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Query: UMLS:C0023418 (leukemia)
93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Risk of cancer mortality from 1973 to 1985 in persons born in the Indian subcontinent who migrated to England and Wales was analysed by ethnicity, and compared with cancer mortality in the England and Wales native population, using data from England and Wales death certificates. There were substantial highly significant raised risks in Indian ethnic migrants for cancers of the mouth and pharynx, gall bladder, and liver in each sex, larynx and thyroid in males, and oesophagus in females. There were also substantial raised risks in these migrants of each sex for non-Hodgkin's lymphoma and myeloma. For the mouth and pharynx, and liver in each sex, and gall bladder in females, there were also raised risks of lesser magnitude in British ethnic migrants. For colon and rectal cancer and cutaneous melanoma in each sex, ovarian cancer in women and bladder cancer in men, there were appreciable significantly reduced risks in the Indian ethnic migrants not shared by those of British ethnicity. Appreciable raised risks in British ethnic migrants not shared by those of Indian ethnicity occurred for nasopharyngeal cancer in males, soft tissue malignancy in both sexes and non-melanoma skin cancer in males. In migrants of both ethnicities there were appreciable significantly raised risks in each sex for leukaemia and decreased risks in each sex for gastric cancer, for lung cancer except in females of British ethnicity and in males for testicular cancer. The results suggest the need for public health measures to combat the high risks of oral and pharyngeal cancers and liver cancer in the Indian ethnic immigrant population of England and Wales, by prevention of betel quid chewing and hepatitis transmission respectively. The data also imply that early exposures or early acquired behaviours in India, or exposures during migration, may increase the risk of leukaemia and reduce the risks of gastric and testicular cancers in the migrants irrespective of their ethnicity. Aetiological studies would be worthwhile to investigate the reasons for the sizeable decreased risk of colon and rectal cancer and increased risk of gall bladder cancer in each sex and the increased risk of thyroid and laryngeal cancer in males and oesophageal cancer in females of Indian ethnicity but not of British ethnicity who have migrated from the Indian subcontinent.
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PMID:Cancer mortality in Indian and British ethnic immigrants from the Indian subcontinent to England and Wales. 757 89

Recent investigations revealed that the 9p arm and 17q arm of human chromosomes harbour tumour suppressor genes (TSGs) with an important role in multistage carcinogenesis. At the 9p arm is located the p16 (MTS1) TSG and probably others with an effect on various human tumours such as acute lymphoblastic leukaemia, bladder cancer, gliomas, malignant mesotheliomas, melanomas and non-small cell lung carcinomas. In addition, the 17q arm harbours BRCA1 TSG which is responsible for approximately 80% of the familial breast/ovarian cancer cases. In order to investigate the implication of these performed a loss of heterozygosity (LOH) analysis with 10 polymorphic microsatellite markers (three at the 17q arm surrounding the BRCA1 region and seven at the 9p arm). Fourteen of the 17 (82%) tumours exhibited deletions at 9p. The highest incidence of LOH (6/13, 46%) was found for the marker D9S157 at 9p22. One sample exhibited deletion of all the informative markers tested indicating deletion of the complete 9p arm. No homozygous deletions were found. LOH at the 17q arm near the BRCA1 locus was found in 6 (35%) among 17 specimens. The results of this study indicate that allelic deletions at 9p are frequent in the development of laryngeal tumours. The highest incidence of LOH was found for the marker D9S157 which is near, but distinct from the location of p16 (MTS1) tumour suppressor gene, indicating the presence of multiple tumour suppressor genes within this chromosomal region. In addition, BRCA1 TSG is implicated in the development of laryngeal tumours.
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PMID:Loss of heterozygosity at 9p and 17q in human laryngeal tumors. 758 72

