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At least 433 records · Page 24Linked to original sources
PubMed2003

Genetic analysis of radiation-associated rectal cancer.

Genetic aberrations in radiation-associated colorectal cancer have not been studied in detail. We analyzed genetic aberrations in five rectal cancers that developed long after radiotherapy had been performed for cervical cancer. Microsatellite instability (MSI) in tumors was examined at five loci: D2S123, D3S966, TP53, DCC, and BAT26. Mutation of simple repeat sequences within the hMSH3, BAX, and transforming growth factor Beta type II receptor ( TGFBetaRII) genes was examined by polymerase chain reaction and single-strand conformation polymorphism (PCR-SSCP). Mutation of p53 exons 5-8 was examined by PCR-SSP and direct sequencing. Mutations of the K- ras gene were analyzed by two-step PCR. No MSI was found in tumor specimens at any of the loci examined, and no mutations in the target genes were observed. K- ras mutation was detected in two carcinomas, but not in their irradiated normal mucosa, while p53 mutation was observed in another two carcinomas, but not in their irradiated normal mucosa. Our results suggest that the radiation-associated rectal carcinomas examined in this study did not develop through the mutator phenotype pathway; rather, tumorigenesis was probably mediated through the multistep carcinogenesis pathway.

Aged↗
PubMed2005

Genetic susceptibility to radiation.

In the context of space radiation, it is important to know whether the human population includes genetically predisposed radiosensitive subsets. One possibility is that haploinsufficiency for ATM confers radiosensitivity, and this defect involves 1-3% of the population. Using knock-out mice we chose to study cataractogenesis in the lens and oncogenic transformation in mouse embryo fibroblasts to assay for effects of ATM deficiency. Radiation induced cataracts appeared earlier in the heterozygous versus wild-type animals following exposure to either gamma rays or 1 GeV/nucleon iron ions. In addition, it was found that embryo fibroblasts of Atm heterozygotes showed an increased incidence of oncogenic transformation compared with their normal litter-matched counterparts. From these data we suggest that Ataxia Telangiectasia heterozygotes could indeed represent a societally significant radio sensitive subpopulation. Knock-out mice are now available for other genes including BRCA1 and 2, and Mrad9. An exciting possibility is the creation of double heterozygotes for pairs of mutated genes that function in the same signal transduction pathway, and consequently confer even greater radiosensitivity.

Aerospace Medicine↗
PubMed2001

[Genetic effects of acute and chronic ionizing irradiation on Pinus sylvestris L., inhabiting the Chernobyl' meltdown area].

The main results of the 12-year radiation-genetic monitoring of radiobiological, cytogenetic, and genetic parameters in Pinus sylvestris forest plantation from the Chernobyl meltdown area are presented. The acute ionizing irradiation at doses > 1 Gy was shown to induce formation of morphoses and depressed growth; at doses > 2 Gy, the reproductive ability of the trees declined. The radiobiological parameters showed a linear or close to linear dose-dependence relationship. The acute irradiation at a dose of 0.5 Gy induced cytogenetic and genetic effects that were significantly higher than the corresponding control values. The relationship between the cytogenetic effects and the absorbed dose was exponential. The dependence of the mutation frequency at specific loci on the absorbed dose was described by a nonlinear curve. The results of cytogenetic analysis of seedlings obtained from seeds annually collected in zones of slight, moderate, and strong damage of Pinus sylvestris L. are presented.

Chromosome Aberrations↗
PubMed2002

Workshop on The Epidemiology of the ATM Gene: Impact on Breast Cancer Risk and Treatment, Present Status and Future Focus, Lillehammer, Norway, 29 June 2002.

