Breast cancer in women with scoliosis exposed to multiple diagnostic x rays

Although exposure to ionizing radiation is a recognized risk factor for breast cancer, the potential hazard from low-dose, fractionated exposures during early breast development has not been thoroughly evaluated. Women with scoliosis represent a valuable population for studying this issue because they are exposed to multiple diagnostic x rays during childhood and adolescence, times when the breast may be highly sensitive to the carcinogenic effects of radiation. A study was conducted of 1,030 women with scoliosis who were seen at four Minneapolis area medical facilities between 1935 and 1965. The average age at diagnosis was 12.3 years; 60% of the women had idiopathic scoliosis. Individual x-ray films were counted and the number per patient ranged from 0 to 618 films (mean, 41.5). On average, the x-ray exposures were given over an 8.7-year period. Ninety percent of the women were located, of whom over 92% responded to a mail questionnaire or telephone interview. The average period of observation was 26 years. Overall, 11 cases of breast cancer were reported, compared with six expected (standardized incidence ratio = 1.82, 90% confidence interval = 1.0-3.0). Excess risk increased with time since exposure and was highest among those followed for more than 30 years (standardized incidence ratio = 2.4). Risk also increased with the number of x rays and with the estimated radiation dose to the breast (mean, 13 rad). These data suggest that frequent exposure to low-level diagnostic radiation during childhood or adolescence may increase the risk of breast cancer.     

Single, split and fractionated dose X-radiation-induced malignant transformation in A31-11 mouse BALB/3T3 cells

Studies were conducted to determine the effects of a single, split and fractionated doses (separated by 1-h intervals) of 100 rad of X-irradiation on the morphological transformation of BALB/c 3T3 clone A31-11 mouse fibroblasts grown in media containing calf serum. Both spontaneous and radiation-induced transformation levels were lower for these cells grown in the cell-serum containing media than previously reported for these cells grown in fetal calf serum containing media. In the studies reported here, cells were irradiated either as density-inhibited plateau phase cultures or as low density cultures at 10-14 h after being reseeded from confluent dishes. We observed that a 4-fraction 100-rad dose resulted in a reduced yield of transformants compared to a single dose of 100 rad when plateau phase cultures were utilized for the radiation exposures, but not in low density cultures in which the cells were allowed to proliferate during the radiation exposures, these results suggest that the growth phase of the cells can play a major role in determining the yield of transformants induced by fractionated doses of radiation. It is noteworthy that, for the other data obtained in these studies, in none of 12 different experimental points (involving 5 separate experiments) did a fractionated dose protocol result in a reduced yield of transformants when compared to a single dose protocol.     

Is family history of breast cancer a marker of susceptibility to exposures in the incidence of de novo adult acute leukemia?

The risk factors for adult acute leukemia incidence have been difficult to establish.Family history of cancer might interact with environmental exposures to produce associations that are otherwise difficult to detect. In addition to family history of leukemia or other hematopoietic cancers, family history of breast cancer could be a marker of susceptibility, because leukemia and breast cancer are known to cluster in families that have specific germ-line mutations. In a population-based case control study of 779 incident adult acute leukemia patients and 625 controls, we estimated the relative risk for exposed individuals with a family history compared with unexposed individuals without a family history (RR(11)), along with a measure of interdependence, the interaction contrast ratio. Combined with a family history of breast cancer, ever-smoking [RR(11) = 2.4, 95% confidence interval (CI): 1.2-4.8], general solvent exposure (RR(11) = 1.9, 95% CI: 1.1-3.4), aromatic hydrocarbon exposure (RR(11) = 3.8, 95% CI: 1.1-14), and diagnostic ionizing radiation exposure (RR(11) = 2.1, 95% CI: 1.2-3.8) were all associated with increased incidence. Furthermore, there was no increased incidence associated with any of these exposures in the absence of a family history of breast cancer and no increased incidence for family history of breast cancer in the absence of exposures. The pattern of relative risks strongly suggested synergy across exposures. Family history of breast cancer might be a marker of susceptibility to a range of leukemia risk factors, whose effects are generally weak or nonexistent when considered alone.     

