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)

Radiotherapy and chemotherapy can effectively control cancer but can also cause new cancers to develop as long-term complications. Almost all types of cancer have been associated with radiotherapy. The breast, thyroid, and bone marrow are the organs most susceptible to radiation carcinogenesis. The bone marrow is also most frequently involved by chemotherapy and the leukemia risk is much higher than after radiotherapy. The combination of intensive radiotherapy and chemotherapy is particularly leukemogenic. The latent period between radiotherapy/chemotherapy and the appearance of a second primary cancer ranges from a few years to several decades. The risk for a second primary cancer following radiotherapy or chemotherapy emphasizes the need for life long follow-up of patients receiving such treatments. This is particularly the case in individuals with long life expectancy, for example, patients treated for childhood neoplasms. The benefits of radiotherapy and chemotherapy in oncology exceed the risks for second primary cancers. Efforts should be directed towards identifying those patients who will benefit from the treatments so that only they are exposed to the risk.
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PMID:Cancer occurring after radiotherapy and chemotherapy. 225 29

The present study, the ninth in a series that began in 1961, extends the time of surveillance 3 more years and covers the period 1950-1985. It is based on the recently revised doses, termed the DS86. The impact of the change from the T65D to the DS86 on the dose-response relationships for cancer mortality was described in the first of this series of reports. Here, the focus is on cancer mortality among the 76,000 A-bomb survivors within the LSS sample for whom DS86 doses have been estimated, with the emphasis on biological issues associated with radiation carcinogenesis. Briefly, the following is found: The excess in leukemia mortality has continued to decline with time, but remains slightly but significantly elevated in 1981-1985 in Hiroshima. For cancers other than leukemia, as a group, excess deaths continue to increase over time in direct proportion to the normal increase in natural cancer mortality with increasing age, and the relative risk seems unchanged over time within age ATB cohorts. The single exception is the cohort under 10 years of age ATB. Within this group of survivors, where the relative risk, although based on relatively few deaths, has been quite high at the higher doses, as judged by deaths before the age of 30, the risk has fallen and has remained fairly constant at a lower level thereafter. Thus the present analysis still supports, in the main, estimation of lifetime risk based on the assumption of a constant relative risk. For the same age ATD, both the relative and absolute risks are higher for younger age ATB cohorts than older ones for cancers other than leukemia. There is no statistically significant difference in excess deaths between males and females except for leukemia, though the relative risk is higher for females than for males, significantly so for cancers of the esophagus and lung, reflecting the higher background cancer rate for males. Significant dose responses are observed for leukemia, cancers of the esophagus, stomach, colon, lung, breast, ovary, and urinary bladder and multiple myeloma, as previously observed. No significant increase is demonstrable as yet for cancers of the rectum, gallbladder, pancreas, uterus, and prostate and malignant lymphoma. In the present report, cancers of the bone, pharynx, nose, and larynx, and skin except melanoma are also examined, but none of these sites show a significant increase with dose.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Studies of the mortality of A-bomb survivors. 9. Mortality, 1950-1985: Part 2. Cancer mortality based on the recently revised doses (DS86). 230 30

The mass screening of lung cancer has been started with financial support of the Japanese Government from 1987. It should be emphasized, however, that mass screening programs of any kind have to be evaluated by means of benefit-risk analysis and cost-effectiveness analysis. This is the first report on the benefit-risk analysis for mass screening program of lung cancer in Japan. The benefit of the lung cancer mass screening is defined as a net elongation of average life expectancy due to early detection of the cancer. It is calculated as a function of age and sex. While, the risk of the screening program is defined as a net shortage of average life expectancy due to radiation carcinogenesis of leukemia and lung cancer. In the case of radiation carcinogenesis, latent time and plateau period are considered in the calculation of the risk. Since the benefit increases with age and the risk decreases with age for both sexes, one can obtain a certain age at which the benefit and the risk cross. Assuming dose equivalent of lung of 1 mSv and risk coefficient of 15.1 X 10(-3) Sv-1, the crossing ages of men and women are about 42 y.o. and 47 y.o. respectively. We consider that these ages are rather high when chest radiograph is to be used as a screening test. It is recommended that the dose equivalent of lung should be lowered to 0.1 mSv if the mass screening of lung cancer is to be performed.
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PMID:[Benefit-risk analysis of mass screening for lung cancer]. 236 90

