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Background Recently, low dose radiotherapy delivered to the whole lung has been proposed as treatment for the pneumonia due to COVID-19. Although there is biological plausibility for its use, the evidence supporting its effectiveness is scarce, and the risks associated with it may be significant. Thus, based on a virtual case simulation, we estimated the risks of radiation-induced cancer (RIC) and cardiac disease. Methods Lifetime attributable risks (LAR) of RIC were calculated for the lung, liver, esophagus, and breast of female patients. The cardiovascular risk of exposure-induced death (REID) due to ischemic heart disease was also calculated. The doses received by the organs involved in the treatment were obtained from a simulation of conformal radiotherapy (RT) treatment, delivering a dose of 0.5 Gy–1.5 Gy to the lungs. We considered a LAR and REID 2% unacceptable. Results The lung was at the highest risk for RIC (absolute LAR below 5200 cases/100,000 and 2250 cases/100,000 for women and men, respectively). For women, the breast had the second-highest LAR, especially for young women. The liver and esophagus had LARs below 700/100,000 for both sexes, with a higher incidence of esophageal cancer in women and liver cancer in men. Regarding the LAR cutoff, we observed an unacceptable or cautionary LAR for lung cancer in all women and men 1 Gy. LAR for lung cancer with an RT dose of 1 Gy was cautionary for women >60 years of age and men

Epstein-Barr virus (EBV) infects most people worldwide and persists for life due to complicated interplay between lytic infection and multiple types of latent infections. While usually asymptomatic, EBV is a causative agent in several types of cancer and has a strong association with multiple sclerosis. Exactly how EBV promotes these diseases and why they are rare consequences of infection are incompletely understood. Here I will discuss current ideas on disease induction by EBV, including the importance of lytic protein expression in the context of latent infection as well as the possible importance of specific EBV variants in disease induction.

Enterococcus faecium é um importante gênero bactérias ácido láticas probióticas que forma parte integrante da microbiota humana saudável. Entretanto, poucos estudos relacionam a capacidade da Enterococcus faecium de origem alimentar para prevenção do câncer colorretal, considerado uma das principais causas de mortalidade nos países ocidentais, estando entre os três cânceres mais incidentes. O nosso estudo se propõe em utilizar uma nova abordagem para avaliar o potencial da cepa Enterococcus faecium 137v – EF137v de queijo de Coalho artesanal no seu desempenho para prevenção e retardo na progressão do câncer colorretal em modelo animal. Para este fim avaliamos, através da ultrassonografia abdominal, os efeitos da administração oral da EF137v sobre o desenvolvimento do câncer colorretal induzido por 1,2-dimetilhidrazina - DMH em diversos grupos objetivando uma análise sistêmica na saúde dos ratos Wistar, bem como observações de possíveis alterações no peso e níveis séricos desses animais. Os resultados obtidos foram importantes para o retardo na progressão tumoral promovido por EF137v em ratos que fizeram uso do probiótico de modo isolado antes (preventivo) e após (curativo) a indução do câncer. Os ratos apresentaram peso corporal estável, sem mudanças bruscas no decorrer do experimento. Níveis séricos de triglicerídeos apresentaram-se altos após o câncer na maioria dos grupos tratados. Uma discussão sobre possíveis alterações metabólicas foi iniciada, bem como a função protetora da EF137v ao câncer colorretal. O probiótico EF137v mostrou-se forte candidato como agente preventivo para o desenvolvimento do câncer e o procedimento ultrassonográfico uma ferramenta adicional para o acompanhar alterações importantes no intestino.

The interest in the induction of secondary tumours following radiotherapy has greatly increased as developments in detecting and treating the primary tumours have improved the life expectancy of cancer patients. However, most of the knowledge on the current levels of risk comes from patients treated many decades ago. As developments of irradiation techniques take place at a much faster pace than the progression of the carcinogenesis process, the earlier results could not be easily extrapolated to modern treatments. Indeed, the patterns of irradiation from historically-used orthovoltage radiotherapy and from contemporary techniques like conformal radiotherapy with megavoltage radiation, intensity modulated radiation therapy with photons or with particles are quite different. Furthermore, the increased interest in individualised treatment options raises the question of evaluating and ranking the different treatment plan options from the point of view of the risk for cancer induction, in parallel with the quantification of other long-term effects. It is therefore inevitable that models for risk assessment will have to be used to complement the knowledge from epidemiological studies and to make predictions for newer forms of treatment for which clinical evidence is not yet available. This work reviews the mathematical models that could be used to predict the risk of secondary cancers from radiotherapy-relevant dose levels, as well as the approaches and factors that have to be taken into account when including these models in the clinical evaluation process. These include the effects of heterogeneous irradiation, secondary particles production, imaging techniques, interpatient variability and other confounding factors.

Biological responses to low-dose and high-dose radiations are markedly different; the former produce beneficial effects and the latter at acute doses cause detrimental health effects such as cancer induction. High-dose radiations (>2 Gy) of low linear energy transfer are widely used in the treatment of cancer, but limitations are imposed due to normal tissue adverse reactions. Low-dose radiations (LDRs), such as X-rays (a few mGy), have been widely used in diagnosis of many diseases without any known adverse health effects. LDR preexposures have been known to suppress cancer induction by acute doses of radiation. This article briefly reviews the possible applications of LDR in cancer therapy and delineates the underlying radiobiological mechanisms in suppressing high-dose-induced cancer. It is further argued to develop LDR technology in preventing and for palliative outcomes in fighting COVID-19 pandemic infection among the populations. Furthermore, it is suggested to examine the average number of people living in high background radiation areas for susceptibility to COVID-19 infection and compare with the average infection rate in the general public for gaining new knowledge on the response of LDR-exposed population.

