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)

Follow-up surveys of patients with ovarian cancer revealed an increased risk of second primary cancers of the uterine corpus, colon, bladder, breast, and hematopoietic system. The excess risk or uterine corpus cancer was independent of therapy. The risk of colon cancer was increased in all treatment groups but was especially high among patients receiving radiation or chemotherapy. The predisposition to other neoplasms was limited to certain treatment groups: bladder cancer to irradiation, leukemia to chemotherapy, and lymphoma to either modality. The pattern of second neoplasms following ovarian cancer appears to be influenced by therapy as well as by common etiologic factors.
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PMID:Second primary neoplasms following ovarian cancer. 28 Jul 6

We compared age-adjusted mortality rates for cancer of selected sites for Chinese, Japanese, and native Indian residents of British Columbia during the years 1964-73 to the corresponding rates for the white population. Mortality from all cancers of the Chinese did not differ significantly from that of whites. Elevated rates are seen for cancer of the nasopharynx in both sexes, of the liver and esophagus in males, and of the lung in females. Chinese males had a lower mortality than whites from stomach, prostate, and bladder cancer and brain tumors, whereas females had a lower mortality from tumors of the colon, breast, and ovary; both sexes had a lower mortality from leukemia. For Japanese males and females, the mortality rates for all cancers combined were similar to those of the white population. The rates for cancer of the stomach and gallbladder were higher in both sexes; males also showed a higher rate of liver cancer. Prostate and breast cancer mortality rates were lower. Native Indian males had a lower mortality rate from all cancers combined; the difference was significant for stomach, colon, lung, and prostate cancers, and for leukemia. Native Indian females showed a lower rate for ovarian cancer and a higher rate of tumors of the gallbladder and uterine cervix, but their overall cancer mortality was similar to that of whites.
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PMID:Cancer mortality among Chinese, Japanese, and Indians in British Columbia, 1964-73. 53 37

Occupational causes of cancer are difficult to establish because of the long latency period and difficulty in identifying occupational linkages. This study provides a regional analysis of cancer incidence and mortality as a method of identifying localizing factors in cancer that can be followed by more specific epidemiologic investigation. In this study we analyze the regional standardized mortality ratios (SMRs) for site-specific cancers, by age, sex and continent of birth for the years 1983-86, for the Jewish population of Israel. Elevated total malignant and benign neoplasm SMRs were found in Acre (SMR 109, P < 0.05), Haifa (104, P < 0.05) and Tel Aviv (107, P < 0.001). The only other statistically significantly elevated SMRs were found in Acre for lung cancer (133, P < 0.05) and leukemia (171, P < 0.05). Age and sex-standardized incidence ratios (SIRs) by regions are also presented for the years 1980-81 for the Jewish population. Haifa had elevated SIRs for colorectal cancer (126, P < 0.001), breast cancer (118, P < 0.01) and lymphomas (126, P < 0.05). Elevated lung cancer SIRs were found in both Acre (145, P < 0.05) and Ramla (143, P < 0.05). Male to female incidence ratios (MFIRs) for ages 30+ for the Israeli Jewish population are also presented. Elevated bladder cancer MFIRs were found in the heavily industrialized Haifa region (7.69 vs. 4.62 P < 0.05). For Ramla residents, bladder and oronasopharyngeal cancer MFIRs were approximately three times the national average (not statistically significant). Ramla also had elevated MFIRs for lung cancer (14.9 vs. 3.4 nationally, P < 0.01), as did Acre (7.6 vs. 3.4 nationally, P = 0.06). These elevated MFIRs are suggestive of occupational exposure from the cement and asbestos factories in the Ramla and Acre regions. Regional analyses of cancer mortality and cancer incidence (using SMRs, SIRs and MFIRs) can serve as a basic tool for identifying sentinel markers of excess rates. Our findings indicate regions where we should undertake case-referent studies in order to identify potential risk factors and where to target possible preventive programs.
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PMID:Regional differences in cancer incidence and mortality in Israel: possible leads to occupational causes. 142 7

