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Radiation-Related Cancer 25 Years After Chernobyl
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Radiation-Related Cancer 25 Years After Chernobyl

A special issue of Genes (ISSN 2073-4425). This special issue belongs to the section "Human Genomics and Genetic Diseases".

Deadline for manuscript submissions: closed (31 October 2011) | Viewed by 78319

Special Issue Editor

Prof. Dr. Horst Zitzelsberger

E-Mail Website
Guest Editor
1. Helmholtz Zentrum München, 85764 Neuherberg, Germany
2. Research Center for Environmental Health (GmbH), Ingolstädter Landstr. 1, 85764 Neuherberg, Germany
Interests: cytogenetics; chromosome aberrations; cancer cytogenetics; molecular cytogenetics; radiation biology; thyroid cancer; radiation-induced carcinogenesis; positional cloning of chromosomal breakpoints

Special Issue Information

Dear Colleagues,

The 26th of April, 2011, marks the 25th anniversary of the Chernobyl accident in northern Ukraine, the largest nuclear plant accident in history. As a consequence, approximately five million people were exposed to the radioactive fallout in the Russian Federation, Ukraine and Belarus. This nuclear disaster along with the atomic bomb explosions in Japan 65 years ago, called to mind the carcinogenic potential of ionizing radiation and its long-term health effects that arise in exposed populations. One of the most surprising health effects of the Chernobyl accident was the appearance and magnitude of cases of thyroid cancer in children that lived in the heavily contaminated areas. In the decades following the accident many researchers have looked at the biological effects occuring in cells that were exposed to radiation in order to understand the molecular mechanisms associated with radiation-related cancer. Although evidence of radiation-induced DNA damage, such as the induction of chromosome aberrations exists, there are only few indications of radiation-specific molecular markers in these tumors. In order to gain a better understanding of the specific actions of ionizing radiation in tumor development, it also might be helpful to identify radiation-specific gene alterations in tumors developed after medical irradiation. To mark the 25th anniversary of the Chernobyl accident, a special issue of the journal Genes will be issued in order to shed light on knowledge about molecular mechanisms in radiation-related cancer. Authors are encouraged to submit original research articles and reviews reporting findings from studies on cancers of radiation-exposed cohorts. Also welcome are papers on animal or cell culture studies modeling the radiocarcinogenic process. This special issue is intented to provide an overview on current knowledge in the research of radiaton-related cancer.

Prof. Dr. Horst Zitzelsberger
Guest Editor

Keywords

  • post-Chernobyl cancer
  • cancers from radiation-exposed cohorts
  • radiation-induced cancers in animals
  • radiation-transformed cell models
  • radiation markers in tumors
  • mechanisms of radiocarcinogenesis

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Published Papers (8 papers)