Purpose The objective of this study was to estimate the probability for cancer development due to radiotherapy for Graves' orbitopathy with 6 MV x rays. Methods Orbital irradiation was simulated with the MCNP code. The radiation dose received by 10 out-of-field organs having a strong disposition for carcinogenesis was calculated with Monte Carlo methods. These dose calculations were used to estimate the organ-dependent lifetime attributable risk (LAR) for cancer induction in 30- and 50-yr-old males and females on the basis of the linear model suggested by the BEIR-VII report. Differential dose-volume histograms derived from patients' three-dimensional (3D) radiotherapy plans were employed to determine the organ equivalent dose (OED) of the brain which was partly exposed to primary radiation. The OED and the relevant LAR for brain cancer development were assessed with the plateau, bell-shaped and mechanistic models. The radiotherapy-induced cancer risks were compared with the lifetime intrinsic risk (LIR) values for unexposed population. Results The radiation dose range to organs excluded from the treatment volume was 0.1-91.0 mGy for a target dose of 20 Gy. These peripheral organ doses increased the LIRs for cancer development of unexposed 30- and 50-yr-old males up to 1.0% and 0.2%, respectively. The corresponding elevations after radiotherapy of females were 2.0% and 0.4%. The use of nonlinear models gave an OED range of the brain of 482.0-562.5 mGy depending upon the model used for analysis and the patient's gender. The elevation of the LIR for developing brain malignancies after radiotherapy of 30-yr-old males and females reached to 13.3% and 16.6%, respectively. The corresponding increases after orbital irradiation at the age of 50 yr were 6.7% and 8.3%. Conclusions The level of the LIR increase attributable to radiation therapy for GO varied widely by the organ under examination and the age and gender of the exposed subject. This study provides the required data to quantify the elevation of these baseline cancer risks following orbital irradiation.

Obtaining a correct dose–response relationship for radiation-induced cancer after radiotherapy presents a major challenge for epidemiological studies. The purpose of this paper is to gain a better understanding of the associated uncertainties. To accomplish this goal, some aspects of an epidemiological study on breast cancer following radiotherapy of Hodgkin’s disease were simulated with Monte Carlo methods. It is demonstrated that although the doses to the breast volume are calculated by one treatment plan, the locations and sizes of the induced secondary breast tumours can be simulated and, based on these simulated locations and sizes, the absorbed doses at the site of tumour incidence can also be simulated. For the simulations of point dose at tumour site, linear and non-linear mechanistic models which predict risk of cancer induction as a function of dose were applied randomly to the treatment plan. These simulations provided for each second tumour and each simulated tumour size the predicted dose. The predicted-dose–response-characteristic from the analysis of the simulated epidemiological study was analysed. If a linear dose–response relationship for cancer induction was applied to calculate the theoretical doses at the simulated tumour sites, all Monte-Carlo realizations of the epidemiological study yielded strong evidence for a resulting linear risk to predicted-dose–response. However, if a non-linear dose–response of cancer induction was applied to calculate the theoretical doses, the Monte Carlo simulated epidemiological study resulted in a non-linear risk to predicted-dose–response relationship only if the tumour size was small (

The present study attempts to calculate organ-absorbed and effective doses for cancer patients to estimate the possible cancer induction and cancer mortality risks resulting from 64-slice abdominopelvic computed tomography (CT) simulations for radiotherapy treatment planning (RTTP).A group of 70 patients, who underwent 64-slice abdominopelvic CT scan for RTTP, voluntarily participated in the present study. To calculate organ and effective doses in a standard phantom of 70 kg, the collected dosimetric parameters were used with the ImPACT CT Patient Dosimetry Calculator. Patient-specific organ dose and effective dose were calculated by applying related correction factors. For the estimation of lifetime attributable risks (LARs) of cancer incidence and cancer-related mortality, doses in radiosensitive organs were converted to risks based on the data published in Biological Effects of Ionizing Radiation VII (BEIR VII).The mean ± standard deviation (SD) of the effective dose for males and females were 13.87 ± 2.37 mSv (range: 9.25-18.82 mSv) and 13.04 ± 3.42 mSv (range: 6.99-18.37 mSv), respectively. The mean ± SD of LAR of cancer incidence was 35.34 ± 13.82 cases in males and 34.49 ± 9.63 cases in females per 100,000 persons. The LAR of cancer mortality had the mean ± SD value of 15.38 ± 4.25 and 16.72 ± 3.87 cases per 100,000 persons in males and females respectively.Increase in the LAR of cancer occurrence and mortality due to abdominopelvic treatment planning CT simulation is noticeable and should be considered.

Consumption of meat is increasing worldwide and to prolong both it's shelf-life and safety companies add various chemicals, some of which are under evaluation to assess their responsible cancer induction. The International Agency of research on Cancer classified red meat and processed meat as probably carcinogenic (Group 2A) and carcinogenic (Group 1) respectively for humans. The aim of this study was to propose a biological sensor able to detect DNA mutations that could lead to cancer induction in beef, and chicken as well as processed meats. Genetically engineered E. coli DPD2794 strain is able to produce bioluminescence in the presence of damages in the DNA molecule, allowing for the screening and discrimination between different meats in terms of potential carcinogenic induction. Unprocessed beef and chicken induced low amounts of bioluminescence, whereas processed beef and chicken induced values above the cut-off limit established. These values where low in comparison to the bioluminescence produced by a strong activator used as our positive reference, leading us to the conclusion that processed meat a low carcinogenic effect.

Diagnostic medical radiation has been the most rapidly increasing component of population background radiation exposure in Western countries over the past decade. This trend is set to increase as CT scanning is readily available with burgeoning use in everyday clinical practice. Consequently, the issue of cancer induction from the doses received during diagnostic medical exposures is highly relevant. In this review we explain current understanding of potential cancer induction at low doses of sparsely ionising radiation. For cancers that may be induced at low doses, a mechanistic description of radiation-induced cancer is discussed, which, in combination with extrapolation of data based on population cohort studies, provides the basis of the currently accepted linear no-threshold model. We explore the assumptions made in deriving risk estimates, the controversies surrounding the linear no-threshold model and the potential future challenges facing clinicians and policy-makers with regards to diagnostic medical radiation and cancer risk, most notably the uncertainties regarding deriving risk estimates from epidemiological data at low doses.

