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At least 811 records · Page 45Linked to original sources
PubMed2004

Direct stenting versus direct stenting followed by centered beta-radiation with intravascular ultrasound-guided dosimetry and long-term anti-platelet treatment: results of a randomized trial: Beta-Radiation Investigation with Direct Stenting and Galileo in Europe (BRIDGE).

OBJECTIVES: We sought to assess the efficacy of vascular brachytherapy (VBT) combined with stenting for the primary prevention of restenosis. BACKGROUND: Intravascular brachytherapy after stent implantation for de novo lesions has been abandoned for the present. We revisited this procedure by optimizing all procedural steps-the use of glycoprotein IIb/IIa blockers, direct stenting, adequate radiation coverage, avoidance of edge damage, source centering, intravascular ultrasound-guided dosimetry, and continuation of a dual anti-platelet regimen for one year. METHODS: The Beta-Radiation Investigation with Direct stenting and Galileo in Europe (BRIDGE) study is a multicenter, randomized controlled trial evaluating the long-term efficacy of VBT with P-32 (20 Gy at 1 mm in the coronary wall) after direct stenting. The primary end point was angiographic intra-stent late loss; secondary end points were six months binary restenosis and neo-intimal hyperplasia. Patients (n = 112) with de novo lesions (2.5 to 4.0 mm in diameter up to 15 mm long) were randomized to either VBT or no-VBT. RESULTS: At six months, intra-stent loss was 0.43 and 0.84 mm (p < 0.001) in the irradiated and control groups, respectively. Intra-stent neo-intimal volume was reduced from 36 mm3 to 10 mm3. However, in the irradiated group there were six late occlusions as well as eight restenoses outside the stented and peri-stented area at the fall-off dose edges of the irradiated area. Accordingly, the target vessel revascularization and major adverse cardiac and cerebrovascular events rates at one year in the VBT group (20.4% and 25.9%, respectively) were higher than in the control group (12.1% and 17.2%, respectively). CONCLUSIONS: Despite the optimization of pre-, peri-, and post-procedural factors and despite the relative efficacy of the brachytherapy for the prevention of the intra-stent neo-intimal hyperplasia, the clinical outcome of the irradiated group was less favorable than that of the control group.

Aged↗
PubMed1999

A prospective, randomized, double-masked trial on radiation therapy for neovascular age-related macular degeneration (RAD Study). Radiation Therapy for Age-related Macular Degeneration.

OBJECTIVE: To determine the efficacy of external beam radiation therapy on choroidal neovascularization (CNV) secondary to age-related macular degeneration (ARMD). DESIGN: Multicenter, parallel, randomized, double-masked clinical trial performed at nine ophthalmic and radiotherapeutic centers. PARTICIPANTS: Two hundred five patients were randomly assigned either to treatment with 8 fractions of 2 Gy external beam irradiation (n = 101) or to control with 8 fractions of 0 Gy (sham treatment, n = 104). Both patients and ophthalmologists were masked with regard to applied treatment. Patients with subfoveal classic or occult CNV, visual acuity of 20/320 or greater on the Early Treatment Diabetic Retinopathy Study chart, lesion size of 6 disc areas or less, history of visual symptoms of 6 months or less, and absence of foveal hemorrhage were recruited. INTERVENTION: In the treatment group, external beam irradiation with 8 fractions of 2 Gy was performed, whereas in the control group, sham treatment with 8 fractions of 0 Gy was applied. MAIN OUTCOME MEASURES: Primary outcome measure was the difference in visual acuity between baseline and after 1 year of follow-up. RESULTS: One hundred eighty-three patients (89.3%) completed the 1-year follow-up. The mean reduction in visual acuity was 3.5 +/- 4.7 lines in 88 patients of the 8- x 2-Gy treatment group and 3.7 +/- 3.8 lines in 95 patients of the 8- x 0-Gy control group. This difference was not statistically significant (P = 0.53, Mann-Whitney U test). At 1 year, 51.1% of treated patients and 52.6% of control subjects lost three or more lines (P = 0.88). Visual acuity in the presence of classic CNV dropped by 3.7 +/- 4.4 lines in 33 patients of the treatment group versus 4.3 +/- 3.9 lines in 36 patients of the control group (P = 0.47). Visual acuity in 114 patients with occult CNV dropped by 3.4 +/- 4.9 in the treatment group (55 patients) versus 3.4 +/- 3.8 lines in the control group (59 patients) (P = 0.80). CONCLUSIONS: In this randomized study, radiation therapy at a dose of 16 Gy applied in 8 fractions of 2 Gy provided no benefit as a treatment for subfoveal CNV secondary to ARMD at 1 year.