A role for specific recombination events at the env region of endogenous murine leukemia virus (MuLV) sequences in radiation carcinogenesis in C57BL mice has been suggested by a number of studies. We characterized env-related cell surface antigens from a primary, x-ray--induced, and several transplanted C57BL/6 thymomas of viral and radiation etiologies by immunoprecipitation and two-dimensional peptide mapping. DNA from lymphoma cells was also analyzed by Southern blotting for evidence of mink cell focus-forming (MCF) type env recombination events. Although gp70 molecules with novel structural determinants were found on all transplanted lymphomas examined, expression of novel env antigens was variable among these lymphomas, and there was a lack of correlation of characteristic MCF-type env recombination events in endogenous retrovirus DNA sequences with novel env antigens on lymphoma cell surfaces. Neither novel gp70 antigens nor MCF-type env provirus recombinant structures were consistent features of the C57BL/6 thymomas of radiation etiology examined in this study, even though MCF-type env recombination events have been suggested as etiologically significant in MuLV-mediated lymphomagenesis in both RadLV and x-ray--induced tumors in C57BL/6 mice.
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PMID:Characterization of env gene recombination in x-ray--induced thymomas of C57BL/6 mice. 267 2

Studies in the 1980s of medically irradiated populations have increased our knowledge of radiation carcinogenesis. (1) Investigations of prenatal x-ray exposures, especially in twins, provide evidence that very low doses of ionizing radiation may cause cancer in humans. (2) Fractionated doses appear as effective as single exposures of the same total dose in causing breast cancer, but seem less effective for lung cancer. (3) Excess breast cancers can occur among women exposed under age 10, indicating that the immature breast is susceptible to the carcinogenic action of radiation. (4) Moderate doses on the order of 1 Gy to the brains of children can cause tumors later in life; moderately high doses to the skin can cause cancer when followed by frequent exposure to ultraviolet light. (5) Radiotherapy for cervical cancer can increase the rate of subsequent leukemia with the best fitting dose-response functions including a negative exponential term to account for cell-killing. (6) Low-dose exposures of about 10 cGy may increase the risk of thyroid cancer. (7) Second cancers following radiotherapy for a variety of cancers occur primarily among long-term survivors. (8) Radiotherapy may not significantly increase the risk of leukemia following childhood cancer, whereas chemotherapy with alkylating agents is a major risk factor. (9) Bone cancer occurs after high-dose radiotherapy for childhood cancer, but children with retinoblastoma are not more susceptible to radiation-induced disease than children with other malignancies. (10) High-dose external beam therapy can cause thyroid cancer, whereas high-dose radioactive 131I may not. (11) Studies of cervical cancer patients indicate that the risk of radiation-induced second malignancies follows a time-response model consistent with a constant multiplication of the underlying background incidence, i.e. a relative risk model seems to hold for projecting risks forward in time.
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PMID:Carcinogenesis--a synopsis of human experience with external exposure in medicine. 304 57

Cancer induction is generally considered to be the most important somatic effect of low doses of ionizing radiation. It is therefore of great concern to assess the quantitative cancer risk of exposure to radiations of different quality and to obtain information on the dose-response relationships for carcinogenesis. Tissues in the human with a high sensitivity for cancer induction include the bone marrow, the lung, the thyroid and the breast in women. If the revised dosimetry estimates for the Japanese survivors of the atomic bomb explosions are correct, there is no useful data base left to derive r.b.e. values for human carcinogenesis. As a consequence, it will be necessary to rely on results obtained in biological systems, including experimental animals, for these estimates. With respect to radiation protection, the following aspects of experimental studies on radiation carcinogenesis are of relevance: Assessment of the nature of dose-response relationships. Determination of the relative biological effectiveness of radiations of different quality. Effects of fractionation or protraction of the dose on tumour development. For the analysis of tumour data in animals, specific approaches have to be applied which correct for competing risks. These methods include actuarial estimates, non-parametric models and analytical models. The dose-response curves for radiation-induced cancers in different tissues vary in shape. This is exemplified by studies on myeloid leukaemia in mice and mammary neoplasms in different rat strains. The results on radiation carcinogenesis in animal models clearly indicate that the highest r.b.e. values are observed for neutrons with energies between 0.5 and 1 MeV. On the basis of such results it might be concluded that the maximum quality factor of 10 for neutrons should be increased. Based on current evidence, an increase by a factor of 2 to 3 seems more realistic than a tenfold rise. The diversity of dose-response relationships point to different mechanisms involved in the induction of different tumours in various species and even in different strains of the same species.
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PMID:Radiation carcinogenesis in experimental animals and its implications for radiation protection. 389 67