José María De la Roca-Chiapas,1 Gloria Barbosa-Sabanero,2 Jorge Antonio Martínez-García,3 Joel Martínez-Soto,1 Víctor Manuel Ramos-Frausto,1 Leivy Patricia González-Ramírez,1 Ken Nowack4 1Department of Psychology, 2Department of Medical Sciences, Division of Health Sciences, Campus Leon-University of Guanajuato, Guanajuato, 3General Regional Hospital of Leon, Guanajuato, Mexico; 4Envisia Learning, Inc., Santa Monica, CA, USA Abstract: Stress is experienced during cancer, and impairs the immune system's ability to protect the body. Our aim was to investigate if isolation stress has an impact on the development of tumors in rats, and to measure the size and number of tumors and the levels of corticosterone. Breast cancer was induced in two groups of female rats (N=20) by administration of a single dose of N-methyl-N-nitrosourea 50 mg/kg. Rats in the control group (cancer induction condition) were allowed to remain together in a large cage, whereas in the second group, rats were also exposed to a stressful condition, that is, isolation (cancer induction and isolation condition, CIIC). The CIIC group displayed anxious behavior after 10 weeks of isolation. In the CIIC group, 16 tumors developed, compared with only eleven tumors in the control cancer induction condition group. In addition, compared with the control group, the volume of tumors in the CIIC group was greater, and more rats had more than one tumor and cells showed greater morphological damage. Levels of corticosterone were also significantly different between the two groups. This study supports the hypothesis that stress can influence the development of cancer, but that stress itself is not a sufficient factor for the development of cancer in rats. The study also provides new information for development of experimental studies and controlled environments. Keywords: breast cancer, corticosterone, isolation condition, psychoneuroimmunology, stress

Computed tomography (CT) examinations have increased significantly in recent years due to technological innovations. In some industrialised countries, CT contributes to the population dose as much as background radiation. In developing countries, the uses and risks of CT have not been well characterised. The purpose of this investigation was to assess potential stochastic and deterministic radiation effects from common CT exams performed in six hospitals of Recife, Pernambuco. Scanning parameters and patient gender and age were collected for a total of 285 patients undergoing CT examinations of the head (90), chest (75), abdomen (60) and abdomen?pelvis (60). The organ doses, which were calculated using the ImPACT dosimetry calculator, varied significantly among institutions. Organs such as the brain, the heart and the eye lenses, which exhibited doses as high as 85, 42 and 100?mGy, respectively, are of concern for the production of cerebrovascular and cardiovascular diseases and cataracts. Effective cancer risks were calculated using Brenner methodology and BEIR-VII risk factors. They range from 1.8 to 110.2 cases per 100?000 persons for cancer induction and from 1.5 to 63.0 cases per 100?000 for cancer mortality. To reduce doses, a quality assurance programme that includes procedural justification and radiation protection optimisation should be implemented.

Ionizing radiation safety standards developed by the International Commission on Radiological Protection (ICRP) during the past 50-plus years have provided guidance for effective protection of workers and the public from the potentially harmful effects of exposure to ionizing radiation, including cancer. Earlier standards were based primarily on radiation dose rate to organs of the body. More recent recommendations have calculated cancer risk as a function of cumulative dose using a linear no-threshold cancer risk model based on the acute high dose rate exposures received by the Japanese atomic bomb survivors. The underlying assumption in these current recommendations is that risk of radiation-induced cancer is proportional to cumulative dose without threshold. In conflict with this position are the studies of protracted exposures from internally-deposited radionuclides in people and laboratory animals that have demonstrated that cancer induction risk is a function of average dose rate for protracted exposures to ionizing radiation. At lower average dose rates, cancer latency can exceed natural lifespan leading to a virtual threshold. This forum statement proposes that the conflict of these two cancer risk models is explained by the fact that the increased risk of cancer observed in the atomic bomb survivor studies was primarily the result of acute high dose rate promotion of ongoing biological processes that lead to cancer rather than cancer induction. In addition, ionizing radiation-induced cancer is not the result of a simple stochastic event in a single living cell but rather a complex deterministic systemic effect in living tissues. It is recommended that the ICRP consider revising its position in light of this important distinction between cancer promotion and cancer induction.

Gastric cancer is often diagnosed at advanced stages and there is no accurate method for its screening and diagnosis, especially in small animals. Here, we explain the application of B-mode ultrasound imaging (BMUI) for screening of gastric changes in the rat. Thus, male Albino Wistar rats, weighing 100-120 grams were randomly divided into two groups. The control group rats (n=10) were given water as routine; the remaining (n=90), were given N-methyl-N-nitro-N-nitrosoguanidine (MNNG, 100 μg/mL) in drinking water ad libitum for 40 weeks. Fifteen rats were killed at different time intervals and the others were sacrificed after 55 weeks. The BMUI of the stomach of animals after MNNG administration show some changes compared with the normal groups. Pathologic investigations of the stomach indicate cancer induction at different levels. The sensitivity and specificity of BMUI is 96.6% and 78.78%, respectively. Thus, it is a useful method of diagnosis of gastric cancer in rats.

The goal of this study is to evaluate the risk of cancer induction in head radiography procedures with a view to promote dose optimization and enhance patient safety. Thermoluminescent dosimeter (TLD 100) was used to determine the entrance surface dose (ESD) of 20 patients presented for head radiography in two tertiary healthcare institutions in Southwest Nigeria. The corresponding effective dose and doses to the brain, oral mucosa and salivary gland were evaluated using PCXMC software. Incidence cancer risks were evaluated using BEIR VII model. The total entrance surface dose (ESDT) for mandible, paranasal sinuses and skull radiography ranged between 3.01-19.12 mGy with a mean of 7.52 mGy. The resulting effective dose, brain dose, oral mucosa dose and salivary gland dose has a mean of 0.25 mGy, 2.84 mGy, 3.06 mGy, and 4.97 mGy respectively. The least incidence of cancer risk obtained in this study is 1: 7000. Failure in the adoption of complete optimization technique was responsible for the increased risk. Periodic dose audit and enforcement of radiation protection policy will help to checkmate the lapses and alleviate patient risk.