Aged↗
PubMed1993

Pelvic failure rate and radiation toxicity in relation to total dose of radiation alone for the treatment of cancer of the uterine cervix.

Seventy-four patients presenting between 1978 and 1989 with carcinoma of the uterine cervix were analysed to compare our results with the published literature, especially with regard to the pelvic failure rate and radiation toxicity. Overall 5-year survival reached 41%. Overall 2-year survival rate for Stage IIB was 85% and Stage IIIB was 32%. For Stage IIB the results agreed with those reported in the literature. Pelvic control was related to total dose and the application of intracavitary irradiation. For Stage IIIB the results were disappointing, partly due to a large number of bulky tumours and also to a relatively low paracentral dose and dose to the pelvic side wall. Percentages of radiation side-effects were low compared with those reported in the literature, probably also due to the relatively low total dose.

Brachytherapy↗
PubMed1998

Radiation therapy or prostatectomy: an old conflict revisited in the PSA era. A radiation oncologist's viewpoint.

A close examination of the outcomes for the radical treatment of prostate cancer in the prostate-specific antigen (PSA) era shows no clear advantage to radical prostatectomy over external-beam radiation. Both modalities are highly effective against small impalpable tumors of low Gleason grade and with PSA values less than 10 ng/mL. Both modalities struggle against all other stages of prostate cancer. Radiation and surgery are currently in states of rapid evolution, and the results emerging become quickly outdated. It is hoped that the newer, more aggressive approaches will help a significant number of patients, perhaps the majority, not currently being cured by radical therapy.

Biomarkers, Tumor↗
PubMed1999

Chromosomal breakpoint positions suggest a direct role for radiation in inducing illegitimate recombination between the ELE1 and RET genes in radiation-induced thyroid carcinomas.

The RET/PTC3 rearrangement is formed by fusion of the ELE1 and RET genes, and is highly prevalent in radiation-induced post-Chernobyl papillary thyroid carcinomas. We characterized the breakpoints in the ELE1 and RET genes in 12 post-Chernobyl pediatric papillary carcinomas with known RET/PTC3 rearrangement. We found that the breakpoints within each intron were distributed in a relatively random fashion, except for clustering in the Alu regions of ELE1. None of the breakpoints occurred at the same base or within a similar sequence. There was also no evidence of preferential cleavage in AT-rich regions or other target DNA sites implicated in illegitimate recombination in mammalian cells. Modification of sequences at the cleavage sites was minimal, typically involving a 1-3 nucleotide deletion and/or duplication. Surprisingly, the alignment of ELE1 and RET introns in opposite orientation revealed that in each tumor the position of the break in one gene corresponded to the position of the break in the other gene. This tendency suggests that the two genes may lie next to each other but point in opposite directions in the nucleus. Such a structure would facilitate formation of RET/PTC3 rearrangements because a single radiation track could produce concerted breaks in both genes, leading to inversion due to reciprocal exchange via end-joining.

Adolescent↗
PubMed2001

Timing of excessive ultraviolet radiation and melanoma: epidemiology does not support the existence of a critical period of high susceptibility to solar ultraviolet radiation- induced melanoma.