Diagnostic X-rays and ultrasound exposure and risk of childhood acute lymphoblastic leukemia by immunophenotype.

The objective of this study was to evaluate the association between in utero diagnostic X-rays and childhood acute lymphoblastic leukemia (ALL) and the less well-studied relationship of this malignancy to preconception and postnatal diagnostic X-rays or fetal ultrasound exposures. The Children's Cancer Group conducted a case-control study including interviews with parents of 1842 ALL cases diagnosed under the age of 15 years and 1986 individually matched controls. Associations of self-reported parental preconception, in utero, and postnatal X-ray exposure with risk of childhood ALL were examined using odds ratios (ORs) and corresponding 95% confidence intervals (CIs) obtained from logistic regression models among the overall group of ALL cases as well as immunophenotypic and age-specific subgroups. Overall, in utero pelvimetric diagnostic X-rays were not associated with the risk of pediatric ALL (OR, 1.2; 95% CI, 0.8-1.7). Childhood ALL, all types combined (OR, 1.1; 95% CI, 0.9-1.2) and specific types were also not linked with postnatal diagnostic X-ray exposures. Neither maternal (OR, 0.9; 95% CI, 0.8-1.2) nor paternal (OR, 1.1; 95% CI, 0.8-1.4) lower abdominal preconception diagnostic X-rays were associated with risk of childhood ALL. Among the multiple comparisons for age-, sex-, and subtype-specific subgroups, we observed an elevated risk of total ALL among children ages 11-14 at diagnosis (OR, 2.4; 95% CI, 1.1-5.0) in relation to in utero pelvimetric diagnostic X-ray exposures and a small increase in pre-B ALL for all ages combined (OR, 1.7; 95% CI, 1.1-2.7) in relation to postnatal diagnostic X-rays. In utero diagnostic ultrasound tests were not linked with risk of childhood ALL. We found little consistent evidence that in utero diagnostic ultrasound tests or X-rays were linked with an increased risk of childhood ALL. Small increases in total or pre-B ALL risks for children in selected age groups to very low ionizing radiation exposures from postnatal or preconception diagnostic X-ray exposures may represent chance findings or biases. Future studies of diagnostic X-rays and childhood leukemia in the United States will require extensive additional efforts and resources to quantify risk because of declining in utero exposures in the general population (thus necessitating large numbers of subjects, particularly cases) and the difficulty in validating reported exposures.     

Ionizing radiation and the risk of brain and central nervous system tumors: a systematic review

Although exposure to moderate-to-high doses of ionizing radiation is the only established environmental risk factor for brain and CNS tumors, it is not clear whether this relationship differs across tumor subtypes, by sex or age at exposure, or at the low-to-moderate range of exposure. This systematic review summarizes the epidemiologic evidence on the association between ionizing radiation exposure and risk of brain/CNS tumors. Articles included in this review estimated radiation exposure doses to the brain and reported excess relative risk (ERR) estimates for brain/CNS tumors. Eight cohorts were eligible for inclusion in the analysis. Average age at exposure ranged from 8 months to 26 years. Mean dose to the brain ranged from 0.07 to 10 Gy. Elevated risks for brain/CNS tumors were consistently observed in relation to ionizing radiation exposure, but the strength of this association varied across cohorts. Generally, ionizing radiation was more strongly associated with risk for meningioma compared with glioma. The positive association between ionizing radiation exposure and risk for glioma was stronger for younger vs older ages at exposure. We did not observe an effect modification on the risk for meningioma by sex, age at exposure, time since exposure, or attained age. The etiologic role of ionizing radiation in the development of brain/CNS tumors needs to be clarified further through additional studies that quantify the association between ionizing radiation and risk for brain/CNS tumors at low-to-moderate doses, examine risks across tumor subtypes, and account for potential effect modifiers.     