Cancer is the abnormal growth of cells in our bodies that can lead to death. Cancer is a leading cause of mortality in the world and it's the cause of more than 20% of all deaths. The major problem in the cancer chemotherapy is the toxicity of the established drugs. Some of the natural product extracts are capable of preventing or inhibiting the process of carcinogenesis. Thousands of herbal and traditional compounds are being examine by many searchers worldwide to validate their use as anti-cancerous drugs. Medicinal plants and their use in various traditional systems of medicine are indeed awe-inspiring. General public consider herbal remedies to be safe, as it causes less side-effects and less likely to cause dependency. Various dietary agents that interfere with these stages of cancer, thus blocking malignancy and thus Cancer induction, growth, and progression are multi-step events and numerous studies have beendemonstrated. Fruits and vegetables contains untapped reservoir ofvarious nutritive and non-nutritive phytochemicals with potential cancer chemo-preventiveactivity. Plants have been used for treating diseases since time immemorial. More than 50% of modern drugs in clinical use are of natural products. Study is required to determine the efficacy of these plant products in treating cancers in humans.

The mathematical cancer evaluation model, the Generalized Moolgavkar‐Venson‐Knudson (G‐MVK) model and the two‐stage MVK model, were applied to Japanese cancer mortality statistics to examine the applicability of the models for estimating the mortality risk with its year and age dependent variation. First the G‐MVK model was simplified with the constant mutation parameters, and was applied to determine the number of stages required for cancer induction for sixteen kinds of cancers and total solid cancer. Then the G‐MVK model and the two‐stage MVK model were compared in their estimation accuracy, and the latter model was calibrated with the Japanese lung cancer and leukemia statistics. The main results obtained under the limits considered in this study are as follows: (1) the number of stages required for cancer induction was determined by numerical fitting with the cancer statistics. The estimated stage number depended on the kind of cancer, and the mortality depended on age and year, (2) the two‐stage MVK...

It is well known that ionizing radiation is a potential hazard for human beings because of its mutagenic and carcinogenic effects. Radiation carcinogenesis is caused by injury to the DNA of irradiated cells in such a way that genetic programming is altered to favor abnormal cellular growth and proliferation. While the risks of cancer from ionizing radiation have been established, there are important uncertainties and ongoing scientific debate concerning cancer risk at low dose rates. The primary safety concern with radiosynoviorthesis is exposure of nonsynovial tissue to ionizing radiation. Two retrospective cohorts were published specific to research on cancer incidence among patients treated with radiosynoviorthesis, and no increase in the risk of cancer was observed. Additionally, the results of biological dosimetry studies indicate that high radiation doses, which would induce genotoxic effects, are not obtained by peripheral blood lymphocytes in patients after radiosynoviorthesis. Chromosomal aberrations and increased micronucleus frequency do occur in some patients as a result of radiosynoviorthesis, but these aberrations are neither specific nor persistent. Review of the literature on safety of radiosynoviorthesis together with clinical experience over 50 years suggests a very low and acceptable risk arising from radiosynoviorthesis compared with the benefit for the patients. On the other hand, because of the complexity of biomonitoring of genotoxicity, we need further investigations to understand the radiation effects in untargeted living systems exactly.

In the past several years, there has been a great deal of attention from the popular media focusing on the alleged carcinogenicity of low-dose radiation exposures received by patients undergoing medical imaging studies such as X-rays, computed tomography scans, and nuclear medicine scintigraphy. The media has based its reporting on the plethora of articles published in the scientific literature that claim that there is “no safe dose” of ionizing radiation, while essentially ignoring all the literature demonstrating the opposite point of view. But this reported “scientific” literature in turn bases its estimates of cancer induction on the linear no-threshold hypothesis of radiation carcinogenesis. The use of the linear no-threshold model has yielded hundreds of articles, all of which predict a definite carcinogenic effect of any dose of radiation, regardless of how small. Therefore, hospitals and professional societies have begun campaigns and policies aiming to reduce the use of certain medical imaging studies based on perceived risk:benefit ratio assumptions. However, as they are essentially all based on the linear no-threshold model of radiation carcinogenesis, the risk:benefit ratio models used to calculate the hazards of radiological imaging studies may be grossly inaccurate if the linear no-threshold hypothesis is wrong. Here, we review the myriad inadequacies of the linear no-threshold model and cast doubt on the various studies based on this overly simplistic model.

High doses of ionizing radiation clearly produce deleterious consequences in humans, including, but not exclusively, cancer induction. At very low radiation doses the situation is much less clear, but the risks of low-dose radiation are of societal importance in relation to issues as varied as screening tests for cancer, the future of nuclear power, occupational radiation exposure, frequent-flyer risks, manned space exploration, and radiological terrorism. We review the difficulties involved in quantifying the risks of low-dose radiation and address two specific questions. First, what is the lowest dose of x- or gamma-radiation for which good evidence exists of increased cancer risks in humans? The epidemiological data suggest that it is approximately 10-50 mSv for an acute exposure and approximately 50-100 mSv for a protracted exposure. Second, what is the most appropriate way to extrapolate such cancer risk estimates to still lower doses? Given that it is supported by experimentally grounded, quantifiable, biophysical arguments, a linear extrapolation of cancer risks from intermediate to very low doses currently appears to be the most appropriate methodology. This linearity assumption is not necessarily the most conservative approach, and it is likely that it will result in an underestimate of some radiation-induced cancer risks and an overestimate of others.

This review presents diverse approaches to cancer biotherapy including bacteriolytic therapy aimed at inducing apoptosis in tumor cells, bacterial vector-based cancer vaccines, and inhibition of tumor neoangiogenesis by microorganisms. The normal microflora in humans and animals may restrain malignant tumor regeneration.

Tobacco use is a major public health problem worldwide. Tobacco-related cancers cause millions of deaths annually. Although several tobacco agents play a role in the development of tumors, the potent effects of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) and N'-nitrosonornicotine (NNN) are unique. Metabolically activated NNK and NNN induce deleterious mutations in oncogenes and tumor suppression genes by forming DNA adducts, which could be considered as tumor initiation. Meanwhile, the binding of NNK and NNN to the nicotinic acetylcholine receptor promotes tumor growth by enhancing and deregulating cell proliferation, survival, migration, and invasion, thereby creating a microenvironment for tumor growth. These two unique aspects of NNK and NNN synergistically induce cancers in tobacco-exposed individuals. This review will discuss various types of tobacco products and tobacco-related cancers, as well as the molecular mechanisms by which nitrosamines, such as NNK and NNN, induce cancer.

