Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Epidemiological studies have suggested that ataxia-telangiectasia (AT) heterozygotes have a predisposition to cancer, especially breast cancer in women. Now, haplotyping can identify heterozygotes for AT mutation (ATM) in AT families, allowing the risk of cancer associated with ATM heterozygosity status to be better assessed. We report a family study of AT patients, in which we estimated the risk of cancer according to ATM heterozygosity status. We analyzed demographic characteristics and occurrence of cancer in 1,423 relatives of AT patients. Haplotyping was performed in living relatives. The probability of being heterozygotes for ATM was calculated for deceased relatives. The risk of developing cancer was estimated in the cohort of relatives, and expected numbers of cancer cases were calculated from French age period-specific incidence rates. The number of cancers at all sites in the total population of relatives was not higher than expected. However, significant heterogeneity was found according to ATM heterozygosity status. This is mainly due to the increased risk of breast cancer previously observed in obligate heterozygotes. In obligate heterozygotes, relative risk (RR) was non-significantly increased for thyroid cancer, leukemia and liver cancer. Risks of ovarian, lung, pancreatic, kidney, stomach and colorectal cancers were non-significantly increased in the group with 0.5 probability of being heterozygotes. The RR was not significantly increased for any site of cancer, except for breast. Therefore, there is no evidence that specific screening of relatives of AT patients would be justified at particular sites other than the breast. However, the amplitude of the risk of breast cancer estimated in heterozygous women does not appear to justify a separate screening program from that already available to women with a first-degree relative affected by breast cancer.
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PMID:Cancer risk in heterozygotes for ataxia-telangiectasia. 1141 Aug 79

The concept of effective dose with its unit, the sievert, is frequently misunderstood. Originally conceived to simplify radiation protection management, this concept is also proposed for another and very ambitions objective: a quantitative evaluation of the risks of radio-induced diseases, whatever the dose, the dose rate, the nature of radiation.... However, using the sievert for the prediction of risks of cancer or hereditary diseases is hazardous, and errors of prediction have been observed these last decades, for example the lack of prediction of the number of thyroid cancer in the very young children after the Chernobyl accident, and the overestimation of the risks such as leukaemia, other cancer and hereditary diseases. What are one sievert and its subunits?
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PMID:The sievert: an enigmatic unit. 1144 65

The Author reviews the problem of neoplasmatic complications of pregnancy focusing mainly on genital tumors such as vulvar, vaginal, cervical, uterine, tubal and ovarian neoplasms as well as on other pelvic tumors originating from the bladder and bowel. Non-genital neoplasms such as breast cancer, Hodgkin's disease, non-Hodgkin lymphoma, leukemia, melanoma and thyroid cancer are also addressed. Literature data on the incidence of tumors in pregnant women are reviewed and the therapeutic options considering both the mother and the fetus are discussed. Management recommendations are given in cases when following the treatment a patient becomes pregnant again.
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PMID:[Pregnancy complicated by a neoplasmatic disease]. 1188 63

Cancer incidence (1950-1995) among 27,011 medical diagnostic x-ray workers was compared by means of O/E system with that of 25,782 other medical specialists employed between 1950 and 1980 to provide evidence of human malignant tumors produced by protracted and fractionated exposure to ionizing radiation and to assess resultant cancer risk. Significant cancer risk was seen among diagnostic x-ray workers (RR = 1.2, 95% CI: 1.1-1.3). Significantly elevated risks were found for leukemia and cancers of skin, female breast, lung, liver, bladder, and esophagus; the RRs were 2.2, 4.1, 1.3, 1.2, 1.2, 1.8, and 2.7, respectively. The patterns of risk associated with years since beginning x-ray work and with age and calendar year of initial employment suggest that the excesses of leukemia, skin cancer, and female breast cancer-and possibly thyroid cancer-were related to occupational exposure to x rays. Because of a lack of individual dosimetry for Chinese medical x-ray workers (CMXW) before 1985, the dose was reconstructed by physical and biological retrospective dosimetry methods. The cancer risk of CMXW was estimated based on the reconstructed dose. The average cumulative dose for the earlier cohort (employed before 1970) was 551 mGy, and for the later cohort (employed from 1970 to 1980) it was 82 mGy. The RRs of leukemia and solid cancer were significantly high for the earlier cohort: 2.4 for leukemia, 1.2 for solid cancer. But no significant increase of RR was evident for the later cohort. The RR of leukemia was 1.7 and 1.1 for solid cancer. This means a significant cancer risk can be induced by long term fractionated exposure to ionizing radiation when the cumulative dose reaches a certain level.
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PMID:Cancer incidence and risk estimation among medical x-ray workers in China, 1950-1995. 1255 57