Polymorphisms in apoptosis- and proliferation-related genes, ionizing radiation exposure, and risk of breast cancer among U.S. Radiologic Technologists.

BACKGROUND: Although genes involved in apoptosis pathways and DNA repair pathways are both essential for maintaining genomic integrity, genetic variants in DNA repair have been thought to increase susceptibility to radiation carcinogenesis, but similar hypotheses have not generally been raised about apoptosis genes. For this reason, potential modification of the relationship between ionizing radiation exposure and breast cancer risk by polymorphic apoptosis gene variants have not been investigated among radiation-exposed women. METHODS: In a case-control study of 859 cases and 1,083 controls within the U.S. Radiologic Technologists cohort, we assessed breast cancer risk with respect to 16 candidate variants in eight genes involved in apoptosis, inflammation, and proliferation. Using carefully reconstructed cumulative breast dose estimates from occupational and personal diagnostic ionizing radiation, we also investigated the joint effects of these polymorphisms on the risk of breast cancer. RESULTS: In multivariate analyses, we observed a significantly decreased risk of breast cancer associated with the homozygous minor allele of CASP8 D302H [rs1045485, odds ratio (OR), 0.3; 95% confidence interval (95% CI), 0.1-0.8]. We found a significantly increased breast cancer risk with increasing minor alleles for IL1A A114S (rs17561); heterozygote OR 1.2 (95% CI, 1.0-1.4) and homozygote OR 1.5 (95% CI, 1.1-2.0), P(trend) = 0.008. Assuming a dominant genetic model, IL1A A114S significantly modified the dose-response relationship between cumulative personal diagnostic radiation and breast cancer risk, adjusted for occupational dose (P(interaction) = 0.004). CONCLUSION: The U.S. Radiologic Technologists breast cancer study provided a unique opportunity to examine the joint effects of common genetic variation and ionizing radiation exposure to the breast using detailed occupational and personal diagnostic dose data. We found evidence of effect modification of the radiation and breast cancer dose-response relationship that should be confirmed in studies with more cases and controls and quantified radiation breast doses in the low-to-moderate range.     

Combined Effects of Ultrasound and Ionizing Radiation on Lymphocyte Chromosomes

The effects of ionizing radiation and ultrasound upon the induction of chromosomal-type aberrations and sister chromatid exchanges were investigated. No statistically significant increase in the frequencies of dicentric and ring chromosomes or sister chromatid exchanges was discovered after ultrasound exposure alone at the diagnostic level. Nor could elevated frequencies of these phenomena be found following exposure to ultrasound before or after ionizing radiation, compared with those resulting from an equivalent dose of ionizing radiation alone. However, simultaneous exposure to ultrasound and ionizing radiation seemed to induce a slight enhancement of sister chromatid exchanges, although no significant change was noted in the yields of dicentric and ring chromosomes.     

Polymorphisms in DNA repair genes, ionizing radiation exposure and risk of breast cancer in U.S. Radiologic technologists

High-dose ionizing radiation exposure to the breast and rare autosomal dominant genes have been linked with increased breast cancer risk, but the role of low-to-moderate doses from protracted radiation exposure in breast cancer risk and its potential modification by polymorphisms in DNA repair genes has not been previously investigated among large numbers of radiation-exposed women with detailed exposure data. Using carefully reconstructed estimates of cumulative breast doses from occupational and personal diagnostic ionizing radiation, we investigated the potential modification of radiation-related breast cancer risk by 55 candidate single nucleotide polymorphisms in 17 genes involved in base excision or DNA double-strand break repair among 859 cases and 1083 controls from the United States Radiologic Technologists (USRT) cohort. In multivariable analyses, WRN V114I (rs2230009) significantly modified the association between cumulative occupational breast dose and risk of breast cancer (adjusted for personal diagnostic exposure) (p = 0.04) and BRCA1 D652N (rs4986850), PRKDC IVS15 + 6C > T (rs1231202), PRKDC IVS34 + 39T > C (rs8178097) and PRKDC IVS31 - 634C > A (rs10109984) significantly altered the personal diagnostic radiation exposure-response relationship (adjusted for occupational dose) (p < or = 0.05). None of the remaining 50 SNPs significantly modified breast cancer radiation dose-response relationships. The USRT genetic study provided a unique opportunity to examine the joint effects of common genetic variation and ionizing radiation exposure on breast cancer risk using detailed occupational and personal diagnostic exposure data. The suggestive evidence found for modification of radiation-related breast cancer risk for 5 of the 55 SNPs evaluated requires confirmation in larger studies of women with quantified radiation breast doses in the low-to-moderate range.     