Iron is the most abundant metal in our body. With different coordinating ligands, iron shows wide variations in reduction-oxidation potential. It thus has advantages as a redox intermediate in many biologic mechanisms. However, the same property makes iron a key participant in free radical production, leading to tissue damage, mutation, and carcinogenesis. Iron is both an essential life component and a free-radical initiator. This review summarizes the laboratory and human studies concerning the relationship between iron and cancer. Also reviewed are the essence of iron metabolism in humans and future perspectives. I have stressed that iron with appropriate ligands becomes carcinogenic, and the free-radical damage to the target organ is an important cause of cancer induction. Iron withholding will become an important strategy in the future to lower the incidence of human cancer.

Background This study provides data on the cumulative life attributable risk (LAR) of radiation-induced cancer from the combination of coronary CT angiography (CCTA), dynamic CT perfusion (CTP) and delayed enhancement (DE) CT scans, required for reliable risk–benefit analysis of the one-stop-shop CCTA+CTP+DECT cardiac examination. Methods Monte Carlo simulation of the dynamic CTP and DECT exposures on 62 adult individuals was employed to determine radiation absorbed dose to exposed radiosensitive organs. Corresponding data for CCTA were derived using patient chest circumference and previously published data. Individual-specific LARs of cancer were estimated using organ/tissue-specific radiogenic cancer risk factors. Total LAR from CCTA+CTP+DECT scans' sequence were estimated and compared to nominal intrinsic risk of cancer. Results The main contribution, up to 80%, to cumulative radiation burden from CCTA+CTP+DECT scan-sequence was found to originate from the CTP scan. The total LAR from CCTA+CTP+DECT for females was found 4–6 times higher, compared to males. The mean cumulative risk of radiogenic cancer associated with the complete CCTA+CTP+DECT scan sequence was found to marginally increase the intrinsic risk for cancer induction by less than 0.6% and 0.1% for females and males, respectively. Conclusions The radiation risk from the 256-slice CCTA+CTP+DECT scan sequence may be considered low and should not constitute an obstacle for the clinical endorsement of the one-stop-shop cardiac CT examination, given that its clinical value has been well verified. Nevertheless, every effort should be made towards optimization of the dynamic CTP component which is the main contributor to patient radiation burden.

Background The irradiation of the ovaries of reproductive age women during fluoroscopically guided selective salpingography and tubal catheterization has raised concern about the safety of the procedure. In addition to the risk of cancer induction, which exists with the irradiation of all tissues, with the gonads, the induction of hereditary disorders is possible. The objective of this study was to estimate these risks and present them in a clinically meaningful way. Methods Retrospective analysis was undertaken of 366 consecutive cases of selective salpingography and tubal catheterization performed at the Birmingham Women's Hospital, UK. The radiation doses of different types of procedure were compared with the background annual radiation dose. The risks of cancer and genetic disorders induction were calculated using conversion coefficients published by the International Commission on Radiological Protection. Results The radiation dose women were exposed to during selective salpingography and tubal catheterization under fluoroscopic guidance was a fraction of the background annual radiation dose. The excess lifetime risks of cancer and hereditary disorders were in the order of four to 13 and two to six per million procedures respectively. Conclusions The long term risks of selective salpingography and tubal catheterization under fluoroscopic guidance are low.

Establishing the biological effects and the safe level of exposure to ionizing radiation remains, so far, an objective to be reached. Mammography is an important exam in the early detection of breast tumors, but since the genes BRCA1 and BRCA2 were identified as a main cause of hereditary breast cancer, there is growing concern of exposing patients carrying those mutations to ionizing radiation. It could increase mutations in these genes and other suppressors, and promote the development of tumor in those patients. In this study we propose an in vitro initial experiment aiming to determine the radiation trigger level for detectable mutations in genes BRCA, and thus a safer level of radiation due to mammography for patients carrying a mutated allele of the genes BRCA1 or BRCA2. Breast cells from one patient were cultivated and irradiated with different doses of X-rays generated by commercial mammography equipment. The results have shown that exposition to ionizing radiation promotes measurable alterations in breast cell grown.

The considerable rise of computed tomography (CT) procedures over the past few decades has urged responsible authorities and researchers to evaluate the risk of carcinogenesis in the population in relation to the radiation dose delivered to the patient. A single patient undergoing CT may receive a radiation equivalent dose that varies between about 2 mSv (head ) to about 20 mSv (CT-based coronary angiography). Whereas the latter represents a substantial dose delivered to one patient it is, however, population-wise far below the area of the so-called low doses, i.e. 50 mSv in children and 100 mSv in adults. While at effective doses above 50 mSv the risk of cancer induction increases linearly with dose, this dose-response relation has not been demonstrated at doses below 50 mSv. Below 50 mSv no convincing epidemiological evidence for cancer risk exists. Calculations on this risk are based on scientifically questionable, if not invalid, extrapolations of data from higher doses. However, the failure to demostrate that a risk of cancer exists does not mean that there is no risk. This paper summarizes the data mentioned in various articles from recent literature discussing cancer risks due to CT and puts the results of these studies in perspective of current scientific knowledge in the field of radiation protection. For this we follow the lead of the ICRP and UNSCEAR. Furthermore, we review the strategies and efforts of various national and international bodies and manufacturers of CT apparatus to lower the radiation dose to the patient.