Late somatic effects of ionizing radiation can be divided into non-stochastic effects with relatively high threshold doses (cataract, fertility problems, chronic radiodermatitis, and radiogenic skin cancer) and non-threshold stochastic effects. Theoretical and epidemiologic aspects of radiocarcinogenesis and various clinical types of radiation-induced neoplasms (leukemia, thyroid cancer, breast cancer) and genetic effects are discussed with special reference to radiation protection measures.
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PMID:[Dermatologic roentgen therapy and radiocarcinogenesis]. 709 82

Several generalizations about radiation carcinogenesis can be made: 1) a single exposure is sufficient to elevate cancer incidence many years later: 2) radiation-induced cancer cannot be distinguished from naturally occurring cancer, i.e., there is not unique radiogenic cancer; 3) all cancers appear to be increased after irradiation with the exception of chronic lymphocytic leukemia, and possibly Hodgkin's disease, cervical cancer, and a few others; 4) the breast, thyroid, and bone marrow appear especially radiosensitive; 5) leukemia is the most prominent radiogenic tumor and shows a wave-like pattern of excess incidence over time, and the excess begins within two to four years, peaks about six to eight years, and decreases to normal levels about 25 years later; 6) solid tumors have a minimum latent period of about ten years, and for several cancers, the temporal pattern of incidence appears to follow the natural incidence, i.e., the cancers do not occur before the ages normally associated with increased incidence, implying that age-dependent factors influence the expression of disease; 7) age at exposure is perhaps the most important host factor influencing subsequent cancer risk; 8) the percentage increase in cancer incidence per rad is not the same for all cancers, i.e., some cancer of high natural incidence, e.g., colon, have low "relative risks" and some cancers of low natural incidence, e.g., thyroid, have high "relative risks;" 9) dose-effect curves are often linear, but curvilinearity is also observed and is possibly associated with the need for "two ionizing events" for transformation to occur at low doses, the influence of cell sterilization at moderate doses, the likelihood of "wasted" dose at high doses, and/or the influence of factors that effect the expression of disease.
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PMID:Cancer following medical irradiation. 723 65

In view of the elevated risk of leukemia among A-bomb survivors, genetic alterations associated with Leukemia can be considered to have been induced by ionizing radiation. Therefore, to clarify this possibility, an examination was made to see whether genetic changes such as BCR-ABL translocation closely associated with chronic myelogenous leukemia (CML) are actually induced by radiation. BCR-ABL translocation is easily detected by means of reverse transcription polymerase chain reaction. One hundred million cells of the promyelocytic leukemia-derived cell line HL60, which do not have such a gene rearrangement, were irradiated with 100 Gy of X-ray, after which RNA was extracted and examined for any rearrangements of BCR and ABL genes. Five kinds of bands were observed in the HL60 cells irradiated with 100 Gy of X-ray, and it became clear that these positive bands contain both BCR gene and ABL gene by the direct sequencing method. Furthermore, these gene rearrangements included not only the rearrangements specifically identified with CML but also atypical rearrangements which are not generally observed clinically. The induction by X-irradiation of such gene changes characteristic of malignant tumors, which are closely associated with radiation carcinogenesis, suggests that they are the initial gene changes in radiation carcinogenesis.
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PMID:[Gene rearrangement and radiation carcinogenesis]. 802 92

There has been no documented increase in childhood leukaemia following the Chernobyl accident. However, different forms of childhood leukaemia may not be equally susceptible to radiation carcinogenesis. Infant leukaemia is a distinct form associated with a specific genetic abnormality. Outside the former Soviet Union, contamination resulting from the Chernobyl accident has been highest in Greece and Austria and high also in the Scandinavian countries. All childhood leukaemia cases diagnosed throughout Greece since 1 January 1980 have been recorded. Here we report that infants exposed in utero to ionizing radiation from the Chernobyl accident had 2.6 times the incidence of leukaemia compared to unexposed children (95% confidence interval, 1.4 to 5.1; P approximately 0.003), and those born to mothers residing in regions with high radioactive fallout were at higher risk of developing infant leukaemia. No significant difference in leukaemia incidence was found among children aged 12 to 47 months. Preconceptional irradiation had no demonstrable effect on leukaemia risk at any of the studied age groups.
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PMID:Infant leukaemia after in utero exposure to radiation from Chernobyl. 915 87


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