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13 pages, 202 KiB  
Communication
The Chernobyl Tissue Bank — A Repository for Biomaterial and Data Used in Integrative and Systems Biology Modeling the Human Response to Radiation
by Geraldine Thomas 1,*, Kristian Unger 1, Marko Krznaric 1, Angela Galpine 1, Jackie Bethel 1, Christopher Tomlinson 2, Mark Woodbridge 2 and Sarah Butcher 2
1 Department of Surgery and Cancer, Imperial College London, Hammersmith Hospital, Du Cane Road, London W12 0HS, UK
2 Bioinformatics Support Service, Imperial College London, Sir Ernest Chain Building, Division of Molecular Biosciences, South Kensington Campus, London SW7 2AZ, UK
Genes 2012, 3(2), 278-290; https://doi.org/10.3390/genes3020278 - 9 May 2012
Cited by 4 | Viewed by 10056
Abstract
The only unequivocal radiological effect of the Chernobyl accident on human health is the increase in thyroid cancer in those exposed in childhood or early adolescence. In response to the scientific interest in studying the molecular biology of thyroid cancer post Chernobyl, the [...] Read more.
The only unequivocal radiological effect of the Chernobyl accident on human health is the increase in thyroid cancer in those exposed in childhood or early adolescence. In response to the scientific interest in studying the molecular biology of thyroid cancer post Chernobyl, the Chernobyl Tissue Bank (CTB: www.chernobyltissuebank.com) was established in 1998. Thus far it is has collected biological samples from 3,861 individuals, and provided 27 research projects with 11,254 samples. The CTB was designed from its outset as a resource to promote the integration of research and clinical data to facilitate a systems biology approach to radiation related thyroid cancer. The project has therefore developed as a multidisciplinary collaboration between clinicians, dosimetrists, molecular biologists and bioinformaticians and serves as a paradigm for tissue banking in the omics era. Full article
(This article belongs to the Special Issue Radiation-Related Cancer 25 Years After Chernobyl)
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13 pages, 106 KiB  
Article
Heritability of Radiation Response in Lung Cancer Families
by Albert Rosenberger 1,*, Ute Rössler 2, Sabine Hornhardt 2, Wiebke Sauter 2, Heike Bickeböller 1, H.-Erich Wichmann 3,4 and Maria Gomolka 2
1 Department of Genetic Epidemiology, University Medical Center, Georg-August-University Göttingen, Humboldtallee 32, 37073 Göttingen, Germany
2 Department of Radiation Protections and Health, Federal Office for Radiation Protection, Ingolstaedter Landstr.1, 85764 Oberschleissheim, Germany
3 Institute of Epidemiology, Helmholtz Center Munich, 85764 Munich, Germany
4 Department of Medical Informatics, Biometry and Epidemiology, Ludwig-Maximilians-University Munich, 80539 Munich, Germany
Genes 2012, 3(2), 248-260; https://doi.org/10.3390/genes3020248 - 29 Mar 2012
Cited by 6 | Viewed by 7381
Abstract
Radiation sensitivity is assumed to be a cancer susceptibility factor due to impaired DNA damage signalling and repair. Relevant genetic factors may also determine the observed familial aggregation of early onset lung cancer. We investigated the heritability of radiation sensitivity in families of [...] Read more.
Radiation sensitivity is assumed to be a cancer susceptibility factor due to impaired DNA damage signalling and repair. Relevant genetic factors may also determine the observed familial aggregation of early onset lung cancer. We investigated the heritability of radiation sensitivity in families of 177 Caucasian cases of early onset lung cancer. In total 798 individuals were characterized for their radiation-induced DNA damage response. DNA damage analysis was performed by alkaline comet assay before and after in vitro irradiation of isolated lymphocytes. The cells were exposed to a dose of 4 Gy and allowed to repair induced DNA-damage up to 60 minutes. The primary outcome parameter Olive Tail Moment was the basis for heritability estimates. Heritability was highest for basal damage (without irradiation) 70% (95%-CI: 51%–88%) and initial damage (directly after irradiation) 65% (95%-CI: 47%–83%) and decreased to 20%–48% for the residual damage after different repair times. Hence our study supports the hypothesis that genomic instability represented by the basal DNA damage as well as radiation induced and repaired damage is highly heritable. Genes influencing genome instability and DNA repair are therefore of major interest for the etiology of lung cancer in the young. The comet assay represents a proper tool to investigate heritability of the radiation sensitive phenotype. Our results are in good agreement with other mutagen sensitivity assays. Full article
