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)

Cancer mortality in relation to radiation dose was evaluated among 4153 women treated with intrauterine radium (226Ra) capsules for benign gynecologic bleeding disorders between 1925 and 1965. Average follow up was 26.5 years (maximum = 59.9 years). Overall, 2763 deaths were observed versus 2687 expected based on U.S. mortality rates [standardized mortality ratio (SMR) = 1.03]. Deaths due to cancer, however, were increased (SMR = 1.30), especially cancers of organs close to the radiation source. For organs receiving greater than 5 Gy, excess mortality of 100 to 110% was noted for cancers of the uterus and bladder 10 or more years following irradiation, while a deficit was seen for cancer of the cervix, one of the few malignancies not previously shown to be caused by ionizing radiation. Part of the excess of uterine cancer, however, may have been due to the underlying gynecologic disorders being treated. Among cancers of organs receiving average or local doses of 1 to 4 Gy, excesses of 30 to 100% were found for leukemia and cancers of the colon and genital organs other than uterus; no excess was seen for rectal or bone cancer. Among organs typically receiving 0.1 to 0.3 Gy, a deficit was recorded for cancers of the liver, gall bladder, and bile ducts combined, death due to stomach cancer occurred at close to the expected rate, a 30% excess was noted for kidney cancer (based on eight deaths), and there was a 60% excess of pancreatic cancer among 10-year survivors, but little evidence of dose-response. Estimates of the excess relative risk per Gray were 0.006 for uterus, 0.4 for other genital organs, 0.5 for colon, 0.2 for bladder, and 1.9 for leukemia. Contrary to findings for other populations treated by pelvic irradiation, a deficit of breast cancer was not observed (SMR = 1.0). Dose to the ovaries (median, 2.3 Gy) may have been insufficient to protect against breast cancer. For organs receiving greater than 1 Gy, cancer mortality remained elevated for more than 30 years, supporting the notion that radiation damage persists for many years after exposure.
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PMID:Cancer mortality following radium treatment for uterine bleeding. 221 30

A mortality study was carried out on 595 workers who were compensated for silicosis in the Latium region, Italy, during the period 1946-84 who died between 1 January 1969 and 31 December 1984. Respiratory disorders, tuberculosis, lung cancer, bone cancer, and cirrhosis of the liver showed significantly increased risk ratios (4.1, 3.7, 1.5, 4.1, and 1.9 respectively); excesses of brain cancer and leukaemia did not reach statistical significance. Lung cancer mortality was further analysed by age, period of compensation, final degree of disability, and occupational activity. The possible confounding role of smoking was assessed by comparing the lifetime smoking habits of a sample of silicotic subjects with those of the general male population as estimated by a national health survey; the prevalence of ever smokers among silicotic subjects (70.7%) was similar to that estimated for the general population (68.5%). The present study indicates that silicosis is associated with lung cancer even though it does not clarify the respective roles of exposure to silica and silicosis.
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PMID:Mortality pattern of silicotic subjects in the Latium region, Italy. 261 Nov 62

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

Recently, the National Cancer Institute published a comprehensive monograph on multiple primary cancers in Connecticut and Denmark. This paper summarizes some of the observations made on the Connecticut population. Data compiled by the Connecticut Tumor Registry have extended our knowledge about the patterns of multiple primary cancers, especially among long-term survivors of cancer and among patients with relatively rare tumors about which little information currently exists. When compared with the general Connecticut population, cancer patients had a 31 percent (RR = 1.31) increased risk of developing a second cancer and a 23 percent (RR = 1.23) elevated risk of second cancer at a different site from the first. Common environmental exposures seemed responsible for the excess occurrence of many second cancers, particularly those related to cigarette smoking, alcohol consumption, or both. For example, persons with epithelial cancers of the lung, larynx, esophagus, buccal cavity, and pharynx were particularly prone to develop new cancers in the same or contiguous tissue throughout their lifetimes. Cancers of the colon, uterine corpus, breast, and ovary frequently occurred together, suggesting underlying hormonal or dietary influences. Only patients with prostate cancer were at significantly low risk for second cancer development; this might be an artifact of case finding, since advanced age at initial diagnosis was generally associated with an underascertainment of second cancers. Radiotherapy may have caused rectal and other cancer among patients with cancers of the female genital tract, and leukemia among patients with uterine corpus cancer. Chemotherapy with alkylating agents probably contributed to the excess of acute nonlymphocytic leukemia following multiple myeloma or cancers of the breast and ovary. Genetic susceptibility seemed to explain some tumor complexes, such as the multiple occurrences of cutaneous melanoma and the excess of bone cancer following retinoblastoma. Research into multiple cancer syndromes should enhance our understanding of carcinogenic factors and mechanisms and the development of strategies for cancer prevention and control.
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PMID:Multiple primary cancers in Connecticut, 1935-82. 354 9