The role of ataxia-telangiectasia mutated (ATM) heterozygosity in cancer is uncertain. In vitro studies of cells from ATM heterozygotes provide strong evidence of radiation sensitivity. Some, but not all, clinical studies suggest an increased risk of breast cancer among ATM gene carriers, and this risk may be greater among those exposed to radiation. This possible excess risk of breast cancer associated with ATM heterozygosity constitutes the basis for several genetic epidemiological studies designed to clarify the role that the ATM gene plays in the etiology of breast and other cancers. The primary focus of this international, multidisciplinary, National Cancer Institute-sponsored workshop was to discuss ongoing and planned epidemiologic studies aimed at understanding the complexities of the ATM gene and its role in carcinogenesis. The invited participants were from diverse disciplines including molecular and clinical genetics, radiation biology and physics, epidemiology, biostatistics, pathology, and medicine. In the present meeting report, the aims of each project are described.

Ataxia Telangiectasia Mutated Proteins↗
PubMedDate not supplied

[The problem of induced genomic instability in the child body cells under conditions of long-term effect of small radiation doses].

The phenomenological aspects of the genomic instability induced in the descendants of the multi-divided cells having been exposed to the radiation are examined. It is demonstrated that the regularity of the chromosome instability induction do not correspond to the classical conception of the radiation genetics (hit principle and target theory). The mechanisms and the biological significance of this new genetic phenomenon in the child organism under conditions of low-intensive effect of small-dose radiation and its connection with the state of health are discussed.

Adult↗
PubMed1981

Effect of recB21, uvrD3, lexA101 and recF143 mutations on ultraviolet radiation sensitivity and genetic recombination in delta uvrB strains of Escherichia coli K-12.

The interaction of the recB21, uvrD3, lexA101, and recF143 mutations on UV radiation sensitization and genetic recombination was studied in isogenic strains containing all possible combinations of these mutations in a delta uvrB genetic background. The relative UV radiation sensitivities of the multiply mutant strains in the delta uvrB background were: recF recB lexA greater than recF recB uvrD lexA, recF recB uvrD greater than recA greater than recF uvrD lexA greater than recF recB, recF uvrD greater than recF lexA greater than recB uvrD lexA greater than recB uvrD greater than recB lexA, lexA uvrD greater than recB greater than lexA, uvrD greater than recF; three of these strains were more UV radiation sensitive than the uvrB recA strain. There was no correlation between the degree of radiation sensitivity and the degree of deficiency in genetic recombination. An analysis of the survival curves revealed that the recF mutation interacts synergistically with the recB, uvrD, and lexA mutations in UV radiation sensitization, while the recB, uvrD, and lexA mutations appear to interact additively with each other. We interpret these data to suggest that there are two major independent pathways for postreplication repair; one is dependent on the recF gene, and the other is dependent on the recB, uvrD, and lexA genes.

DNA Repair↗
PubMed1980

Medical radiation exposure and genetic risks.

Everyone is exposed to background radiation throughout life (100 mrem/year to the gonads or 4 to 5 rem during the reproductive years). A lumbosacral series might deliver 2,500 mrem to the male or 400 mrem to the female gonads. A radiologic procedure is a cost/benefit decision, and genetic risk is a part of the cost. Although cost is usually very low compared to benefit, if the procedure is unnecessary then the cost may be unacceptable. On the basis of current estimates, the doubling dose is assumed to be 40 rem (range 20 to 200) for an acute dose, and 100 rem for protracted exposure. Although there is no satisfactory way to predict the size of the risk for an individual exposed, any risk should be incentive to avoid unnecessary radiation to the gonads. Conception should be delayed for at least ten months for women and three or four months for men after irradiation of the gonads. The current incidence of genetically related diseases in the United States population is 60,000 per million live births. Based on the most conservative set of assumptions, an average gonadal dose of 1,000 mrem to the whole population would increase the incidence of genetically related diseases by 0.2%.

Abnormalities, Radiation-Induced↗
PubMed1975

Genetic effects of radiation.