(This article belongs to the Special Issue Radiation-Related Cancer 25 Years After Chernobyl)
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25 pages, 223 KiB  
Review
Biological Complexities in Radiation Carcinogenesis and Cancer Radiotherapy: Impact of New Biological Paradigms
by Hossein Mozdarani
Department of Medical Genetics, Faculty of Medical Sciences, Tarbiat Modares University, Tehran P.O. Box 14115-111, Iran
Genes 2012, 3(1), 90-114; https://doi.org/10.3390/genes3010090 - 20 Jan 2012
Cited by 31 | Viewed by 13410
Abstract
Although radiation carcinogenesis has been shown both experimentally and epidemiologically, the use of ionizing radiation is also one of the major modalities in cancer treatment. Various known cellular and molecular events are involved in carcinogenesis. Apart from the known phenomena, there could be [...] Read more.
Although radiation carcinogenesis has been shown both experimentally and epidemiologically, the use of ionizing radiation is also one of the major modalities in cancer treatment. Various known cellular and molecular events are involved in carcinogenesis. Apart from the known phenomena, there could be implications for carcinogenesis and cancer prevention due to other biological processes such as the bystander effect, the abscopal effect, intrinsic radiosensitivity and radioadaptation. Bystander effects have consequences for mutation initiated cancer paradigms of radiation carcinogenesis, which provide the mechanistic justification for low-dose risk estimates. The abscopal effect is potentially important for tumor control and is mediated through cytokines and/or the immune system (mainly cell-mediated immunity). It results from loss of growth and stimulatory and/or immunosuppressive factors from the tumor. Intrinsic radiosensitivity is a feature of some cancer prone chromosomal breakage syndromes such as ataxia telangectiasia. Radiosensitivity is manifested as higher chromosomal aberrations and DNA repair impairment is now known as a good biomarker for breast cancer screening and prediction of prognosis. However, it is not yet known whether this effect is good or bad for those receiving radiation or radiomimetic agents for treatment. Radiation hormesis is another major concern for carcinogenesis. This process which protects cells from higher doses of radiation or radio mimic chemicals, may lead to the escape of cells from mitotic death or apoptosis and put cells with a lower amount of damage into the process of cancer induction. Therefore, any of these biological phenomena could have impact on another process giving rise to genome instability of cells which are not in the field of radiation but still receiving a lower amount of radiation. For prevention of radiation induced carcinogenesis or risk assessment as well as for successful radiation therapy, all these phenomena should be taken into account. Full article
(This article belongs to the Special Issue Radiation-Related Cancer 25 Years After Chernobyl)
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16 pages, 889 KiB  
Review
Discriminating Gene Expression Signature of Radiation-Induced Thyroid Tumors after Either External Exposure or Internal Contamination
by Catherine Ory 1,*, Nicolas Ugolin 1, Martin Schlumberger 2, Paul Hofman 3,4,5 and Sylvie Chevillard 1
1 CEA, DSV, IRCM, SREIT, Laboratoire de Cancérologie Expérimentale, BP6, Fontenay-aux-Roses, F-92265, France
2 Institut Gustave Roussy, Department on Nuclear Medicine and Endocrine Oncology, Villejuif, and University Paris-Sud, F-94800, France
3 INSERM ERI-21, Nice, F-06002, France
4 University of Nice-Sophia Antipolis, IFR 50, Nice, F-06002, France
5 Laboratory of Clinical and Experimental Pathology and CHU-CRLCC-UNSA tumour tissue bank of Nice area, Louis Pasteur Hospital, Nice, F-06002, France
Genes 2012, 3(1), 19-34; https://doi.org/10.3390/genes3010019 - 21 Dec 2011
Cited by 7 | Viewed by 7893
Abstract
Both external radiation exposure and internal radionuclide contamination are well known risk factors in the development of thyroid epithelial tumors. The identification of specific molecular markers deregulated in radiation-induced thyroid tumors is important for the etiological diagnosis since neither histological features nor genetic [...] Read more.