The genetic and environmental components in 15 common cancers were estimated using the nationwide Swedish Family-Cancer Database. Tetrachoric correlations were used to describe similarity in cancer liability among family members. Structural equation modeling was used to derive estimates of the importance of genetic and environmental effects. Statistically significant estimates of proportion of cancer susceptibility, accounted for by genetic effects, were obtained for all studied cancers except for leukemia. The estimate was highest in thyroid cancer (53%), followed by tumors at endocrine glands (28%), testis (25%), breast (25%), cervix (22%), melanoma (21%), colon (13%), nervous system (12%), rectum (12%), non-Hodgkin lymphoma (10%), lung (8%), kidney (8%), urinary bladder (7%), stomach (1%) and leukemia (1%). The estimates of shared environmental effects ranged from 0% (cervix) to 15% (stomach). The childhood shared environmental effects were most important in testicular cancer (17%), stomach cancer (13%) and cervix in situ (13%). Our results indicate that environment has a principal causative role in cancer at all studied sites except for thyroid. The relatively large effect of heritability in cancer at some sites, on the other hand, indicates that even though susceptibility genes have been described at many cancer sites, they are likely to explain only part of the genetic effects.
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PMID:Environmental and heritable causes of cancer among 9.6 million individuals in the Swedish Family-Cancer Database. 1197 42

The Chernobyl nuclear accident on 26th April, 1986, led to a massive release of radionuclides into the environment. Although vast areas of Europe were affected by Chernobyl-related ionising radiation, the accident had the greatest impact in Belarus, Ukraine, and the Russian Federation. Epidemiological studies that have investigated the link between the Chernobyl accident and cancer have largely focused on malignant diseases in children, specifically thyroid cancer and leukaemia. There is good evidence to suggest that rates of thyroid cancer in children from the countries that were formally part of the Soviet Union have risen as a consequence of the Chernobyl accident. The findings for childhood leukaemia are less conclusive. Overall rates for this disease do not seem to have been affected by the Chernobyl-related ionising radiation, but there may be a larger risk of infant leukaemia in contaminated areas of Europe. Among adult populations, there is no strong evidence to suggest that risk of thyroid cancer, leukaemia, or other malignant disease has increased as a result of the Chernobyl accident.
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PMID:Chernobyl-related ionising radiation exposure and cancer risk: an epidemiological review. 1221 89

The current paper presents the methods and design of two case-control studies among Chernobyl liquidators-one of leukaemia and non-Hodgkin lymphoma, the other of thyroid cancer risk-carried out in Belarus, Estonia, Latvia, Lithuania and Russia. The specific objective of these studies is to estimate the radiation induced risk of these diseases among liquidators of the Chernobyl accident, and, in particular, to study the effect of exposure protraction and radiation type on the risk of radiation induced cancer in the low-to-medium- (0-500 mSv) radiation dose range. The study population consists of the approximately 10000 Baltic, 40000 Belarus and 51 000 Russian liquidators who worked in the 30 km zone in 1986-1987, and who were registered in the Chernobyl registry of these countries. The studies included cases diagnosed in 1993-1998 for all countries but Belarus, where the study period was extended until 2000. Four controls were selected in each country from the national cohort for each case, matched on age, gender and region of residence. Information on study subjects was obtained through face-to-face interview using a standardised questionnaire with questions on demographic factors, time, place and conditions of work as a liquidator and potential risk and confounding factors for the tumours of interest. Overall, 136 cases and 595 controls after receiving their consent were included in the studies. A method of analytical dose reconstruction has been developed, validated and applied to the estimation of doses and related uncertainties for all the subjects in the study. Dose-response analyses are underway and results are likely to have important implications to assess the adequacy of existing protection standards, which are based on risk estimates derived from analyses of the mortality of atomic bomb survivors and other high dose studies.
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PMID:Studies of cancer risk among Chernobyl liquidators: materials and methods. 1240 Sep 62