Cancer mortality was compared between a three-county region in southwestern Utah and the remainder of Utah in an investigation of reported excess cancer risks associated with residence in southwestern Utah during the period of above-ground nuclear tests at the Nevada Test Site. Because most of the fallout in southwestern Utah was deposited during 1953-1957, comparisons were limited to persons born before 1958, and deaths from leukemia and bone cancer during 1955-1980 and from other cancers during 1964-1980. There was no excess risk of cancer mortality in southwestern Utah, for single or grouped sites, with the single exception of leukemia which showed statistically significant odds ratios of 1.45 based on 62 deaths at all ages, and 2.84 based on nine deaths at ages 0-14. The finding for childhood leukemia was based on different time periods and geographic comparisons from those of two earlier studies in which no such excess was found. Mortality from all cancer sites combined was significantly lower in southwestern Utah than in the remainder of the state, even after adjustment for the higher proportion of (lower risk) Mormons in southwestern Utah. The present results, including the positive association for leukemia, are inconsistent with the high excess risks reported by Johnson (JAMA 1984;251:230-6) based on an interview survey of cancer incidence among long-term Mormon residents of southwestern Utah.
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PMID:Cancer mortality and radioactive fallout in southwestern Utah. 378 54

Several recent studies (animal and human) have suggested an association between lung cancer and silica exposure. To test the hypothesis, we have studied death benefit records of 1,905 members of the Granite Cutters Union. A proportionate mortality analysis (PMR) was conducted, using U.S. deaths as a comparison population. Statistically (PMR) was conducted, using U.S. deaths as a comparison population. Statistically significant excesses were observed for death from nonmalignant respiratory significant excesses were observed for death from nonmalignant respiratory disease (largely silicosis) (183 obs, 43.7 exp) and for tuberculosis (largely silicotuberculosis) (262 obs, 19.3 exp). Other significant excesses were observed for bone cancer (6 obs, 1.9 exp) and arthritis (5 obs, 1.5 exp). A significant decrease was observed for leukemia (5 obs, 13.0 exp). For lung cancer a slight but nonsignificant excess was observed (97 obs, 81.1 exp, PMR = 1.19, 95% CI 0.97-1.46). A proportionate cancer mortality analysis (PCMR) showed similar results for lung cancer (PCMR = 1.09, 95% CI 0.89-1.33). Lung cancer mortality also failed to show any trend with either calendar time or duration of exposure. Although no significant excess of lung cancer was observed for the entire silica-exposed cohort, there was an indication that those who were silicotic had an excess risk of lung cancer, based on a review of contributing causes on the death certificate.
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PMID:A proportionate mortality study of granite cutters. 396

Exposures in southwestern Utah to radioactive fallout (1951 through 1962) from atmospheric nuclear detonations at the Nevada Test Site (NTS) were followed by smaller exposures (1962 through 1979) from venting of underground nuclear detonations. The cancer incidence in a 1951 cohort (4, 125) of Mormon families in southwestern Utah near the NTS was compared with that of all Utah Mormons (1967 through 1975). There were 109 more cases of cancer than expected (288[observed]/179[expected]). Leukemia was most prominent early (1958 through 1966), with 19 cases, five times more than expected (3.6). The excess of leukemia persisted into the later period (1972 through 1980), with 12 cases observed, 3.4 expected. There was an increase in lymphoma. Excess cases of thyroid cancer appeared early and a notable excess appeared later (14/1.7). An excess of breast cancer was noted later (27/14). There were more cancers of the gastrointestinal tract than expected. There was an excess of melanoma (12/4.5), bone cancer (8/0.7), and brain tumors (9/3.9). A subgroup with history of acute fallout effects had a higher cancer incidence. That these cases can be associated with radiation exposures is supported by a comparison between groups of the ratio of cancers of more radiosensitive organs with all other types of cancer.
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PMID:Cancer incidence in an area of radioactive fallout downwind from the Nevada Test Site. 669 Jul 81