BACKGROUND: The existence of a 'critical period' early in life characterized by a high susceptibility to melanoma initiation due to excessive ultraviolet (UV) radiation has been suggested by various authors based on epidemiological findings from migration studies and some case-control studies. However, the evidence so far is controversial as several epidemiological investigations failed to corroborate these results. Objective To compare the increase in melanoma risk due to excessive UV radiation between different periods in life. METHODS: In a multicentre case-control study we recruited 603 melanoma cases and 627 population controls in seven European countries. We obtained data on the history of sunburns during 'childhood' (</= 15 years) and 'adulthood' (> 15 years), respectively, in standardized personal interviews. We employed logistic regression analyses to estimate the impact of the exposure factors under study, while simultaneously controlling for the effect of a variety of confounding variables. RESULTS: We found a very similar upward gradient of melanoma risk in exposure categories related to the frequency of sunburns during both periods in life. More than five sunburns doubled the melanoma risk, irrespective of their timing in life. CONCLUSIONS: Our data do not provide supporting evidence for the existence of a 'critical period'. The hazardous impact of sunburns seems to persist lifelong and thus activities concerned with melanoma prevention should be directed to the entire population rather than being focused only on younger age groups.

Adolescent↗
PubMed2001

Non-targeted radiation effects in radiotherapy--roles of radiation-induced genomic instability and of the bystander effect in cancer cure by radiotherapy.

Local tumour control by radiotherapy requires the complete sterilization of all tumour 'stem' cells in the tumour volume. Neither bystander effect nor radiation-induced genomic instability is able to contribute substantially to the probability of local tumour control of the primary cancer by radiotherapy. However, the progeny of these surviving tumour 'stem' cells are likely to suffer from radiation-induced genomic instability, which results in the persistent appearance of non-stem cells, i.e. a reduced probability of self-maintenance. This results in a slower growth rate of the recurrent tumour, a reduced stem-cell fraction and, as a consequence, an increased radiosensitivity of the recurrent tumour. In some recurrent tumours, particularly those that develop very late and grow very slowly, radiosensitivity may be further increased by increased intrinsic radiosensitivity, which could be related to the as yet poorly defined phenotype of 'small colony formation'.

Bystander Effect↗
PubMed2002

Limits imposed by ionizing radiation on the long-term survival of trapped bacterial spores: beta radiation.

PURPOSE: A model is presented for determining the survival time T(F) of a fraction F of a population of bacterial spores trapped within a fluid inclusion and subject to genetic damage from beta radiation. METHODS: The limiting factor to survival is the production of double-strand breaks (DSB) in the DNA resulting from single-track cleaving and from the cumulative effects of single-strand breaks (SSB) induced by the presence of ionizing radiation in the environment. The model considers the probability that radicals and ions formed by the passage of high-energy particles will interact with a DNA molecule and induce damage. RESULTS: The survival time T(F) for a fraction F of a trapped population is a weak function of both F and the length L in base pairs of the genome. For irradiation due to a beta source trapped with the spores within the inclusion, the survival time is also inversely proportional to the concentration of the radionuclide, the dominant factor in limiting survival time. CONCLUSIONS: The predictions of the model are consistent with measured DSB formation rates, the observed survival of trapped spores over time periods as long as 250 Ma, and track structure models which address low physical dose rates.

Bacteria↗
PubMed1978

Extensive and equivalent repair in both radiation-resistant and radiation-sensitive E. coli determined by a DNA-unwinding technique.

The extent of strand breakage and repair in irradiated E. coli B/r and Bs-1 was studied using a DNA-unwinding technique in denaturing conditions of weak alkali. Although these two strains show widely different responses to the lethal effects of ionizing radiation, they both have an equal capacity to repair radiation-induced breaks in DNA. Oxygen enhancement ratios for the killing of B/r and Bs-1 were respectively 4 and 2; but after repair in non-nutrient or nutrient post-irradiation conditions, the oxygen enhancement values for the residual strand breaks were always the same for the two strains. The equal abilities of E. coli B/r and E. coli Bs-1 to remove the strand breaks measured by this weak-alkali technique leads us to suggest that some other type of damage to either DNA or another macromolecule may play a major role in determining whether or not the cells survive to proliferate.

DNA, Bacterial↗
PubMed1979

Interaction between radiation and drug damage in mammalian cells. III. The effect of adriamycin and actinomycin-D on the repair of potentially lethal radiation damage.