Tumors of thyroid follicular cells provide a very interesting model to understand the development of human cancer. It is becoming apparent that distinct molecular events are associated with specific stages in a multistep tumorigenic process with good genotype/ phenotype correlation. For instance, mutations of the gsp and thyroid-stimulating hormone receptor genes are associated with benign hyperfunctioning thyroid nodules and adenomas while alterations of other specific genes, such as oncogenic tyrosine kinase alterations (RET/PTC, TRK) in papillary carcinoma and the newly discovered PAX8/peroxisome proliferator-activated receptor gamma rearrangement, are distinctive features of cancer. Although activating RAS mutations occur at all stages of thyroid tumorigenesis, evidence is accumulating that they may also play an important role in tumor progression, a role that is well documented for p53. Environmental factors (iodine deficiency, ionizing radiations) have been shown to play a crucial role in promoting the development of thyroid cancer, influencing both its genotypic and phenotypic features. It is possible that the follicular thyroid cell has unique ways to respond to DNA damage. Similarly to leukemia or sarcomas (and unlike most epithelial cancers), numerous specific rearrangements are being discovered in thyroid cancer suggesting preferential activation of DNA repair instead of cell death programs after environmentally induced genetic alterations.
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PMID:Molecular pathobiology of thyroid neoplasms. 1266 46

Radioodine-131 has an important place in the management of well-differentiated thyroid cancer. Patient preparation for radioiodine-131 administration must be rigorous and is based on the stimulation of endogenous TSH production, which requires a hypothyroid state after withdrawal of suppressive T4-therapy. The introduction of recombinant human TSH would simplify the protocol of preparation and improve the quality of life of patients. The diagnosis place of radioiodine-131 knew significant changes following the introduction of the serum thyroglobulin measurement. This tumour marker has a central role in the strategy of follow-up and tends to be the principal element of indication for a diagnosis exploration with radioidine-131. The systematic ablation of thyroid remnants remains controversial particularly in patients with good prognosis factors; the efficacy of low activities is also still debatable. The optimal follow-up strategy and the indication of remnant ablation must take in account the prognosis factors of survival and recurrence. Radioiodine-131 therapy permits frequently the cure of distant metastases, particularly in infraradiological pulmonary forms. This fact outlines the importance of an early detection of tumour recurrence based on the conjunction of radioiodine-131 and thyroglobulin. Side effects of radioiodine-131 therapy are generally limited if the precautionary measures are well applied; leukaemia constitutes the main risk but this complication is very uncommon and occurs after a high cumulative activity.
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PMID:[Role of iodine-131 in the management of differentiated thyroid cancers (vesicular origin)]. 1270 21

Exposure to ionizing radiation is a well-known risk factor for a number of human cancers, including leukemia, thyroid cancer, soft tissue sarcomas, and many others. Although it has been known for a long time that radiation exposure to the cell results in extensive DNA damage, including double strand DNA breaks, the exact mechanisms of radiation-induced carcinogenesis remain unknown. Recently, a large increase in incidence of thyroid cancer was observed in children exposed to radiation after the Chernobyl nuclear accident. A high prevalence of chromosomal rearrangements involving the RET gene was found among these radiation-induced thyroid tumors. As a result of such rearrangement, a portion of the RET gene is fused with another gene, typically with the H4 or ELE1 . However, since the DNA targets of ionizing radiation are randomly distributed throughout the cell nucleus, the reason for predilection for the RET rearrangements in thyroid cells was unclear.
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PMID:Spatial positioning of RET and H4 following radiation exposure leads to tumor development. 1280 63


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