Mortality is described in a cohort of 18,869 white males who were employed between 1943 and 1947 at a uranium conversion and enrichment plant in Oak Ridge, Tenn. Workers in certain departments (especially chemical workers) were exposed to high average air levels of uranium dust. Based on deaths reported in 1974 by the Social Security Administration (SSA) and using mortality rates for U.S. white males, standardized mortality ratios (SMRs) for various causes in the entire cohort were generally less than 1.00. After correction for unascertained deaths and missing death certificates, the SMR for lung cancer was 1.22 (95% confidence limits, 1.10 and 1.36). SMRs for various causes, including lung cancer, did not tend to be higher in 8,345 workers employed in areas where uranium dust was present or in 4,008 of these 8,345 workers employed for one year or longer at the plant. Other causes of particular interest (i.e., bone cancer, leukemia, diseases of respiratory and genitourinary systems) did not exhibit high SMRs. The suggestive finding of the authors was an increased number of lung cancer deaths in a group of chemical workers hired at greater than or equal to 45 years of age. Continued follow-up of the cohort is necessary for further evaluation of the long-term health effects of exposure to uranium.
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PMID:Mortality among men employed between 1943 and 1947 at a uranium-processing plant. 698 20

The occurrence of soft-tissue tumors in beagles given 90Sr (88 dogs), 228Ra (76 dogs), or 228Th (81 dogs) as young adults and followed throughout their lifespans was compared with that of 133 control beagles given no radioactivity. For animals injected with 228Ra, tumors of the eye were more prominent (p < 0.05) than in the controls, and soft-tissue tumors of cavities in the head (excluding the brain, mouth, and eye) were more prominent in dogs given 90Sr than in the controls (p < 0.05). There was some indication that eye tumors in animals given about 0.56 kBq 228Th kg-1 were associated with their radionuclide exposure. For tumors at a few other locations, the relative occurrence was greater (p < 0.05) in the controls. These included malignant tumors of the testis and malignant plus benign tumors of the mammae and vagina in 228Th dogs; both malignant and malignant plus benign tumors of the mouth and testis, and malignant plus benign tumors of the mammae and vagina in 228Ra dogs; and malignant plus benign tumors of the mammae in 90Sr dogs (p > 0.05 by Odds Ratio Chi Square analysis but p < 0.05 by Fisher's Exact Test). Differences in relative occurrence between radioactive dogs and controls of all other tumor types that appeared in any of the animals (notably lymphosarcoma, lymph node tumors, leukemia, mast cell tumors, liver tumors, etc.) were not statistically significant (p > 0.05). Intercurrent mortality, mainly from bone cancer, was higher in the radioactive dogs than in the controls. Mean survival was reduced in the dogs given 90Sr, 228Ra, or 228Th (13.17 +/- 2.64 y in controls, 10.95 +/- 4.06 y in 90Sr dogs, 9.07 +/- 3.61 y in 228Ra dogs, and 9.20 +/- 4.15 y in 228Th dogs). Attenuated lifespans could account, at least in part, for the relative paucity of soft-tissue tumors not induced by radiation among the groups of dogs given radioactivity and occurring near the end of life for control animals.
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PMID:Soft tissue tumors among beagles injected with 90Sr, 228Ra, OR 228Th. 762 76

The cause-specific mortality (1940-1993) of 2,985 male workers employed in three oil refineries was examined using a proportionate mortality study design. Separate analyses were undertaken by race, refinery, employment status (active and retired), and time since entry into the Oil, Chemical, and Atomic Workers (OCAW) union. Proportionate cancer mortality ratio (PCMR) analyses also were conducted. Proportionate mortality ratios (PMR) were significantly increased (P < 0.05) for cancers of the lip (PMR = 384), stomach (PMR = 142), unspecified sites of the liver (PMR = 238), pancreas (PMR = 151), connective tissues (PMR = 243), prostate (PMR = 135), eye (PMR = 407), brain (PMR = 181), benign and unspecified neoplasms (PMR = 289), and leukemia (PMR = 175) for the entire cohort. Significantly decreased mortality was observed for respiratory tuberculosis (PMR = 29), esophageal cancer (PMR = 45), rectal cancer (PMR = 49), and cancers of the bladder and other urinary organs (PMR = 40). Skin cancer was observed to be significantly increased (PMR = 242) for workers with less than 20 years since union initiation. Significantly increased PCMRs were seen for cancers of unspecified sites of the liver (PCMR = 205), brain (PCMR = 147), benign and unspecified neoplasms (PCMR = 243), and leukemia (PCMR = 146). Among nonwhites, an increased risk of bone cancer was observed in the PCMR analysis (PCMR = 704), although based on only two deaths. Analyses of mortality patterns for white males by refinery revealed similar patterns in each refinery as was seen in the overall cohort of refinery workers. Mortality patterns for whites and nonwhites also were similar. Additional analyses of deaths between 1960 and 1993 demonstrated increased mortality due to asbestosis (PMR = 683) and multiple myeloma (PMR = 124), although the multiple myeloma excess was not statistically significant. Ten deaths due to mesotheliomas were observed among these refinery workers.
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PMID:Proportionate mortality among union members employed at three Texas refineries. 988 51


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