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PubMed2006

Radiobiology of breast cancer.

Advances in molecular and cellular biology are transforming our understanding of breast cancer and promise the same for radiotherapy over the next few years. At the clinical level, the molecular basis of fractionation dependency and other tumour and normal tissue responses are likely to become clearer. More importantly, they will become useful in the clinic, where molecular characterisation of the patient and tumour will start to determine therapeutic options. Although many of the fundamental processes are only amenable to study in laboratory systems, the power of array-based technologies makes it possibly to address highly relevant questions in the clinic, using functional imaging and/or tissue biopsies. To help clinical oncologists exploit these opportunities in translational research, some aspects of the molecular and cellular basis of radiotherapy are described below in their relation to breast cancer.

Biomedical Technology↗
PubMed2003

Long-term genetic effects of radiation exposure.

To date, there has been little experimental knowledge on the genetic risks of human exposure to ionising radiation for humans. Recent data suggest that hypervariable tandem repeat minisatellite loci provide a useful and sensitive experimental approach for monitoring radiation-induced germline mutation in humans. Here, I review the results of studies on minisatellite mutation rates in human populations exposed to radioactive fallout after the Chernobyl accident and nuclear weapon tests in Kazakhstan.

Environmental Exposure↗
PubMed1978

Induced radioresistance in four strains of Escherichia coli, two with lambda lysogens.

Cells of E. coli that are recA+ and lex+ show a phenomenon of induced radioresistance. A preexposure to ultraviolet light, or ionizing radiation followed by incubation to allow protein synthesis, followed by treatment with rifampin to prevent further induction, renders the cells resistant to further doses of radiation. When this is attempted with lambda lysogens of the same strains, no radioresistance is seen, even though the preexposure is too small to induce lambda itself. If the lysogens are ind-, namely lambda C1857, about the normal radioresistance can be developed by pretreatment. These findings suggest that the lambda repressors can bind to single-strand breaks caused by the inducing agent and can modify the course of induction.

Coliphages↗
PubMed1975

Does x-radiation of the preconceptional mammalian ovum lead to sterility and/or congenital anomalies?

Sexually mature CF1 female mice were x-radiated with 10 to 500 R prior to mating with normal males of the same strain, and no exposure rendered the mice sterile immediately; estrous was not altered, so that normal matings occurred; the litter size of females exposed to the 500-R dose was reduced, possibly due to induction of dominant lethal genes. The second and third meiotic maturations following x-radiation gave rise to fertilizable ova which resulted in offspring that did not show any increase in the incidence of congenital anomalies. With increasing levels of exposure to x-rays, there was a decrease in the reproductive live-span. If the interval between x-radiation and mating was lengthened to 60 days, none of those exposed to 300 R or more was fertile; those exposed to 100 R showed variable fertility, evidenced by reduced litter sizes, but there were no anomalies. None of the offspring of the x-radiated females showed a significant weight loss, even to 2 months of age. Thus, when ova were x-rayed before fertilization with normal sperm, normal fertilization occurred and normal offspring were produced from at least the first three successive estrous cycles; after that, various degrees of sterility were evident, depending upon the dose level of the original exposure. Since resorptions (but not anomalies) were increased with the higher doses, dominant lethal and recessive mutatuions may have been obscured by the normal alleles of the unirradiated male mates. The ovarian ovum could not readily be sterilized by x-rays, nor could it be so damaged as to cause congenital anomalies. Nevertheless, one must be aware that all x-rayed ova may carry recessive mutatuions which might be phenotypically evident if they are on the female sex (X) chromosome, unmasked by an allelomorph on the male (Y) chromosome, or might even surface in future generations, if chance combines them with similar genes.

Animals↗
PubMed2002

On key lesions and all that: a tribute to Paul Lohman.

This paper is a tribute to Paul Lohman at the occasion of his retirement from the position of Professor in the Medical Faculty at the Leiden University in The Netherlands and as Director of its Department of Radiation Genetics and Chemical Mutagenesis. Paul's contributions to the science of genetic toxicology are discussed in the context of more recent insights as to how mammalian cells process DNA damage, and how this may lead to cancer and, possibly, aging. Starting with his work on the characterization of UV-induced DNA repair in cultured cells from xeroderma pigmentosum patients and the development of methodology for monitoring the removal of UV-induced lesions in human cells, the concept of the key lesion is introduced. Among the myriad of DNA lesions that can be induced in DNA as a consequence of exposure to a range of natural or synthetic mutagens, key lesions are the ones responsible for subsequent adverse effects, for example, because they give rise to mutation. The development of methods using immunofluorescence microscopy to detect and identify such key lesions and quantitate them at the single cell level, is one of the highlights of Paul's career. Based on the perceived need to evaluate mutational end points in vivo in relation to specific lesions identified by his immunofluorescence methods, Paul subsequently made crucial contributions to the development of the first transgenic mouse model to measure mutations in chromosomally integrated reporter genes. In parallel to his experimental work, Paul greatly contributed to genetic toxicology at the theoretical level by his work on the development and evaluation of methods for assessment or prediction of risks of exposure to environmental mutagens. Finally, Paul has served the discipline of genetic toxicology in a more administrative role in various ways, both locally as one of the founders of the Medical Genetics Center South-West Netherlands and internationally by playing a prominent role in organizations such as ICPEMC. Here, his numerous contributions to the journal Mutation Research, both as author on many papers and as Executive Managing Editor should not go unmentioned.

Genetics↗
PubMedDate not supplied

Re-analysis of radiation-induced specific locus mutations in the mouse.

A re-analysis of published data on mouse mutation rates induced by X and gamma rays suggests that the kinetics of induction can be analysed by fitting the data to a parabolic curve. We interpret this to mean that a substantial proportion of the induced mutations results from gross chromosomal changes such as deletions, some of which are one-track and some of which are two-track. This analysis is based on the assumption that the shape of the dose curve, which in the female is concave upward, reflects the manner in which the mutations are induced rather than representing a one-track (linear) curve whose shape has been modified by differential repair.

Animals↗