antioxidant synthesis, cell-mediated immune responses, induction of DNA damage repair systems, and differentiation of regulatory T cells.

Ultraviolet Radiation-Induced p53 Responses in the Epidermis are Differentiation-Dependent

1999 ◽  
Vol 3 (5) ◽  
pp. 280-283 ◽  
Author(s):  
Victor A. Tron ◽  
Gang Li ◽  
Vincent Ho ◽  
Martin J. Trotter
Keyword(s):  
Cellular Responses ◽  
Mutant P53 ◽  
Induced Responses ◽  
Dna Damaging Agents ◽  
Normal Keratinocytes ◽  
Proposed Model ◽  
Multiple Copies ◽  
Radiation Induced ◽  
Tumour Suppressor P53 ◽  
Harmful Effects

Background: The tumour suppressor, p53, is recognized as a crucial molecule in regulating cellular responses to various DNA-damaging agents. Very early on in the development of nonmelanoma cancers p53 is mutated or lost, suggesting that p53 is crucial in protecting normal keratinocytes from the harmful effects of ultraviolet (UV) radiation. Objective: Using two mouse models, one with multiple copies of mutant p53 and the other a p53 “knockout,” our laboratory has examined a role for p53 in UV-induced DNA damage and determined if these effects are differentiation dependent. Conclusion: We outline in this review a proposed model reflecting differentiation-dependent p53 regulation of UV-induced responses in keratinocytes. After exposure to UV, basal keratinocytes repair damaged DNA, whereas differentiating keratinocytes undergo cell death, both processes are regulated by p53.

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