Breast cancer incidence in U.S. radiologic technologists

BACKGROUND: Studies of atomic bomb survivors and medically exposed populations have demonstrated an increased risk of breast cancer associated with acute or protracted, intermediate-dose or high-dose, ionizing radiation; however, the risks associated with low-dose and low-dose-rate (protracted) exposures are less certain. METHODS: The authors evaluated incident breast cancer risks from 1983 to 1998 according to employment characteristics and a 4-level proxy index for cumulative radiation exposure based on 2 mail surveys among 56,436 U.S. female radiologic technologists who were certified from 1925 to 1980, adjusting for established breast cancer risk factors. RESULTS: During follow-up, 1050 new breast cancer diagnoses were ascertained. Compared with radiologic technologists who began working in 1970 or later, adjusted breast cancer risks for those who first worked in the 1960s, 1950s, 1940s, from 1935 to 1939, and before 1935 were 1.0 (95% confidence interval [CI], 0.8-1.2), 1.2 (95% CI, 0.9-1.6), 1.0 (95% CI, 0.7-1.5), 1.8 (95% CI, 1.0-3.2), and 2.9 (95% CI, 1.3-6.2), respectively. The risk rose with the number of years worked before 1940 (P value for trend = .002) and was elevated significantly among those who began working before age 17 years (relative risk, 2.6; 95% CI, 1.3-5.1; 10 women) but was not related to the total years worked in the 1940s or later. Compared with technologists who had a Level 1 (minimal) proxy index for cumulative radiation exposure, breast cancer risks were 1.0 (95% CI, 0.9-1.2), 1.0 (95% CI, 0.7-1.3), and 1.5 (95% CI, 1.0-2.2), respectively, for technologists who had Level 2, Level 3, and Level 4 (highest) exposure. CONCLUSIONS: Breast cancer risk was elevated significantly in female radiologic technologists who experienced daily low-dose radiation exposures over several years that potentially resulted in appreciable cumulative exposure. The increased risk for total years worked before 1940, but not later, was consistent with decreasing occupational radiation exposures, improvements in radiation technology, and more stringent radiation protection standards over time.     

Cancer and other causes of mortality among radiologic technologists in the United States

Data are limited on the role of chronic exposure to low-dose ionizing radiation in the etiology of cancer. In a nationwide cohort of 146,022 U.S. radiologic technologists (73% female), we evaluated mortality risks in relation to work characteristics. Standardized mortality ratios (SMRs) were computed to compare mortality in the total cohort vs. the general population of the United States. Mortality risks were low for all causes (SMR = 0.76) and for all cancers (SMR = 0.82) among the radiologic technologists. We also calculated relative risks (RR) for the 90,305 technologists who responded to a baseline mailed questionnaire, using Poisson regression models, adjusted for known risk factors. Risks were higher for all cancers (RR = 1.28, 95% confidence interval [CI] = 0.93-1.69) and breast cancer (RR = 2.92, 95% CI = 1.22-7.00) among radiologic technologists first employed prior to 1940 compared to those first employed in 1960 or later, and risks declined with more recent calendar year of first employment (p-trend = 0.04 and 0.002, respectively), irrespective of employment duration. Risk for the combined category of acute lymphocytic, acute myeloid and chronic myeloid leukemias was increased among those first employed prior to 1950 (RR = 1.64, 95% CI = 0.42-6.31) compared to those first employed in 1950 or later. Risks rose for breast cancer (p-trend = 0.018) and for acute lymphocytic, acute myeloid and chronic myeloid leukemias (p-trend = 0.05) with increasing duration of employment as a radiologic technologist prior to 1950. The elevated mortality risks for breast cancer and for the combined group of acute lymphocytic, acute myeloid and chronic myeloid leukemias are consistent with a radiation etiology given greater occupational exposures to ionizing radiation prior to 1950 than in more recent times.     