The effects of radiation on biologic systems as manifested through genetic changes have been reviewed. The use of x-radiation by the health professions represents the largest contribution of radiation dose to the people of the United States. It is apparent that the genetic effect of radiation results in the production of chromosomal aberrations and gene mutations. Recognizing this, it becomes mandatory that appropriate measures are instituted to reduce to an absolute minimum the total amount of radiation that patients receive. Strict utilization of all known protective measures and adherence to protective guidelines promulgated by the ICRP and NCRP IS IMPERATIVE. Every attempt must be made to obtain maximal diagnostic yield from all radiation exposures used for diagnostic purposes, thereby assuring maximal benefit for our patients with minimal risk to our ancestors.

Cell Division↗
PubMed1992

[A.S. Serebrovskiĭ's experimental studies on induced mutagenesis].

The paper is devoted to A.S. Serebrovskiĭ's studies on induced mutagenesis. His first publication on X-ray induction of mutations in Drosophila appeared in 1928; this became a classical work and entered the golden fund of modern radiation genetics. Investigations of the scientists in the A.S. Serebrovskiĭ's laboratory as will as his own works on the analysis of radiation mutations at the achaete-scute complex have led to the development of the teaching about gene subdivision and made it possible to draw up a linear array of a gene from elementary subgenes, which have laid down the foundations of the modern molecular-genetic theory of gene.

Animals↗
PubMedDate not supplied

[Mutagenesis in Muridae from regions with increased radiation level].

Genetic monitoring of wild populations of mouse-like rodents has been carried out since 1992 in areas with the increased radioactivity in the south of the Bryansk region. The radioactive background ranged from 0.20 to 2.20 mkGy/h. Over 400 rodents of different species have been examined. Bank vole constituted more than a half of the examined animals. The genetic effect of radiation was estimated by the frequency of micronuclei in normochromatic erythrocytes of peripheral blood and by the frequency of abnormal sperm heads. In house mice the frequency of reciprocal translocations and the level of embryo mortality were studied in the progeny of the caught male mice mated with intact laboratory females. The data obtained demonstrate that the yield of induced genetic disorders by all tests was relatively low and only in a few cases the frequency of disturbances tended to increase with an increase in the level of radionuclide contamination in the examined areas.

Animals↗
PubMed2005

Genetic variation in XPD, sun exposure, and risk of skin cancer.

The XPD gene is involved in the nucleotide excision repair pathway removing DNA photoproducts induced by UV radiation. Genetic variation in XPD may exert a subtle effect on DNA repair capacity. We assessed the associations between two common nonsynonymous polymorphisms (Asp312Asn and Lys751Gln) with skin cancer risk in a nested case-control study within the Nurses' Health Study (219 melanoma, 286 squamous cell carcinoma, 300 basal cell carcinoma, and 874 controls) along with exploratory analysis on the haplotype structure of the XPD gene. There were inverse associations between the Lys751Gln and Asp312Asn polymorphisms and the risks of melanoma and squamous cell carcinoma. No association was observed between these two polymorphisms and basal cell carcinoma risk. We also observed that the association of the 751Gln allele with melanoma risk was modified by lifetime severe sunburns, cumulative sun exposure with a bathing suit, and constitutional susceptibility score (P for interaction = 0.03, 0.04, and 0.02 respectively). Similar interactions were also observed for the Asp312Asn. Our data suggest these two XPD nonsynonymous polymorphisms may be associated with skin cancer risk, especially for melanoma.

Adult↗
PubMed1975

Unsealed radioactive materials in medical practice in New Zealand.

Information has been collected on numbers and types of radionuclide procedures in medical practice in New Zealand over a three-month period in the latter half of 1973. For in vivo procedures data on the age and sex of patients and the activities of radioactive materials administered were also collected. The changes in numbers of such procedures carried out over a seven-year period are discussed. A genetic radiation dose to the population of 0.24 mrad per person is derived for the year 1973, about 0.20 mrad of this dose arising from diagnostic procedures and 64 percent being attributable to brain imaging. Whereas formerly genetic doses have been estimated from data on activities of 131I and 32P used, this is no longer possible.