Background and Purpose Most information on the dose-response of radiation-induced cancer is derived from data on the A-bomb survivors. 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. However, estimates of cancer risk for doses larger than one Gy are becoming more important for radiotherapy patients. Therefore in this work, emphasis is placed on doses relevant for radiotherapy with respect to radiation induced solid cancer. Materials and methods For various organs and tissues the analysis of cancer induction was extended by an attempted combination of the linear-no-threshold model from the A-bomb survivors in the low dose range and the cancer risk data of patients receiving radiotherapy for Hodgkin's disease in the high dose range. The data were fitted using organ equivalent dose (OED) calculated for a group of different dose-response models including a linear model, a model including fractionation, a bell-shaped model and a plateau-dose-response relationship. Results The quality of the applied fits shows that the linear model fits best colon, cervix and skin. All other organs are best fitted by the model including fractionation indicating that the repopulation/repair ability of tissue is neither 0 nor 100% but somewhere in between. Bone and soft tissue sarcoma were fitted well by all the models. In the low dose range beyond 1 Gy sarcoma risk is negligible. For increasing dose, sarcoma risk increases rapidly and reaches a plateau at around 30 Gy. Conclusions In this work OED for various organs was calculated for a linear, a bell-shaped, a plateau and a mixture between a bell-shaped and plateau dose-response relationship for typical treatment plans of Hodgkin's disease patients. The model parameters (α and R) were obtained by a fit of the dose-response relationships to these OED data and to the A-bomb survivors. For any three-dimensional inhomogenous dose distribution, cancer risk can be compared by computing OED using the coefficients obtained in this work.

Approximately 1.800.000 CT examinations are performed every year in Belgium. With a mean dose 0,5 mSv, the annual collective dose from CT could induce up to 450 cancer. This number has to be compared to the 45 000 observed new cancers yearly. The deleterious effect of scanner radiation is thus undetectable among cancers induced by smoking, alcohol, and western diet. Risk from radiation is based on cancer mortality rates observed among atomic bomb survivors who underwent high level radiation. Overestimation of collective radiation risks in the filed of low level radiation (below 0,2 Sv) as used for CT is suspected first because a majority of patients undergoing CT are aged 60 years or more, and second because the numerous defense mechanisms that prevent cancer induction at lowdoses in human bodies are not taken into account by the linear no threshold model of carcinogenesis used as legal rule for risk calculations.

Current progress in molecular biology is rapid, and the identification of successive stages in cancer induction, the role of individual oncogenes and tumor supressor genes in specific organ cancers, and possible biomarkers for radiation-induced tumors, as well as for many others, are becoming commonplace. These will offer the prospect not only of understanding the whole process but also the possibility of preventing molecular changes from progressing to a tumor. This possibility may eventually reduce the importance of risk estimates. Risk estimates for radiation-induced cancer have dominated low-dose radiation protection for the last two decades at least. Their recent reevaluation has led to the first reduction in dose limits for radiation workers in 30 years. It behooves us to follow developments in these risk estimates carefully, as they seen likely to continue to be the most important element in the background science of radiation protection.

This paper briefly reviewed recent reports on the epidemiological and experimental data on low dose radiation effects that support the concept of radiation hormesis. These reports point to the possibility of existence of a threshold dose in cancer induction by ionizing radiation and in some cases the occurrence of hormetic effects with stimulation of host defense mechanisms. The possibility of the use of low dose radiation in cancer treatment to improve the outcome of conventional radiotherapy was raised by citing previous reports on experimental studies, which showed increased efficacy in tumor control with significant reduction of total dose of radiation when low dose radiation was used in the combined treatment protocol.

With emerging trends in the incidence of cancer of various organ sites, additional approaches are needed to control human malignancies. Intervention or prevention of cancer by dietary constituents, a strategy defined as chemoprevention, holds great promise in our conquest to control cancer, because it can be implemented on a broader population base with less economic burden. Consistent with this, several epidemiological studies have shown that populations that consume diets rich in fruits and vegetables have an overall lower cancer incidence. Based on these encouraging observations, research efforts from across the globe have focused on identifying, characterizing, and providing scientific basis to the efficacy of various phytonutrients in an effort to develop effective strategy to control various human malignancies. Cancer induction, growth, and progression are multi-step events and numerous studies have demonstrated that various dietary agents interfere with these stages of cancer, thus blocking malignancy. Fruits and vegetables represent untapped reservoir of various nutritive and nonnutritive phytochemicals with potential cancer chemopreventive activity. Grapes and grape-based products are one such class of dietary products that have shown cancer chemopreventive potential and are also known to improve overall human health. This review focuses on recent advancements in cancer chemopreventive and anticancer efficacy of grape seed extract and other grape-based products. Overall, completed studies from various scientific groups conclude that both grapes and grape-based products are excellent sources of various anticancer agents and their regular consumption should thus be beneficial to the general population.

The linear nonthreshold (LNT) model plays a central role in low-dose radiation risk assessment for humans. With the LNT model, any radiation exposure is assumed to increase one's risk of cancer. Based on the LNT model, others have predicted tens of thousands of deaths related to environmental exposure to radioactive material from nuclear accidents ( e.g., Chernobyl) and fallout from nuclear weapons testing. Here, we introduce a mechanism-based model for low-dose, radiation-induced, stochastic effects (genomic instability, apoptosis, mutations, neoplastic transformation) that leads to a LNT relationship between the risk for neoplastic transformation and dose only in special cases. It is shown that nonlinear dose-response relationships for risk of stochastic effects (problematic nonlethal mutations, neoplastic transformation) should be expected based on known biological mechanisms. Further, for low-dose, low-dose rate, low-LET radiation, large thresholds may exist for cancer induction. We summarize previously published data demonstrating large thresholds for cancer induction. We also provide evidence for low-dose-radiation-induced, protection (assumed via apoptosis) from neoplastic transformation. We speculate based on work of others ( Chung 2002 ) that such protection may also be induced to operate on existing cancer cells and may be amplified by apoptosis-inducing agents such as dietary isothiocyanates.