Both external radiation exposure and internal radionuclide contamination are well known risk factors in the development of thyroid epithelial tumors. The identification of specific molecular markers deregulated in radiation-induced thyroid tumors is important for the etiological diagnosis since neither histological features nor genetic alterations can discriminate between sporadic and radiation-induced tumors. Identification of highly discriminating markers in radiation-induced tumors is challenging as it relies on the ability to identify marker deregulation which is associated with a cellular stress that occurred many years before in the thyroid cells. The existence of such a signature is still controversial, as it was not found in several studies while a highly discriminating signature was found in both post-radiotherapy and post-Chernobyl series in other studies. Overall, published studies searching for radiation-induced thyroid tumor specificities, using transcriptomic, proteomic and comparative genomic hybridization approaches, and bearing in mind the analytical constraints required to analyze such small series of tumors, suggest that such a molecular signature could be found. In comparison with sporadic tumors, we highlight molecular similarities and specificities in tumors occurring after high-dose external radiation exposure, such as radiotherapy, and in post-Chernobyl tumors that occurred after internal 131I contamination. We discuss the relevance of signature extrapolation from series of tumors developing after high and low doses in the identification of tumors induced at very low doses of radiation. Full article
(This article belongs to the Special Issue Radiation-Related Cancer 25 Years After Chernobyl)
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17 pages, 325 KiB  
Review
Modeling the Risk of Secondary Malignancies after Radiotherapy
by Uwe Schneider 1,2
1 Vetsuisse Faculty, University of Zürich, Zürich 8057, Switzerland
2 Radiotherapy Hirslanden AG, Rain 34, Aarau 5000, Switzerland
Genes 2011, 2(4), 1033-1049; https://doi.org/10.3390/genes2041033 - 29 Nov 2011
Cited by 63 | Viewed by 10700
Abstract
In developed countries, more than half of all cancer patients receive radiotherapy at some stage in the management of their disease. However, a radiation-induced secondary malignancy can be the price of success if the primary cancer is cured or at least controlled. Therefore, [...] Read more.
In developed countries, more than half of all cancer patients receive radiotherapy at some stage in the management of their disease. However, a radiation-induced secondary malignancy can be the price of success if the primary cancer is cured or at least controlled. Therefore, there is increasing concern regarding radiation-related second cancer risks in long-term radiotherapy survivors and a corresponding need to be able to predict cancer risks at high radiation doses. Of particular interest are second cancer risk estimates for new radiation treatment modalities such as intensity modulated radiotherapy, intensity modulated arc-therapy, proton and heavy ion radiotherapy. The long term risks from such modern radiotherapy treatment techniques have not yet been determined and are unlikely to become apparent for many years, due to the long latency time for solid tumor induction. Most information on the dose-response of radiation-induced cancer is derived from data on the A-bomb survivors who were exposed to γ-rays and neutrons. Since, for radiation protection purposes, the dose span of main interest is between zero and one Gy, the analysis of the A-bomb survivors is usually focused on this range. With increasing cure rates, estimates of cancer risk for doses larger than one Gy are becoming more important for radiotherapy patients. Therefore in this review, emphasis was placed on doses relevant for radiotherapy with respect to radiation induced solid cancer. Simple radiation protection models should be used only with extreme care for risk estimates in radiotherapy, since they are developed exclusively for low dose. When applied to scatter radiation, such models can predict only a fraction of observed second malignancies. Better semi-empirical models include the effect of dose fractionation and represent the dose-response relationships more accurately. The involved uncertainties are still huge for most of the organs and tissues. A major reason for this is that the underlying processes of the induction of carcinoma and sarcoma are not well known. Most uncertainties are related to the time patterns of cancer induction, the population specific dependencies and to the organ specific cancer induction rates. For radiotherapy treatment plan optimization these factors are irrelevant, as a treatment plan comparison is performed for a patient of specific age, sex, etc. If a treatment plan is compared relative to another one only the shape of the dose-response curve (the so called risk-equivalent dose) is of importance and errors can be minimized. Full article