Adult↗
PubMed2005

Protection against UV-light-induced skin carcinogenesis in SKH-1 high-risk mice by sulforaphane-containing broccoli sprout extracts.

Aerobic life, UV solar radiation, genetic susceptibility, and immune status contribute collectively to the development of human skin cancers. In addition to direct DNA damage, UV radiation promotes the generation of reactive oxygen intermediates that can cause oxidative damage and inflammation, and ultimately lead to tumor formation. Treatment of murine and human keratinocytes with the isothiocyanate sulforaphane elevated phase 2 enzymes and glutathione and protected against oxidant toxicity. Topical application of sulforaphane-containing broccoli sprouts extracts induced the phase 2 response in mouse skin in vivo. Sulforaphane inhibited cytokine-dependent (gamma-interferon or lipopolysaccharide) induction of iNOS in RAW 264.7 macrophages. The UV-radiation-induced skin carcinogenesis in "initiated high-risk mice" was substantially inhibited by broccoli sprout extracts containing sulforaphane. After completion of the UV irradiation schedule (30 mJ/cm(2)/session twice a week for 20 weeks), groups of approximately 30 mice were treated topically on their backs (5 days a week for 11 weeks) with broccoli sprout extract containing either the equivalent to 0.3 micromol (low dose) or 1.0 micromol (high dose) sulforaphane, respectively. At this time point, the tumor incidence had reached 100% in the control mice. Tumor burden, incidence, and multiplicity were reduced by 50% in the animals that received the high dose of protector. Tumor incidence and multiplicity did not differ between the low dose-treated and the control groups, but the low dose treatment resulted in a substantial reduction of the overall tumor burden. Thus, topical application of sulforaphane-containing broccoli sprout extracts is a promising strategy for protecting against skin tumor formation after exposure to UV radiation.

Animals↗
PubMed1993

Expression of p210 bcr/abl increases hematopoietic progenitor cell radiosensitivity.

PURPOSE: The cytogenetic finding of the Ph1+ chromosome and its molecular biologic marker bcr/abl gene rearrangement in cells from patients with chronic myeloid leukemia are associated with a proliferative advantage of the Ph1+ clone in vivo. Although the transition to the acute terminal phase or blastic crisis is often associated with additional cytogenetic abnormalities, the molecular events which correlate the initial cytogenetic lesion with the terminal phase are poorly understood. Defective cellular DNA repair capacity is often associated with chromosomal instability, increased mutation frequency, and biologic alterations. METHODS AND MATERIALS: We, therefore, tested whether the protein product of the bcr/abl translocation (p210) could alter DNA repair after gamma-irradiation of murine cell lines expressing the bcr/abl cDNA. RESULTS: The 32D cl 3 parent, 32D cl 3 pYN (containing the control vector plasmid) and each of two sources of 32D cl 3 cells expressing p210 bcr/abl cDNA (32D-PC1 cell line and 32D-LG7 subclone) showed a D0 of 1.62, 1.57, 1.16, and 1.27 Gy, respectively. Thus, expression of the p210 bcr/abl product induced a significant (p < 0.05) increase in radiosensitivity at the clinically relevant radiation therapy dose-rate (1.16 Gy/min). The increased radiosensitivity of p210 bcr/abl expressing cells persisted if cells were held before plating in a density-inhibited state for 8 hr after gamma-irradiation, indicating little effect on the repair of potentially lethal gamma-irradiation damage. The IL-3 dependent parent 32D cl 3 cells demonstrated programmed cell death in the absence of growth factor or following gamma-irradiation to 200 cGy. Expression of bcr/abl cDNA in the 32D-PC1 and 32D-LG7 sub clones abrogated IL-3 requirement of these cell lines and inhibited gamma-irradiation induced programmed cell death. CONCLUSION: These data suggest a role for bcr/abl p210 in amplifying gamma-irradiation DNA damage or broadly inhibiting DNA repair, conditions that may stimulate further cytogenetic alterations in hematopoietic cells.

Biomarkers↗