Epidemiologic studies of occupational groups have been central to the identification of human carcinogens. The incorporation of a biochemical component into occupational studies of cancer can expand the possibilities for identifying human carcinogens and for understanding the disease process. Two epidemiologic studies of occupation and cancer which include evaluation of biomarkers are described. The association of acetylator phenotype with bladder cancer risk was studied in benzidine-exposed workers. The association of benzene-related leukopenia with leukemia is being studied in benzene-exposed workers. These investigations illustrate issues in the use of biomarkers in epidemiologic studies of cancer risk. Such studies require the identification and characterization of the population at risk. Disease susceptibility factors are amenable for inclusion in these studies and can be statistically modeled as exposure-effect modifiers. Biomarkers of exposure are mainly of importance in short-term longitudinal and cross-sectional studies of exposure and intermediate outcomes and for validation of other data sources. Several sources of error can affect the results of molecular epidemiologic studies. Aside from minimizing laboratory error, consideration must be given in the design and execution of these studies to potential problems in subject selection and field collection of biologic samples and other relevant data.
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PMID:Biomarkers in occupational cancer epidemiology: considerations in study design. 148 44

Cancer has been the leading cause of deaths since 1981 in Japan and is still on the increase accounting for 27% of all causes of deaths in 1989. The crude death rate of cancer has been increasing in both sexes, but the age-adjusted death rate has been stable in males and decreasing in females. Among various cancers cancers of the stomach, uterus, liver (females only), and esophagus (females only) have been decreasing. Leukemia and bladder cancer also tend to show a declining trend. Other cancers, especially cancers of the lung, colo-rectum, pancreas, biliary tract liver (males only), prostate, ovary, and breast are increasing in Japan. Trends in the cancer incidence are similar to those of cancer mortality. Causes of the marked secular trends in the cancer mortality and incidence are not clear, but the major causes are suspected to be changes in dietary habits, smoking and drinking habits, and other socio-environmental factors such as marital and reproductive factors. The five year survival rates of several cancers have been improved in the last decades. Thus, progresses in the diagnostic and therapeutic techniques and promotion of cancer screening may have also contributed to the decrease of cancer deaths. If the present trends in cancer mortality and incidence continue, cancer deaths/incidences will still increase and cancers of the lung, colo-rectum, liver (males only), pancreas, biliary tract, etc. will become major cancers in Japan in the future. To combat with ever increasing cancer it is necessary to further promote cancer research, cancer screening, programs for primary prevention of cancer, especially smoking control and improvement of dietary habits.
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PMID:Trends in cancer mortality, incidence and survival in Japan. 151 21

Cancer mortality was studied in 10,552 Swedish hyperthyroid patients treated with 131I between 1950 and 1975. The patients were matched with the Swedish Cause-of-Death Register and the cases of 977 patients who died from cancer or leukemia were studied. The patients had been followed up for an average of 15 years (range 0 to 35 years), and the overall standardized mortality ratio (SMR) was 1.09 [95% confidence interval (CI) = 1.03 to 1.16], with a higher risk for women. The highest mortality was seen during the first year after exposure (SMR = 1.15) and decreased for the following 9 years (SMR = 1.04). The risk of dying from a cancer in the digestive tract and respiratory organs was significantly elevated more than 10 years after exposure, as was the overall cancer mortality (SMR = 1.14). No increased risk was seen for leukemia, bladder cancer or breast cancer. Younger patients and those receiving 131I at higher activity had higher SMRs than older patients and those receiving lower activity. Patients with toxic nodular goiter had higher risk than those with Graves' disease. The lack of increasing mortality over time and with increasing activity of 131I administered argues against a carcinogenic effect of 131I. However, in the case of cancers of the stomach, the 131I exposure could have contributed to the excess mortality from these cancers.
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PMID:Cancer mortality after iodine-131 therapy for hyperthyroidism. 155 88

There have been a series of reports on the association of a genetic polymorphism at the cytochrome P450 CYP2D6 gene locus with cancer susceptibility. Many of these reports have remained contradictory either because of small numbers of patients studied or because of the limitations and controversy surrounding the pharmacokinetic assay used to identify affected individuals (poor metabolizers; PMs). We have recently developed a DNA-based assay that will allow the unequivocal identification of poor metabolizers and have applied this to the study of 1635 patients with different forms of cancer. Out of 361 lung cancer patients studied no statistically significant change in the proportion of PMs relative to controls was found. However, a significant increase in the proportion of poor metabolizers or heterozygotes was seen in leukaemia, bladder cancer and melanoma patients. This could be explained by a role for CYP2D6 in carcinogen detoxification or by linkage to another cancer-causing gene.
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PMID:Relationship between the debrisoquine hydroxylase polymorphism and cancer susceptibility. 160 Jun 8