Myeloid leukaemia frequency after protracted exposure to ionizing radiation: experimental confirmation of the flat dose-response found in ankylosing spondylitis after a single treatment course with X-rays

The dose-response for leukaemia induction by exposure to ionizing radiation protracted over several weeks was largely independent of dose not only in X-rayed patients with ankylosing spondylitis but also in experimentally gamma-rayed CBA/H mice. In the experiment the induced leukaemia frequency of acute myeloid leukaemia was independent of a several thousand-fold variation in physical dose rate. Any difference in leukaemia induction between brief and protracted exposures must therefore depend on specifically biological consequences of protracted exposures. Experimental analysis is required to provide the guides for inference about risks of low level exposure from observations on relatively heavily irradiated populations.     

Cancer risks associated with external radiation from diagnostic imaging procedures

The 600% increase in medical radiation exposure to the US population since 1980 has provided immense benefit, but increased potential future cancer risks to patients. Most of the increase is from diagnostic radiologic procedures. The objectives of this review are to summarize epidemiologic data on cancer risks associated with diagnostic procedures, describe how exposures from recent diagnostic procedures relate to radiation levels linked with cancer occurrence, and propose a framework of strategies to reduce radiation from diagnostic imaging in patients. We briefly review radiation dose definitions, mechanisms of radiation carcinogenesis, key epidemiologic studies of medical and other radiation sources and cancer risks, and dose trends from diagnostic procedures. We describe cancer risks from experimental studies, future projected risks from current imaging procedures, and the potential for higher risks in genetically susceptible populations. To reduce future projected cancers from diagnostic procedures, we advocate the widespread use of evidence‐based appropriateness criteria for decisions about imaging procedures; oversight of equipment to deliver reliably the minimum radiation required to attain clinical objectives; development of electronic lifetime records of imaging procedures for patients and their physicians; and commitment by medical training programs, professional societies, and radiation protection organizations to educate all stakeholders in reducing radiation from diagnostic procedures. CA Cancer J Clin 2012. © 2012 American Cancer Society.     

Low-dose medical radiation exposure and breast cancer risk in women under age 50 years overall and by estrogen and progesterone receptor status: results from a case–control and a case–case comparison

Although moderate to high-dose ionizing radiation exposure is an established risk factor for breast cancer, the effect of low-dose radiation exposure has not been clarified by epidemiological data. We evaluated the effect of low-dose radiation from medical procedures on risk of breast cancer overall and by joint estrogen and progesterone receptor (ER/PR) status in 1,742 population-based case patients aged 20–49 years and 441 control subjects identified from neighbourhoods of case patients in Los Angeles County. After excluding radiation exposures in the 5 years prior to case’s diagnosis or control’s initial household contact date we found an elevated breast cancer risk among women who reported having had multiple chest X-rays (P _trend = 0.0007) or 7 or more mammograms (odds ratio [OR] = 1.80, 95% confidence interval [CI] = 0.95–3.42). Risk was also increased among women who received dental X-rays without lead apron protection before age 20 years (OR = 1.81, 95% CI = 1.13–2.90). Women, who had their first exposure to these medical radiation procedures during childhood, had a greater increase in risk than those who were first exposed at older ages. Although not statistically significantly different, risk estimates were somewhat stronger for nulliparous than for parous women. We found no effect modification by ER/PR status. In conclusion, our findings support the hypothesis that low-dose ionizing radiation, and particularly exposures during childhood, increase breast cancer risk.     