We have studied the effects of actinomycin-D (AMD) and Adriamycin (ADRM) on the repair of radiation damage in Chinese hamster cells (V79) in plateau phase growth. Suppression of potentially lethal damage repair (PLDR) was observed in the presence of non-toxic levels of AMD and minimally toxic levels of ADRM. The suppression of PLDR by AMD persisted as long as the drug was present. Removal of AMD was followed by prompt repair of potentially lethal injury suggesting that suppression of PLDR by AMD was not accompanied by fixation of injury to a non-repairable state. On the other hand, irradiated cells exposed to ADRM eventually repair potentially lethal injury in the presence of drug after an initial delay. AMD, but not ADRM, inhibited repair of sublethal radiation damage.

Animals↗
PubMed1987

Effects of ionizing radiation on artificial (planar) lipid membranes. I. Radiation inactivation of the ion channel gramicidin A.

The ion channel formed by the pentadecapeptide gramicidin A in planar lipid membranes is extremely sensitive to ionizing radiation. The membrane conductance may drop by several orders of magnitude under appropriate experimental conditions (low pH and presence of oxygen). The radiation sensitivity is strongly reduced for gramicidin M-. This analogue has the four tryptophan residues replaced by phenylalanines. Experiments performed in the presence of various radical scavengers suggest that the inactivation of the channel is due to a combined action of OH and of HO2 radicals at the tryptophan residues. The shape of the inactivation curves following continuous radiolysis or pulse radiolysis were found to be in fair agreement with a simple model which assumes that the damage of a single tryptophan residue is sufficient for channel inactivation. The conductance of inactivated channels could not be resolved within the experimental accuracy. This is contrary to photolysis of gramicidin channels found by Busath and Waldbilling (1983), where a broad distribution of low conductance states was observed. The inactivation by radiolysis seems to represent an 'all-or-none-process' of the channel conductance.

Dose-Response Relationship, Radiation↗
PubMed1988

The dose-response for low-LET radiation-induced DNA double-strand breakage: methods of measurement and implications for radiation action models.

There is considerable controversy over the form of the dose-response for DNA double-strand breakage (dsb) induction in mammalian cells by low-LET type radiation. This controversy centres on the techniques used for measuring DNA dsb. The applications and shortcomings of the four major techniques for estimating DNA size--sedimentation, viscoelastometry, electrophoresis, and non-denaturing filter elution--are examined. In particular, the criticisms of the results obtained using the non-denaturing filter elution technique, which have suggested that the DNA dsb dose-response is non-linear, are discussed. It is concluded that these results may require a re-evaluation of the basic assumptions of many radiation action models.

Animals↗
PubMed1996

Interstitial radiation and hyperthermia in the Dunning R3327 prostate tumour model: therapeutic efficacy depends on radiation dose-rate, sequence and frequency of heating.

To determine the most effective means by which to apply the combined treatments of local tumour hyperthermia (LTH) with interstitial low dose-rate irradiation (IRT) we examined the significance of such factors as dose-rate of radiation, and the sequence and frequency of hyperthermia applications in the anaplastic Dunning prostate tumour subline R3327-AT1. IRT was carried out by the insertion of a single Ir-192 seed into the center of the tumour. For LTH treatments, the tumour-bearing leg was positioned in a circulating constant temperature water bath (43.5 +/- 0.1 degrees C) for 35 min. Neither LTH treatment alone nor the insertion of a dummy seed produced any change in tumour growth compared with sham-treated controls. With regard to the sequence of heating and IRT our results showed that during a 72-h treatment time (30 Gy, 40 cGy/h) a single heat treatment given just before the start of IRT was more efficient (TER = 1.47) in terms of growth delay than LTH given in the middle or the end of radiation treatment (TER approximately 1.0). The growth delay for both the 20 and 40 cGy/h groups appear to be linear with increasing dose for the IRT as well as the IRT + LTH groups. The higher dose-rate was more effective especially with respect to long-term delay in tumour growth in some of the animals. As TER at 40 cGy/h decreased subsequently with increasing treatment time from 1.47 to 1.25 at 60 Gy, we conclude that for treatment times > 72 h, one LTH just before IRT might not be sufficient. If multiple heat treatments are applied during a comparable time course, two LTH treatments one just before the start, the other at the end yielded the greatest local tumour control. In contrast, three LTH given daily were not more effective than the one LTH given just before the start of IRT. These data indicate a clear thermal enhancement of low dose-rate irradiation, with maximal sensitization when hyperthermia was given just before IRT. For multiple heatings a better understanding of the underlying mechanisms of sequencing and timing hopefully provides guidelines how to apply optimally both modalities in the treatment of cancer.

