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Hermann J. Muller (1890–1967)
Published in Krishna Dronamraju, A Century of Geneticists, 2018
With Julian Huxley’s help, Muller obtained a temporary position at the Institute for Animal Genetics at Edinburgh University. He was then 50 years old. Muller attracted several students during that period, including some who became well-known geneticists in their own right, such as Charlotte Auerbach, Guido Pontecorvo, and S.P. Ray Chaudhury. With Pontecorvo, Muller worked out the breakage–fusion–bridge cycle (dicentric chromosome formation), independently of Barbara McClintock, and used it to explain the curious dominant lethals he had observed in large numbers since his X-ray work in 1927. The dicentric chromosomes led to cell death and aborted embryos (Pontecorvo and Muller 1942). With his student S.P. Ray Chaudhury, Muller extended his radiation studies to chronic and acute doses. Another finding was that, for gene mutations, it made no difference whether a dose of 400 R was administered in a few minutes or drawn out over a month-long period. In either case, the mutation rate was the same, confirming Muller’s belief that gene mutations were punctiform events (Muller and Chaudhury 1939). The same observation got him embroiled in a dispute with British radiologists who considered it inappropriate it to extrapolate from flies to humans and that Muller’s view might unnecessarily alarm the public about the uses of radiation.
A Brief Review of Cancer
Published in C.S. Sureka, C. Armpilia, Radiation Biology for Medical Physicists, 2017
Aberrant activation of CDKs, regulatory proteins, and p53 proteins (>50%) leads to irregularities in the cell cycle. Further, activation of telomerase (~90% contribution) triggers the cell to achieve an infinite life (referred to as immortalization). This also happens when the cell repairs its dicentric chromosome using a non-homologous end-joining mechanism (discussed in Chapter 3). Hence, a normal cell is transformed into a malignant cell due to its irregular cell cycle, failure in apoptosis, and cell immortalization.
Cell death after irradiation: How, when and why cells die
Published in Michael C. Joiner, Albert J. van der Kogel, Basic Clinical Radiobiology, 2018
Why does irradiation cause proliferating cells to undergo mitotic catastrophe and cell death? This appears to result from the fact that although DDR pathways remove much of the initial damage caused by irradiation, they are unable to prevent some cells with DNA breaks or DNA rearrangements from entering mitosis. The consequences of incomplete or improper DNA repair become readily visible as chromosomes condense in metaphase as a series of different types of chromosome aberrations. The fate of cells harbouring chromosome aberrations is largely determined by the nature of the chromosome aberration itself (Figure 3.3) (1). Studies have demonstrated approximately equal numbers of reciprocal translocations and non-reciprocal translocations (a dicentric chromosome + acentric fragment) are formed after irradiation. Both of these types of aberrations result from misrepair in which chromosome ends are incorrectly ligated together in a largely stochastic process. However, whereas cells with dicentrics and acentric fragments all die, those with reciprocal translocations often survive. The presence of two centromeres in dicentric chromosomes prevents their separation at metaphase, and consequently leads to mitotic catastrophe and eventually cell death. Some cells with dicentric chromosomes may manage to complete mitosis, however, loss of genetic material present in the acentric fragment (which forms a ‘micronuclei’) in subsequent mitosis may lead to subsequent death at a later time. This explains the good correlation which has been observed between the formation of dicentric chromosomes or micronuclei formation and cell survival. Reciprocal translocations do not cause problems at metaphase, and thus do not cause mitotic catastrophe or cell death. In fact, these types of aberrations can be found in cells from people exposed to irradiation many years later.
Construction and evaluation of an α-particle-irradiation exposure apparatus
Published in International Journal of Radiation Biology, 2021
Zacharenia Nikitaki, Evangelia Choulilitsa, Spyridon A. Kalospyros, Sofia Kaisaridi, Georgia I. Terzoudi, Mike Kokkoris, Alexandros G. Georgakilas
The dicentric chromosome is the aberration type that is most frequently used in biological dosimetry. Dicentric chromosome is called an aberrant chromosome bearing two centromeres derived from the misrepair of two broken chromosomes (IAEA 2011). The International Organization for Standardization (ISO), in 2004, accepted the Dicentric Chromosome Analysis (DCA) as an International Standard for laboratories performing radiation biological dosimetry by cytogenetics. The DCA technique is particularly useful when it comes to the evaluation of cases of suspected or verified radiation exposure as well as for dose estimation in the absence of physical dosimetry (IOfS 2004). Although radiation induces many types of chromosomal changes in addition to dicentric chromosomes, dicentric analysis is considered the “gold standard” for assessing radiation dose. Finally, this analysis is both specific and sensitive to radiation exposure even at low doses. Dicentric analysis has been performed by McNally et al to compare α-particle irradiation with X-rays, concluding that their levels are proved to be similar to that of 6 Gy for X-rays, 24 h upon irradiation with 2 Gy of alpha particles – (Manti 1997).
An intercomparison exercise to compare scoring criteria and develop image databank for biodosimetry in South Korea
Published in International Journal of Radiation Biology, 2021
Yang Hee Lee, Younghyun Lee, Hyo Jin Yoon, Su San Yang, Hae Mi Joo, Ji Young Kim, Seong-Jun Cho, Wol Soon Jo, Soo Kyung Jeong, Su Jung Oh, Yeong-Rok Kang, Ki Moon Seong
Variations in scoring dicentrics were often found when chromosomes with centromeres in terminal positions (D or G group) formed dicentrics, which were similarly reported in a previous study (Romm et al. 2017). Chromosomes 13, 14, 15, 21, and 22 are acrocentric chromosomes, which have short p arms and the centromere is located near one end of the chromosome. One laboratory identified dicentric chromosomes based on the specific morphology of each chromosome (Figure 2), whereas the others considered it a fragment due to less visible centromeres. All participating laboratories agreed that understanding the morphology of D and G group chromosomes would help to identify dicentrics correctly. In addition, scoring results were different when chromosomes were twisted. Some scorers confused a twisted chromosome with a dicentric chromosome. According to experienced scorers’ comments, the twisted area in a chromosome is darker than centromere, including the centromere (Figure 3), which should allow easy discrimination of dicentrics and twisted chromosomes.
Low-dose radiobiology program at Canadian nuclear laboratories: past, present, and future
Published in International Journal of Radiation Biology, 2019
Yi Wang, Laura A. Bannister, Soji Sebastian, Yevgeniya Le, Youssef Ismail, Candice Didychuk, Richard B. Richardson, Farrah Flegal, Laura C. Paterson, Patrick Causey, Ali Fawaz, Heather Wyatt, Nicholas Priest, Dmitry Klokov
CNL maintains a biodosimetry capability that is part of a pan-Canadian biodosimetry network (Wilkins et al. 2015) that is also part of the international network coordinated by the WHO in Geneva. Radiological incidents affecting mass populations would require the fast and reliable dosimetric assessment of those exposed for triage purposes. This has traditionally been done using the dicentric chromosome aberration analysis (IAEA 2011). The biodosimetry team at CNL, in collaboration with Canadian and European partners, has contributed to the development, validation, and advancement of the method (Flegal et al. 2010; Oestreicher et al. 2017). Moreover, current research at CNL is examining novel sensitive markers of radiation exposure suitable for radiological triage purposes. Among the current candidates are the molecular content of exosomes and the automated scoring of γH2AX foci.