Ionizing radiations are x-rays, γ-rays, and small atomic particles that have sufficient energy to ionize atoms. The local deposition of energy involved can damage or kill cells. It may also produce subtle changes in a cell genetic make-up. Much has been learned about effects of radiation from experiments on cell cultures. These experiments have shown that large particle radiations are more damaging than x-rays for the amount of energy released. They have also shown that when similar doses of x-rays are delivered at lower dose rates, less damage is produced because the cells are able to effectively repair much of the damage. The effects of radiation on human populations have been assessed through epidemiological studies of groups exposed to very large doses, such as the survivors of the atomic bombs exploded over Japan. Exposure to large doses of radiation above a certain threshold produces tissue reactions in the short term. Longer-term effects may occur after exposure to low doses of radiation, which are referred to as stochastic effects, as their occurrence is governed by the laws of chance. Stochastic effects are the induction of cancer and of genetic effects. Cancer induced by radiation will not develop until many years after exposure and the risks are greater among those exposed as children. Risks have been estimated from epidemiological studies, by extrapolating dose-response data down to the low doses received by radiation workers, but debate exists about whether the current extrapolation model may be too conservative. Keywords: radiobiology; biological effects; ionizing radiation; x-rays; radiation protection; cancer induction; chromosome mutation; stochastic effects; tissue reactions; radiotherapy

The effective-dose method which was proposed by the ICRP (International Commission of Radiation Protection) for the estimation of risk to the general population from occupational or environmental, low-dose radiation exposure is not adequate for estimating the risk of cancer induction by radiotherapy of malignant or nonmalignant diseases. The risk of cancer induction by radiotherapy of benign diseases should be based on epidemiologic data directly derived from follow-up studies of patients who had been given radiotherapy for nonmalignant diseases in the past. Risk factors were derived from epidemiologic studies of patients treated with irradiation for nonmalignant diseases to be used for selecting treatment options and optimizing treatment procedures. In most cases, cancer risks estimated by the effective-dose method may overestimate the true risks by one order of magnitude, yet in other cases even may underestimate it. The proposed method using organ-specific risk factors may be more suitable for treatment planning.

I would like to discuss (a) how important discoveries over the last 100 years help to quantify the risk of cancer in populations exposed to man-made sources of ionizing radiation, and (b) how periodic episodes of contamination of the environment with radioactive elements have created public health problems.

The problem of 2011 nuclear accident crisis draws attention of physicians and medical scientists around the world. The cancer induction is an important adverse effect of exposure to radionuclide. In this specific article, the multiple myeloma, an important hematological cancer, in the post nuclear accident crisis will be discussed.

This is a brief review of what is known from experimental studies about the effects of low doses of radiation, and approaches that might improve risk estimates are discussed. The dose-response relationships for cancer induction by radiation vary markedly between tissues. The evidence suggests that 1) the induction of the initial events is dependent on the cell type because the size and/or the number of targets and how the cells handle the initial lesions differs between cell types; and 2) there are marked differences among tissues how initial lesions are expressed and proceed to overt cancer. The recent findings about adaptive responses are discussed in the context of what they contribute to our understanding about the response to irradiation. Lastly, the possibility of extending the approach of determining "The probability of causation," which Vic Bond played such an important role in establishing, is raised.

Summary Ionizing radiation at high doses is known human carcinogen. Numerous population studies involving military, medical, and occupational uses of radiation clearly show that leukemia and a variety of solid tumors may be induced by radiation. However, at low doses of radiation, typically encountered in diagnostic radiology and nuclear medicine, the evidence for cancer causation is much less compelling. Most epidemiological studies are inconsistent. Only a few studies suggest a significant association between radiation and cancer. Even in these investigations, the causal nature of such associations and the levels of risk remain uncertain. Radiation risks for cancer have been based primarily on studies of Japanese survivors of the atomic bombings. Extrapolation of data derived from these studies, using a linear no-threshold model, has been the basis for predicting cancer risk at low doses. The derived risk estimates suggest that radiodiagnostic studies, including nuclear medicine and X-ray examinations, are associated with small risks for cancer. Radiotherapy for cancer, which involves substantially higher doses, are associated with higher risks, but these risks are still very small considering the benefits derived from the treatments.

“Repeated irradiation gives rise to a unique threshold-type dose response in skin tumor induction.” This statement is the main subject of this paper. Although information on radiation-induced tumors has been accumulated from experimental data (Upton et al. 1986), most has come from experiments using a single exposure or a few fractionated exposures to radiation. Estimation of radiation risk for humans is mainly based upon data obtained from cases of single exposure: very few data are available on the dose-response relationship of tumor incidence to continuous or repeated exposures to radiation. However, such data are necessary for evaluating the risk of continuous exposure of humans to environmental radiation.

The rationale of this study stems from the concern of radiation-induced second malignancies after a course of definitive radiation therapy or the possibility of a terrorist-mediated nuclear attack resulting in large populations of people exposed to non-lethal radiation doses, which would substantially increase the risk for cancer induction post-exposure. Currently, there are no safe and effective interventions to reduce this risk to humans. Previous studies have shown that chronic administration of Tempol (nitroxide antioxidant) in the diet of mice results in decreased weight and spontaneous tumorigenesis, and increased tumor latency (Mitchell JB, et al., Free Radic Biol Med 34:93-102, 2003). In the current study we tested the hypothesis that Tempol (TP) administered in the diet of mice would reduce radiation-induced cancer when given after the radiation exposure. Total body radiation (3 Gy) was administered to female C3H and CBA mice. Along with various control groups, immediately after radiation one group of animals from each strain was placed on a TP diet. Food consumption and animal weights were monitored throughout the study. Animals were followed for their entire lifespan (>1300 mice). The endpoint for the study was tumor formation or until the animal reached a humane endpoint at which time the animal was euthanized and evaluated for the presence of tumor (pathology evaluated on all animals). TP food supplementation after radiation: a) did not alter food consumption compared to animals on a control food diet, b) compared to animals on control food diet, the TP diet resulted in decreased weights in both mouse strains (40% for C3H and 20% for CBA), and c) TP food supplementation post-radiation significantly enhanced the survival of both mouse stains. Median survival values for 0 Gy, 3 Gy, 0 Gy TP, and 3 Gy TP for C3H mice was 706, 434, 764, and 670 days, respectively. For CBA mice median survival values for 0 Gy, 3 Gy, 0 Gy TP, and 3 Gy TP for C3H mice was 901, 660, 939, and 782 days, respectively. The incidence of hematopoietic neoplasms (predominantly lymphomas) was significantly reduced in both mouse strains by TP treatment and both the onset and incidence of solid neoplasms was significantly reduced in CBA mice treated with TP. These results encourage more research on nitroxide-based antioxidants in the chemoprevention of cancer to elucidate the mechanism(s) involved. Citation Information: Cancer Prev Res 2010;3(12 Suppl):A4.