I-131 was administered to 298 patients with thyroid cancer, and there has been a follow-up of at least two years. Follow-up periods were: 2.5 to 30 years (median 14.5) in living patients, 2.5 to 15 years (median 5.5) in patients dead of tumour greater than or equal to 2 years after first treatment and 2.5 to 23 years (median nine) in patients dead without tumour. Person-years at risk were (total applied activity of I-131): 1119 (3 to 21 GBq), 1477 (22 to 65 GBq), 521 (61 to 170 GBq). 33 subsequent malignancies in 31 patients were observed, compared to an expected number of 17. The relative risk of subsequent malignancies is therefore 1.94 with a 95% confidence interval of 1.15 to 3.05. This increase in the incidence of subsequent malignancies after I-131 treatment is largely due to the significantly increased incidence of leukemia and bladder cancer. Estimated radiation doses to the bone marrow in the patients with leukemia were 301 cGy to 792 cGy and the doses to the bladder in patients with bladder cancer were 2250 cGy to 10, 350 cGy. After a total activity of less than 37 GBq I-131, no cases of bladder cancer or leukemia were observed. The observed number of subsequent malignancies are compared with the expected number according to several dose-effect estimations.
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PMID:Subsequent malignancies in patients treated with 131-iodine for thyroid cancer. 162 Dec 12

The effect of calcium antagonist verapamil on the uptake and efflux of Etoposide (VP16), a semi-synthetic derivative of podophylotoxin and a broad spectrum antineoplastic agent, has been investigated and compared in sensitive (UM-UC-2) and resistant (UM-UC-9) human bladder cancer cells, and L1210 leukemia cells, by using both radioisotope (3[H]-VP16) liquid scintillation and high performance liquid chromatography assay with electrochemical detection. The uptake of VP16 was rapid in all three cell lines, showing an initial rapid linear phase followed by a second slower phase, but at steady state the ratios of intracellular to extracellular VP16 concentrations were only 0.004-0.006. No significant difference in drug uptake was observed in sensitive UM-UC-2 and resistant UM-UC-9 cells at all concentrations studied. Verapamil at a concentration of 10 microM enhanced the intracellular VP-16 levels in all sensitive and resistant cell lines. The increments were 21.5% for UM-UC-2, 11.8% for UM-UC-9, and 31.0% for L1210 cells after 30 minutes incubation with 1 microM VP16. A slower efflux of VP16 was observed in verapamil treated cells in all three cell lines. There was a small increase in the nonexchangeable components in verapamil treated cells, although only 5-10% of VP16 was retained. No peak other than that of VP16 was detected in the HPLC chromatogram of extracts from both cell pellet and influx or efflux medium.
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PMID:Effect of verapamil on the uptake and efflux of etoposide (VP16) in both sensitive and resistant cancer cells. 175 30

The rubber industry, acknowledged by the International Agency for Research on Cancer (IARC) to be a cancer risk technology is, because of difficulty in identifying causal factors, the subject of intensive epidemiological studies in many countries. In the presented study, cancer risk in the rubber industry was evaluated on the basis of long-term observation (1945-1985) of a cohort of 6978 male workers employed in a rubber goods factory, predominantly engaged in producing rubber footwear. The reference group was the general male population of Poland. Standardized mortality ratios (SMRs), calculated by means of the person-years method, were used in the evaluation of death risk. The observation of a whole cohort indicated an excess of cancer, in general (approx 12%), lung cancer (approx 40%) and gallbladder cancer (approx fourfold). In the subcohorts, distinguished according to peculiarities of individual production sections, cancer risk of the large intestine and larynx was significantly increased. The highest cancer risk was found in compounding, mixing, milling and vulcanizing sections. Hence, beta-naphthylamine, benzidine and solvents (benzene) were used in technological processes in the past, bladder cancer and leukemia were considered as most specific for the rubber industry. In the cohort observed, the risk of death from bladder cancer was significantly increased only in those who had been employed during the years 1945-1953, namely during the period when beta-naphthylamine was in use. No excess of deaths from leukemia was observed.
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PMID:Cancer mortality among male workers in the Polish rubber industry. 179 40


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