Animals↗
PubMed1981

Self recognition in allogeneic radiation bone marrow chimeras. A radiation-resistant host element dictates the self specificity and immune response gene phenotype of T-helper cells.

The specificity of the self-recognition repertoire in fully allogeneic (A {arrow} B), semiallogeneic (A {arrow} A x B and A x B {arrow} A), and double donor (A + B {arrow} A) radiation bone marrow chimeras was assessed by the ability of their spleen cells to generate in vitro primary plaque-forming cell (PFC) responses to trinitrophenyl- keyhole limpet hemocyanin. In contrast to spleen cells from semiallogeneic and double donor chimeras, intact spleen cells from fully allogeneic BI0 {arrow} B10.A and B10.A {arrow} B10 chimeras were not capable of generating responses to trinitrophenyl (TNP)-keyhole limpet hemocyanin. However, cultures containing a mixture of both B10 {arrow} B10.A and B10.A {arrow} B10 spleen cells did respond, demonstrating that all the cell populations required for the in vitro generation of T-dependent PFC responses were able to differentiate into functional competence in a fully allogeneic major histocompatibility complex (MHC) environment. The self recognition repertoire of T-helper cells from fully allogeneic A {arrow} B chimeras was determined to be specific for the recognition of host, not donor, MHC determinants in that they were able to collaborate with cells expressing only host MHC determinants but not with cells expressing only donor MHC determinants, even though the functional lymphocytes in these chimeras were shown to be of donor origin. Experiments utilizing double donor A + B {arrow} A chimeras further demonstrated that the ability of chimeric T cells to recognize allogeneic MHC determinants as self structures was a function of a radiation-resistant host element and not simply a consequence of the tolerization of T cell precursors to allogeneic MHC determinants, because strain A lymphocytes isolated from A + B {arrow} A chimeras were tolerant to both A and B MHC determinants but were restricted to the self recognition of syngeneic host type A MHC determinants. Finally, the Ir gene phenotype expressed by B10 {arrow} B10.A and B10.A {arrow} B10 chimeric lymphocytes was determined by their ability to function in the Ir gene controlled response to TNP-poly-L-(Tyr,Glu)-poly-D,L-Ala-poly- L-Lys [(T,G)-A--L]. The ability of lymphocytes to function in TNP-(T,G)-A--L responses was not determined by their genotype but rather paralleled the specificity of their self recognition repertoire for high responder (H-2 (b)) determinants. The possible degeneracy of the MHC-specific self recognition repertoire is discussed, and a model is proposed for Ir gene regulation in which expression of Ir gene function by lymphocytes is an antigen-nonspecific consequence of the specificity and cross-reactivity of their self recognition repertoire.

Animals↗
PubMed1975

Secondary radiation from a spherical tissue-equivalent phantom irradiated with 60Co gamma radiation and 6 MV X-rays.

The angular dependence and the dependence on the phantom mass of the secondary exposure rate from spherical tissue-equivalent phantoms irradiated with 60Co gamma radiation and 6 MV X-rays have been investigated both by measurement and by calculation using the Monte Carlo method and approximate methods. A nonlinear dependence on the phantom mass was found. Calculation of the differential photon fluence was also made. These measurements and calculations can be used when calculating the required barrier thickness for walls which are not hit by primary radiation.