For decades investigators have suggested a correlation between personality (1) or emotional stress (2) and the growth of cancer. Links have been made between helpless behavior in the face of stressful impairment and reduction in clearance of tumor cells in experimental animal models (3, 4). Humans might be affected in a similar fashion but the possibilities to obtain this evidence in humans are limited. Some recent results concerning the link between stressful life events and breast cancer are contradictory and usually dependent on the different methodologies of investigation of this link (5).

In this paper, we consider the possible role of nitroarenes as causative compounds for human cancer. At the outset, it is important to recognize that adequate data to answer this question are not available. However, we will evaluate existing data with respect to three major cancer sites: lung, bladder, and breast. These sites were chosen because either experimental or epidemiologic studies, as summarized below, suggested that nitroarenes were possible etiologic agents. Our evaluation of the role of nitroarenes in each of these diseases will be based on their abilities to induce the relevant tumors in experimental animals, on their concentrations in the appropriate environments, and on data from analyses of human tissues or blood. We recognize that this approach is limited by the complex interactions that occur in environmental mixtures to which humans are exposed. Interactions between carcinogens and cocarcinogens, inhibitors, or promoters as well as host factors such as levels of carcinogen metabolizing enzymes tend to confound analyses of this type. Nevertheless, we have found it useful to focus on individual compounds within complex mixtures as this can lead to new insights regarding mechanisms of cancer induction.

The lifespan studies of animals exposed to low doses of ionizing radiation with a view to determining the relationships between radiation dose and cancer incidence have been identified and corresponding publications have been reviewed. The information on experimental conditions and cancer incidence data in exposed and control animals have been entered into a database intended for a global analysis of the relationship between low doses of ionizing radiation and cancer incidence. Data concerning about 85,000 exposed animals and their 45,000 corresponding controls, with a total of over 60,000 and 12,000 cancers in exposed and control animals, respectively, have been collected. Experiments were conducted with all types of ionizing radiation, at doses ranging from 10 mGy to 3.3 Gy for gamma radiation, 40 mGy to 4 Gy for X-rays, 2 mGy to several hundred Gy for beta radiation, 2 mGy to 9 Gy to alpha radiation, and 5 mGy to 3.3 Gy of neutrons. Within a specific experiment, data are grouped into datasets, which concern animals of a particular species, strain, sex, age at exposure, exposed to a range of doses under specific exposure conditions. In this body of data, no cancers were observed in the control groups of about 30% of the datasets, which makes it impossible to detect a possible decrease in cancer rates in exposed animals. When cancers were observed in control animals, either no effect or an apparent reduction in cancer risk was observed in 40% of the datasets for neutron exposure, 50% of the datasets for X-rays, 53% of the datasets for gamma radiation, and 61% of the datasets for alpha radiation. Apparent reductions in cancer rate, significant at up to 10 standard deviations, were observed in mice exposed to 100 and 250 mGy of gamma radiation. This review confirmed that, in some experiments, exposed animals live considerably longer (up to 40%) than their controls. In some experiments for which pathological observations were reported on non-malignant diseases, there appears to be apparent beneficial effects of low doses of radiation, coupled with an apparently increased longevity. The statistical strength of the overall observations has not been determined yet and is subject to further work. However, the frequency of an apparent lack of effect or of protective effects, and of increased longevity in exposed animals, challenges the general validity of the Linear No Threshold Theory (LNT) and calls for research aimed at confirming or disproving the existence of beneficial effects of low-dose radiation on malignant and nonmalignant diseases and at determining the mechanisms that subtend them.

There have been allegations in the media and in the courts that cell phones and other types of hand-held transceivers are a cause of cancer. There have also been numerous public objections to the siting of TV, radio and cell phone transmission facilities because of a fear of cancer induction. A recent publication in Radiation Research by Repacholi et al. (147, 631-640, 1997) which suggests that exposure to radiofrequency (RF) radiation may increase lymphoma incidence in mice has contributed to this controversy. The goal of this review is to provide biomedical researchers a brief overview of the existing RF radiation-cancer studies. This article begins with a brief review of the physics and technology of cell phones. It then reviews the existing epidemiological studies of RF radiation, identifying gaps in our knowledge. Finally, the review discusses the cytogenetics literature on RF radiation and the whole-animal RF-radiation carcinogenesis studies. The epidemiological evidence for an association between RF radiation and cancer is found to be weak and inconsistent, the laboratory studies generally do not suggest that cell phone RF radiation has genotoxic or epigenetic activity, and a cell phone RF radiation-cancer connection is found to be physically implausible. Overall, the existing evidence for a causal relationship between RF radiation from cell phones and cancer is found to be weak to nonexistent.

The objectives of the trip were: to take part in and to give the summary of a Symposium on Radiation Carcinogenesis at Tokyo, and to give a talk at the National Institute of Radiological Sciences at Chiba. The breadth of the aspects considered at the conference was about as broad as is possible, from effects at the molecular level to human epidemiology, from the effects of tritium to cancer induction by heavy ions. The events induced by cancer that lead to cancer and the events that are secondary are beginning to come into better focus but much is still not known. Interest in suppressor genes is increasing rapidly in the studies of human tumors and many would predict that the three or four suppressor genes associated with cancer are only the first sighting of a much larger number.

Oncogenic viruses, able to elicit tumour formation in animals, have been on the scientific scene for many years. After the early discovery of Ellerman and Bang at the beginning of this century, Peyton Rous opened up the field in its second decade and in prophetic words gave a good hint of things to come. However, these discoveries were soon forgotten and only after a long eclipse was interest in oncogenic viruses revived in the fifties. My involvement in this field began at that time when Rubin and Temin worked in my laboratory with the Rous Sarcoma Virus. When in 1958 polyoma virus, a new oncogenic virus with different properties, was isolated, I jumped at the new opportunity and started working with it. Within a short time polyoma virus became the main interest of my laboratory, to be joined, a few years later by SV40, another papovavirus. It became clear fairly soon that the molecular biology of these viruses could be worked out, and I set out to find the molecular basis of cancer induction. The results that I and a number of brilliant young collaborators have obtained during the following fifteen years have brought us close to that goal. I will review the most interesting steps of our work and will then ask some questions concerning the nature of cancer and about perspectives for prevention and treatment. I stress the relevance of my work for cancer research because I believe that science must be useful to man.