X-ray exposure and premature aging

An hypothesis of an aging effect of exposure to ionizing radiation in humans is proposed and given precise mathematical expression. The assumption is made that the biological changes which occur when humans are exposed to ionizing radiation from medical x ray are comparable to those occuring through the natural aging process, since both factors are known to increase the relative risk of nonlymphatic leukemia. This assumption focuses on this one aspect of aging only. The hypothesis that aging and exposure to ionizing radiation are comparable for increasing the relative risk of nonlymphatic leukemia is tested against the data from the Tri-State Leukemia Survey. It is shown to explain the data in a statistically acceptable way, giving an estimate of 1 rad skin dose exposure to the trunk as comparable to 1 year natural aging. This research raises further questions concerning the effects of exposure to ionizing radiation, and presents a new methodology by which these questions may be researched.     

Lung cancer at autopsy in A-bomd survivors and controls, Hiroshima and Nagasaki, 1961-1970. II. Smoking, occupation, and A-bomb exposure.

The apparent effect of ionizing radiation on lung cancer in A-bomb survivors has not been large enough to still doubts as to its validity. It has seemed essential to determine whether the apparent radiation effect could have resulted from a confounding of heavy smoking and high radiation dose, or if the occupational exposure of high-dose subjects with lung cancer was suggestive of the influence of environmental hazards other than radiation. The available series consists of 204 subjects with lung cancer verified by autopsy, 61 of whom were low-dose (less than 1 rad) and 13 high-dose (200 + rads) subjects. No evidence could be found that the influence of either smoking or occupational exposure upon lung cancer was exerted so as to suggest that the apparent radiation effect is other than real. The study also provides additional evidence of the relationship between lung cancer and smoking in Japanese.     

Radiation therapy in the treatment of meningioma: the Joint Center for Radiation Therapy experience 1970 to 1982

The standard treatment for meningioma is complete resection. However, complete resection is often not possible because of tumor location and extent. To evaluate the usefulness of radiation therapy in patients with unresected or residual tumor, we reviewed the Joint Center for Radiation Therapy experience from 1970 to 1982 (n = 31). Histologic diagnosis was available in 27 patients. The patients were treated with megavoltage radiation to a mean dose of 5,280 rad (3,780 to 6,050 rad) in 180- to 200-rad daily fractions using multiple static or rotational fields. The median follow-up period was 45 months, with a range of four to 156 months. The overall four-year relapse-free survival (RFS) rate was 72%. All relapses occurred within the first 37 months; the mean time to relapse was 31 months. The four-year RFS was the same whether patients were treated at initial presentation or after recurrence (74% v 67%, respectively). There was no difference in RFS for patients treated after partial resection or those patients with no resection (76% v 64%). No patients with malignant meningioma were relapse free three years after radiation therapy. Complications included decreased auditory acuity in three patients and retinopathy in one patient. These data suggest that moderate dose radiation therapy can offer long-term symptom-free survival with few complications in patients having unresected or partially resected benign meningioma.     

Risk of melanoma among radiologic technologists in the United States

Our study examines the risk of melanoma among medical radiation workers in the U.S. Radiologic Technologists (USRT) study. We evaluated 68,588 white radiologic technologists (78.8% female), certified during 1926-1982, who responded to a baseline questionnaire (1983-1989) and were free of cancer other than nonmelanoma skin at that time. Participants were followed through completion of a second questionnaire (1994-1998). We identified 207 cases, 193 subjects who reported first primary melanoma and 14 decedents with melanoma listed as an underlying or contributory cause of death. We examined risks of occupational radiation exposures using work history information on practices, procedures, and protective measures reported on the baseline questionnaire. Based on Cox proportional hazards regression, melanoma was significantly associated with established risk factors, including constitutional characteristics (skin tone, eye and hair color), personal history of nonmelanoma skin cancer, family history of melanoma and indicators of residential sunlight exposure. Melanoma risk was increased among those who first worked before 1950 (RR = 1.8, 95% CI = 0.6-5.5), particularly among those who worked 5 or more years before 1950 (RR = 2.4; 0.7-8.7; p (trend) for years worked before 1950 = 0.03), when radiation exposures were likely highest. Risk was also modestly elevated among technologists who did not customarily use a lead apron or shield when they first began working (RR = 1.4; 0.8-2.5). Clarifying the possible role of exposure to chronic ionizing radiation in melanoma is likely to require nested case-control studies within occupational cohorts, such as this one, which will assess individual radiation doses, and detailed information about sun exposure, sunburn history and skin susceptibility characteristics.     