(This article belongs to the Special Issue Radiation-Related Cancer 25 Years After Chernobyl)
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23 pages, 770 KiB  
Article
Delineating Chromosomal Breakpoints in Radiation-Induced Papillary Thyroid Cancer
by Heinz-Ulrich G. Weier 1, Yuko Ito 1,2, Johnson Kwan 1, Jan Smida 3, Jingly F. Weier 1,4, Ludwig Hieber 5, Chun-Mei Lu 1,6, Lars Lehmann 1,5,7, Mei Wang 8, Haig J. Kassabian 1, Hui Zeng 1 and Benjamin O’Brien 1,9,10,*
1 Life Sciences Division, E.O. Lawrence Berkeley National Laboratory, 1 Cyclotron Road, Berkeley, CA 94720, USA
2 National Institute of Science and Technology Policy (NISTEP), Ministry of Education, Culture, Sports, Science and Technology, Tokyo 100-0005, Japan
3 Clinical Cooperation Group Osteosarcoma, Helmholtz Zentrum München, German Research Center for Environmental Health, Ingolstädter Landstrasse 1, 85764 Neuherberg, Germany
4 Clinical Labs–Cytogenetics, University of California, 185 Berry Street Suite 290, San Francisco, CA 94143-0100, USA
5 Department of Radiation Cytogenetics, Helmholtz Zentrum München, German Research Center for Environmental Health, Ingolstädter Landstr.1, Neuherberg 85764, Germany
6 Department of Chemical and Materials Engineering, National Chin-Yi University of Technology, No.35, Lane 215, Section 1, Chungshan Road, Taiping City, Taichung 411, Taiwan
7 Roche Diagnostics GmbH, Nonnenwald 2, 82377 Penzberg, Germany
8 Department of Diabetes, City of Hope, 1500 Duarte Road, Duarte, CA 91010-3012, USA
9 William Harvey Research Institute, Translational Medicine and Therapeutics, Barts and The London School of Medicine, Charterhouse Square, London, EC1M 6BQ, UK
10 Department of Anesthesiology, German Heart Institute Berlin, Augustenburger Platz 1, 13353 Berlin, Germany
Genes 2011, 2(3), 397-419; https://doi.org/10.3390/genes2030397 - 28 Jun 2011
Cited by 5 | Viewed by 9938
Abstract
Recurrent translocations are well known hallmarks of many human solid tumors and hematological disorders, where patient- and breakpoint-specific information may facilitate prognostication and individualized therapy. In thyroid carcinomas, the proto-oncogenes RET and NTRK1 are often found to be activated through chromosomal rearrangements. However, [...] Read more.
Recurrent translocations are well known hallmarks of many human solid tumors and hematological disorders, where patient- and breakpoint-specific information may facilitate prognostication and individualized therapy. In thyroid carcinomas, the proto-oncogenes RET and NTRK1 are often found to be activated through chromosomal rearrangements. However, many sporadic tumors and papillary thyroid carcinomas (PTCs) arising in patients with a history of exposure to elevated levels of ionizing irradiation do not carry these known abnormalities. We developed a rapid scheme to screen tumor cell metaphase spreads and identify candidate genes of tumorigenesis and neoplastic progression for subsequent functional studies. Using a series of overnight fluorescence in situ hybridization (FISH) experiments with pools comprised of bacterial artificial chromosome (BAC) clones, it now becomes possible to rapidly refine breakpoint maps and, within one week, progress from the low resolution Spectral Karyotyping (SKY) maps or Giemsa-banding (G-banding) karyotypes to fully integrated, high resolution physical maps including a list of candiate genes in the critical regions. Full article
(This article belongs to the Special Issue Radiation-Related Cancer 25 Years After Chernobyl)
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10 pages, 298 KiB  
Article
Allelic Imbalances in Radiation—Associated Acute Myeloid Leukemia
by Sergiy V. Klymenko 1,2,†, Jan Smida 2,4,†, Michael J. Atkinson 2,3, Volodymir G. Bebeshko 1, Michaela Nathrath 3,4 and Michael Rosemann 2,3,4,*
1 Institute of Clinical Radiology, Research Centre for Radiation Medicine, 53 Melnikova, 04050 Kyiv, Ukraine
2 Institute of Pathology, Helmholtz Zentrum Muenchen–German Research Center for Environmental Health, Ingolstaedter Landstrasse 1, 85764 Neuherberg, Germany
3 Institute of Radiobiology, Helmholtz Zentrum Muenchen–German Research Center for Environmental Health, Ingolstaedter Landstrasse 1, 85764 Neuherberg, Germany