Cobalt Radioisotopes↗
PubMed2004

Acute radiation toxicity assessment of a 3-D conformal head and neck radiation treatment technique.

Patients undergoing radiation treatment for head and neck cancer have many critical structures within or adjacent to the treatment area. Avoiding these critical structures is more efficient and easier using 3-D conformal planning. At Sir Charles Gairdner Hospital an investigation into the acute radiation toxicity was undertaken when the head and neck treatment technique was changed from the conventional 2-D plan to the conformal 3-D plan. Although the primary target volume (PTV), fraction size and overall dose remain the same for the two techniques, differing beam configurations mean that treatment fields enter and exit through different parts of the head and neck. Ten patients were initially assessed to gain a baseline appearance of their head and neck region, and then graded weekly according to the toxicity criteria during treatment and at 4, 8 and 12 weeks after treatment. The results of the assessment indicate that there is no increase in toxicity as a result of treating using the conformal head and neck technique.

Acute Disease↗
PubMed2002

Dose to radiation therapists from activation at high-energy accelerators used for conventional and intensity-modulated radiation therapy.

The increased beam-on times which characterize intensity-modulated radiation therapy (IMRT) could lead to an increase in the dose received by radiation therapists due to induced activity. To examine this, gamma ray spectrometry was used to identify the major isotopes responsible for activation at a representative location in the treatment room of an 18 MV accelerator (Varian Clinac 21EX). These were found to be 28Al, 56Mn, and 24Na. The decay of the dose rate measured at this location following irradiation was analyzed in terms of the known half-lives to yield saturation dose rates of 9.6, 12.4, and 6.2 microSv/h, respectively. A formalism was developed to estimate activation dose (microSv/week) due to successive patient irradiation cycles, characterized by the number of 18 MV fractions per week, F, the number of MU per fraction, M, the in-room time between fractions, td (min), and the treatment delivery time t'r (min). The results are represented by the sum of two formulas, one for the dose from 28Al 1.8 x 10(-3) F M (1-e(-03t'(r))/t'r and one for the dose from the other isotopes approximately 1.1 x 10(-6) F(1.7) Mt(d). For conventional therapy doses are about 60 microSv/week for an 18 MV workload of 60,000 MU/week. Irradiation for QA purposes can significantly increase the dose. For IMRT as currently practiced, lengthy treatment delivery times limit the number of fractions that can be delivered per week and hence limit the dose to values similar to those in conventional therapy. However for an IMRT regime designed to maximize patient throughput, doses up to 330 microSv/week could be expected. To reduce dose it is recommended that IMRT treatments should be delivered at energies lower than 18 MV, that in multienergy IMRT, high-energy treatments should be scheduled in the latter part of the day, and that equipment manufacturers should strive to minimize activation in the design of high-energy accelerators.

Algorithms↗
PubMed2004

Increased metastatic dissemination in human melanoma xenografts after subcurative radiation treatment: radiation-induced increase in fraction of hypoxic cells and hypoxia-induced up-regulation of urokinase-type plasminogen activator receptor.

Cancer patients showing local failure after radiation treatment have increased probability for developing metastatic disease. The mechanisms behind this observation have not been identified. In the present work, metastatic spread after inadequate radiation therapy was studied by using R-18 human melanoma xenografts as models of cancer in humans. Pimonidazole was used as a hypoxia marker, and hypoxia and urokinase-type plasminogen activator receptor (uPAR) expression were detected by immunohistochemistry. R-18 tumors regrowing after subcurative irradiation showed a higher frequency of lymph node metastasis than unirradiated tumors. The expression of uPAR was up-regulated in hypoxic tumor regions, and the fractions of hypoxic and uPAR-positive cells were approximately 2-fold higher in regrowing irradiated tumors than in untreated tumors. Treatment with anti-uPAR antibody blocked metastasis almost completely in irradiated as well as unirradiated tumors. The metastatic frequency was higher in tumors regrowing after irradiation than in unirradiated tumors because the irradiation induced tumor hypoxia, and tumor hypoxia induced up-regulation of uPAR.

Animals↗