Medical radiation exposure and breast cancer risk: findings from the Breast Cancer Family Registry

Moderate to high-dose radiotherapy is known to increase the risk of breast cancer. Uncertainties remain about the effects of low-dose chest X-rays, particularly in individuals at increased genetic risk. We analyzed case-control data from the Breast Cancer Family Registry. Self-reported data on therapeutic and diagnostic radiation exposures to the chest were available for 2,254 breast cancer cases and 3,431 controls (1,556 unaffected sisters and 1,875 unrelated population controls). We used unconditional logistic regression analyses to estimate odds ratios (OR) and 95% confidence intervals (CI) associated with radiation exposure, after adjusting for age, study center, country of birth, and education. Increased risks for breast cancer were found for women who had radiotherapy for a previous cancer (OR=3.55, CI=1.47-8.54) and diagnostic chest X-rays for tuberculosis (OR=2.49, CI=1.82-3.40) or pneumonia (OR=2.19, CI=1.38-3.47). Risks were highest for women with a large number of exposures at a young age or exposed in earlier calendar years. There was no evidence of increased risk associated with other diagnostic chest X-rays (not including tuberculosis or pneumonia), both in women with and without indicators of increased genetic risk (i.e., diagnosed at age <40 years or family history of breast cancer). Given the widespread and increasing use of medical diagnostic radiation, continued surveillance of breast cancer risk is warranted, particularly in women at specific genetic risk, such as those carrying mutations in BRCA1 or BRCA2.     

No association between immunohistochemical expression of p53, c-erbB-2, Ki-67, estrogen and progesterone receptors in female papillary thyroid cancer and ionizing radiation

An association has previously been reported between exposure to medical diagnostic ionizing radiation and papillary thyroid cancer in women. To further evaluate potential mechanisms in carcinogenesis, the expression of p53, c-erbB-2, as well as Ki-67, estrogen and progesterone receptors were analyzed by immunohistochemistry in 19 women exposed to X-rays and for comparison in nine women without such reported exposure. They all had papillary thyroid cancer. No difference was found between these groups. The results of this study showed that p53, c-erbB-2, Ki-67, estrogen and progesterone receptors are not involved in papillary thyroid cancer associated with exposure to medical diagnostic ionizing radiation.     

Syrian hamster dermal cell immortalization is not enhanced by power line frequency electromagnetic field exposure.

Several epidemiological studies have suggested associations between exposure to residential power line frequency electromagnetic fields and childhood leukaemia, and between occupational exposure and adult leukaemia. A variety of in vitro studies have provided limited supporting evidence for the role of such exposures in cancer induction in the form of acknowledged cellular end points, such as enhanced mutation rate and cell proliferation, though the former is seen only with extremely high flux density exposure or with co-exposure to ionizing radiation. However, in vitro experiments on a scale large enough to detect rare cancer-initiating events, such as primary cell immortalization following residential level exposures, have not thus far been reported. In this study, large cultures of primary Syrian hamster dermal cells were continuously exposed to power line frequency electromagnetic fields of 10 100 and 1000 microT for 60 h, with and without prior exposure to a threshold (1.5 Gy), or sub-threshold (0.5 Gy), immortalizing dose of ionizing radiation. Electromagnetic field exposure alone did not immortalize these cells at a detectable frequency (> or = 1 x 10(-7)); furthermore, such exposure did not enhance the frequency of ionizing radiation-induced immortalization.