Neoplastic Cell Transformation by Heavy Charged Particles

Yang, T. C.; Craise, Laurie M.; Mei, Mantong; Tobias, Cornelius A.

doi:10.2307/3576645

Cited by 153 publications

(21 citation statements)

References 14 publications

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“…In addition, the suppression of PLD repair was reported in high LET with a 90 keV/μm carbon beam [27]. PLDR was also observed in experiments using mouse embryo cells with other beam species such as silicon and neon beams [28]. …”

Section: Discussionmentioning

confidence: 90%

Modeling the biological response of normal human cells, including repair processes, to fractionated carbon beam irradiation

Wada

Suzuki²,

Liu³

et al. 2013

Journal of Radiation Research

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To understand the biological response of normal cells to fractionated carbon beam irradiation, the effects of potentially lethal damage repair (PLDR) and sublethal damage repair (SLDR) were both taken into account in a linear-quadratic (LQ) model. The model was verified by the results of a fractionated cell survival experiment with normal human fibroblast cells. Cells were irradiated with 200-kV X-rays and monoenergetic carbon ion beams (290 MeV/u) at two irradiation depths, corresponding to linear energy transfers (LETs) of approximately 13 keV/μm and 75 keV/μm, respectively, at the Heavy Ion Medical Accelerator in Chiba of the National Institute of Radiological Sciences. When we only took into account the repair factor of PLDR, γ, which was derived from the delayed assay, the cell survival response to fractionated carbon ion irradiation was not fully explained in some cases. When both the effects of SLDR and PLDR were taken into account in the LQ model, the cell survival response was well reproduced. The model analysis suggested that PLDR occurs in any type of radiation. The γ factors ranged from 0.36–0.93. In addition, SLD was perfectly repaired during the fraction interval for the lower LET irradiations but remained at about 30% for the high-LET irradiation.

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Section: Discussionmentioning

confidence: 90%

Modeling the biological response of normal human cells, including repair processes, to fractionated carbon beam irradiation

Wada

Suzuki²,

Liu³

et al. 2013

Journal of Radiation Research

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“…(83) RBE values for the induction of in-vitro neoplastic transformation in C3H10T1/2 cells increase up to a value of approximately 10 for LET of 100-200 keV mm À1 (Yang et al, 1985(Yang et al, , 1996. RBE values for 14, 30, and 172 keV mm À1 carbon ions for transformation of HeLa X human skin fibroblast cell line CGL1 are 1.0, 2.5, and 12, respectively (Bettega et al, 2009).…”

Section: Rbe For Ion Beam Radiation In Stochastic Effectsmentioning

confidence: 99%

Cellular mechanisms underlying failed beta cell regeneration in offspring of protein-restricted pregnant mice

Cox

Beamish

Carter

et al. 2013

Exp Biol Med (Maywood)

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Low birth weight and poor foetal growth following low protein (LP) exposure are associated with altered islet development and glucose intolerance in adulthood. Additionally, LP-fed offspring fail to regenerate their β-cells following depletion with streptozotocin (STZ) in contrast to control-fed offspring that restore β-cell mass. Our objective was to identify signalling pathways and cellular functions that may be critically altered in LP offspring rendering them susceptible to developing long-term glucose intolerance and decreased β-cell plasticity. Pregnant Balb/c mice were fed a control (C; 20% protein) or an isocaloric LP (8% protein) diet throughout gestation and C diet thereafter. Female offspring were injected intraperitoneally with 35 mg/kg STZ or vehicle on days 1 to 5 for each dietary treatment. At 30 days of age, total RNA was extracted from pancreatic tissue for microarray analysis using the Affymetrix GeneChip Mouse Genome 430 2.0. Gene and protein expression were quantified from isolated islets. Finally, β-cell proliferation was determined in vitro following REG1α treatment. The microarray data and GO enrichment analysis indicated that foetal protein restriction alters the early expression of genes necessary for many cell functions, such as oxidative phosphorylation and free radical scavenging. Expression of Reg1 was upregulated following STZ, whereas protein content was decreased in LP + STZ islets. Furthermore, REG1α failed to stimulate β-cell proliferation in vitro in LP + STZ islets. Therefore, early nutritional insults may programme the Reg1 pathway resulting in a limited ability to increase β-cell mass during metabolic stress. In conclusion, this study implicates the Reg1 pathway in β-cell regeneration and describes altered programming of gene expression in LP offspring, which underlies later development of cell dysfunction and glucose intolerance in adulthood.

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“…This is in agreem ent w ith evidence from other typ es of studies, suggesting (Fertil et al 1988). The dep endence of PLD on LET has been studied experim entally by Yang et al (1985) that m ost DN A dsb in m am m alian cells are rep aired (Radford 1986).…”

Section: Et D Ep E Nd En Ce O F P Ote Ntially Le Thal Through a Celmentioning

confidence: 99%

Parameters of linear-quadratic radiation dose-effect relationships: dependence on LET and mechanisms of reproductive cell death

Barendsen

1997

International Journal of Radiation Biology

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Neoplastic Cell Transformation by Heavy Charged Particles

Cited by 153 publications

References 14 publications

Modeling the biological response of normal human cells, including repair processes, to fractionated carbon beam irradiation

Modeling the biological response of normal human cells, including repair processes, to fractionated carbon beam irradiation

Cellular mechanisms underlying failed beta cell regeneration in offspring of protein-restricted pregnant mice

Parameters of linear-quadratic radiation dose-effect relationships: dependence on LET and mechanisms of reproductive cell death

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