4 Clinical Cooperation Group Osteosarcoma, Helmholtz Zentrum Muenchen, German Research Center for Environmental Health and Department of Pediatrics, Technische Universitaet Muenchen, Ingolstaedter Landstrasse 1, 85764 Neuherberg, Germany
† These authors contributed equally to this work.
Genes 2011, 2(2), 384-393; https://doi.org/10.3390/genes2020384 - 31 May 2011
Cited by 5 | Viewed by 7027
Abstract
Acute myeloid leukemia (AML) can develop as a secondary malignancy following radiotherapy, but also following low-dose environmental or occupational radiation exposure. Therapy-related AML frequently carries deletions of chromosome 5q and/or 7, but for low-dose exposure associated AML this has not been described. For [...] Read more.
Acute myeloid leukemia (AML) can develop as a secondary malignancy following radiotherapy, but also following low-dose environmental or occupational radiation exposure. Therapy-related AML frequently carries deletions of chromosome 5q and/or 7, but for low-dose exposure associated AML this has not been described. For the present study we performed genome-wide screens for loss-of-heterozygosity (LOH) in a set of 19 AML cases that developed after radiation-exposure following the Chernobyl accident. Using Affymetrix SNP arrays we found large regions of LOH in 16 of the cases. Eight cases (42%) demonstrated LOH at 5q and/or 7, which is a known marker of complex karyotypic changes and poor prognosis. We could show here for the first time that exposure to low-dose ionizing radiation induces AML with molecular alterations similar to those seen in therapy-related cases. Full article
(This article belongs to the Special Issue Radiation-Related Cancer 25 Years After Chernobyl)
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10 pages, 268 KiB  
Review
Clinical Experiences with Radiation Induced Thyroid Cancer after Chernobyl
by Christoph Reiners
Department of Nuclear Medicine, University of Würzburg, Oberdürrbacherstr.6, D-97082 Würzburg, Germany
Genes 2011, 2(2), 374-383; https://doi.org/10.3390/genes2020374 - 31 May 2011
Cited by 4 | Viewed by 9144
Abstract
The risk of developing thyroid cancer increases considerably after exposure to external or internal radiation, especially in children below the age of 10. After the Chernobyl reactor accident, the yearly incidence of childhood thyroid cancer in Belarus increased to approximately 40 per 1.000.000 [...] Read more.
The risk of developing thyroid cancer increases considerably after exposure to external or internal radiation, especially in children below the age of 10. After the Chernobyl reactor accident, the yearly incidence of childhood thyroid cancer in Belarus increased to approximately 40 per 1.000.000 in girls and to roughly 20 per 1.000.000 in boys compared to approximately 0.5 cases per 1.000.000 prior to the accident. Typically, young children with thyroid cancer after radiation exposure present in ≈95% of the cases as papillary cancers, in ≈50% as invasive tumors growing outside the thyroid capsule, in ≈65% with lymph node metastases and in ≈15% with distant metastases. A joint Belarusian-German project starting in April 1993 that combined treatment with surgery and radioiodine was organized in 237 selected children from Belarus who were exposed to the Chernobyl fallout and had advanced stages of thyroid cancer. The study group included 141 girls and 96 boys. Their median age at the time of the accident was 1.7 years; whereas the median age at the time of diagnosis was 12.4 years. With the exception of two cases with follicular histology, the majority of the patients had been diagnosed with papillary thyroid cancers. In 63%, the tumor had grown outside the thyroid capsule and invaded the tissue of the neck (pT4). Nearly all of the selected cases (96%) showed-up with lymph node metastases (pN1) and 43% of the patients with distant metastases mainly to the lungs (pM1). In 58% of the children, complete remissions of thyroid cancer could be achieved until December 31st 2010 and in 34% of the children, stable partial remissions; in the remaining 8% of the patients, partial remissions were observed. The risk of radiation-induced thyroid cancer increased considerably in children and adolescents who were affected by the Chernobyl reactor accident. In spite of the fact, that thyroid cancers in young children seem to behave more aggressively than in older patients, the results of combined treatment with thyroidectomy, radioiodine therapy and thyroid hormone replacement are excellent. Full article
(This article belongs to the Special Issue Radiation-Related Cancer 25 Years After Chernobyl)
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