Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “RADIATION GENETICS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,189 records · Page 66Linked to original sources
PubMed2004

Lauriston S. Taylor Lecture: The evolution of radiation protection--from erythema to genetic risks to risks of cancer to...?

Radiation Protection has evolved and will continue to evolve as new information becomes available, as the result of changes in public perception and concern and, perhaps in the future, as a result of enormous expenditures on reducing small risks. In the early part of the last century it was a sense of real danger among medical Practitioners that prompted the first set of exposure limiting suggestions. Addressing medical concerns continued to be the basis of guidance until after the Second World War. An array of new sources and applications led to new approaches, which modified many of the technical issues but didn't result in substantial changes in the dose limits. Fallout from the first generation of thermonuclear weapons in the 1950's resulted in focusing attention on genetic effects, which continued until the middle 1970's. Data from the Japanese Survivor Studies provided the information for risk based recommendations beginning in 1977 and continue to do so today. Both the ICRP and the NCRP are heavily criticized by both those groups of individuals which believe the risk estimates are underestimated and by those which believe the risks are greatly overestimated. Perhaps both organizations can take some comfort in Saint Thomas Aquinas' suggestion, "In medio virtus."

Age Factors↗
PubMedDate not supplied

Cumulative genetic damage in children exposed to preconception and intrauterine radiation.

Using a mathematical model and newly developed computer software, the data from the Tri-State Leukemia Survey involving different combinations of radiation exposures to the father and mother prior to conception and to the mother during pregnancy were analyzed. The hypothesis that radiation exposure produces genetic damage which may be expressed in the child both as indicator disease and as leukemia was tested. The genetic damage was estimated in terms of the proportion affected by a given exposure. The relative risk of leukemia and certain other indicator diseases among those "affected" could then be estimated. The results were obtained by direct minimization of the total chi-square. The results show that there are at least two distinguishable risk groups, one group with lower (one or two exposures), and the other group with higher (two or three) radiation exposures. The estimates for the proportion affected are 0.13 and .04 for the lower and higher exposure groups, respectively. The relative risks of leukemia and indicator diseases are 25.0 and 5.0, respectively. The 95% confidence intervals for the proportion affected in the lower and higher exposure categories are (.0075, .02) and (.028, .055), respectively, and for the relative risk of leukemia are (16.0, 35.0). These results have confirmed and extended the findings of our preliminary report published in the Journal of the American Medical Association in May 1977.

Adolescent↗
PubMed2001

Evidence of genetic instability in 3 Gy X-ray-induced mouse leukaemias and 3 Gy X-irradiated haemopoietic stem cells.

PURPOSE: If radiation-induced genetic instability is causal in mouse radiation leukaemogenesis, then genetic instability should be detectable in the irradiated target untransformed haemopoietic stem cell, and evidence of genetic instability detected in the clonal radiation-induced leukaemia. We have tested this hypothesis using the CBA/H mouse model of radiation-induced acute myeloid leukaemia (r-AML). MATERIALS AND METHODS: Fluorescence in situ hybridisation (FISH) was employed to screen for chromosomal aberrations in mouse 3 Gy X-ray-induced r-AMLs and in the clonal descendents of control and 3 Gy X-irradiated bone marrow haemopoietic stem cells using the in vitro clonogenic CFU-A colony assay. RESULTS: High levels of clonal non-specific chromosomal aberrations were detected in the r-AML (approximately 4-5 aberrations/r-AML), and ongoing chromosomal instability as defined by subclonal variants detected in 5/10 r-AML. A similar analysis of CFU-A colonies revealed chromosomal aberrations in 25% of colonies derived from irradiated bone marrow (2% in controls). However, 66% of the aberrant colonies (2% in controls) exhibited ongoing genetic instability as defined by non-clonal chromosomal aberrations. Overall, 6% (121/1884) of the CFU-A cells derived from irradiated bone marrow were aberrant (0.05% in controls) of which 12% (15/121) were subclonal. No one CFU-A cell exhibited aberrations on more than one of the three chromosomes painted. CONCLUSIONS: The high levels of non-specific genetic damage observed in the r-AMLs is therefore attributed to the accumulation of genetic lesions in the target haemopoietic stem cell over a longer time-scale after exposure than assessed in the in vitro CFU-A clonogenic assay. This is consistent with the long latency of the multi-stage radiation leukaemogenic process, and a role for radiation-induced genetic instability is inferred.

Animals↗
PubMedDate not supplied

Induction of genetic instability by ionizing radiation.

Evidence is presented to support the hypothesis that radiation may induce a heritable, genome-wide process of instability that leads to an enhanced frequency of genetic changes occurring among the progeny of the original irradiated cell. This instability is transmissible over many generations of cell replication. Mutational instability is induced in a relatively large fraction (approximately 10%) of the cell population, and may be modulated by factors acting in vivo. Thus, it cannot be a targeted event involving a specific gene or set of genes. There is no dose-response relationship in the range 2-12 Gy, suggesting that the instability phenotype may be induced by quite low radiation doses. The molecular mechanisms associated with the genesis of mutations in unstable populations differ from those for direct X-ray-induced mutations. These results suggest that it may not be possible to predict the nature of the dose-response relationship for the ultimate genetic effects of radiation based on a qualitative or quantitative analysis of the original DNA lesions.

Alpha Particles↗