Exposure to perchloroethylene (PCE) occurs in a number of occupational settings in which organic solvents are used, and, in particular, is widely prevalent in the dry-cleaning industry. This review summarizes the results of studies of the occurrence of the individual types of cancer in dry cleaners. Two of those cancers of greatest a priori concern (because of results in PCE-exposed experimental animals)--liver cancer and leukemia--have not occurred with increased frequency among persons employed in the dry-cleaning industry. Rates were elevated by about a factor of two for esophageal and bladder cancers, but not increased clearly for any other site. The excess mortality from esophageal cancer was well beyond the limits of chance, based on a total of 23 deaths that occurred in the two principal cohort-studies of dry cleaners. There was some indication of a particularly high risk associated with prolonged employment and a long interval since first employment. However, the possible confounding effect of the combination of cigarette smoking and heavy alcohol consumption, a very strong risk factor for the development of esophageal cancer, could be taken into account only partially in these studies. With regard to bladder cancer, the limited data available suggest that the observed increased risk could be due to exposure to other solvents than PCE used in dry cleaning. The potential influence of occupational exposure to PCE on the occurrence of esophageal and bladder cancer needs continued examination in further follow-up of existing cohorts of dry cleaners, the assembly of additional cohorts, and in large case-control studies that ascertain occupational exposures in some detail.
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PMID:Cancer in relation to occupational exposure to perchloroethylene. 761 5

Genitourinary cancers--bladders, testis and prostate--account for almost 50,000 deaths per year. Epidemiologic data suggest that individuals with low serum retinoid levels or low dietary intake of retinoid-containing foodstuffs have an increased risk of bladder and prostate cancer. Preclinical investigations show that a variety of retinoids suppress the proliferation of prostate and bladder cancer cells and induce differentiation in teratocarcinoma cells. Retinoids prevent the emergence of murine bladder and prostate cancers in carcinogen-treated animals. Clinical data are disappointing or inconclusive. A single well-conducted phase 2 trial of 13-cis retinoic acid in patients with germ cell tumors was negative. Several historically controlled as well as prospectively randomized, placebo-controlled trials of retinoids in superficial bladder cancer have failed to provide evidence of the efficacy of retinoids. Two studies of all-trans-retinoic acid in advanced prostate cancer have been negative. Despite compelling preclinical rationale, retinoids have failed to yield positive results in the clinical management of prostate, bladder or testis cancers. Further work is needed to define subsets of patients in whom retinoids might be active, and whether new retinoids or new approaches to retinoid delivery will improve the clinical usefulness of retinoids in these tumors.
Leukemia 1994
PMID:Retinoids in bladder, testis and prostate cancer: epidemiologic, pre-clinical and clinical observations. 780 25

Cytochrome P450 CYP2D6 polymorphism is an autosomal recessive trait associated with impaired debrisoquine metabolism in 5-10% of caucasian populations. This polymorphism has been associated with susceptibility to Parkinson's disease, bladder cancer, various forms of leukemia and possibly melanoma. In many other cancer forms, the data remained contradictory due to the technical limitations for identifying affected individuals (poor metabolizers). A recently developed polymerase chain reaction-based assay allows convenient screening of approximately 80% of known mutations. We have tested brain tumors correlated with chromosome 22 deviations for genetic polymorphism in the cytochrome P450 CYP2D6 locus localized on chromosome 22q13. Thirty-one meningioma samples were analyzed and the observed frequency of heterozygotes and homozygotes for the G to A mutation did not deviate significantly from the distribution in a normal population. These data are comparable to previous observations in for example breast and colon cancer and indicate that the CYP2D6 locus on chromosome 22q13 is not involved in the pathogenesis of meningiomas.
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PMID:Debrisoquine hydroxylase gene polymorphism in meningioma. 784 77

Many agents used in cancer chemotherapy are known carcinogens. However, few secondary malignancies have been definitely linked to chemotherapy, since studies on this problem are complicated by methodological problems. A causal relationship has been established between alkylating agents and leukaemia and between cyclophosphamide and bladder cancer. The risk of leukaemia peaks at 5-10 years after beginning of chemotherapy and declines steadily after its end. The interaction between chemotherapy and radiotherapy has not been fully clarified, nor has the leukaemogenic potency of individual drugs, although combinations without nitrogen mustard seem to entail a lower risk. Other tumours reported at increased incidence, in particular among Hodgkin's disease patients, for whom a carcinogenic effect of chemotherapy seems plausible, are non-Hodgkin's lymphoma and lung cancer. Other secondary solid tumors have also been reported, but for none of them an independent effect of chemotherapy has been demonstrated.
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PMID:Secondary malignancies following cancer chemotherapy. 794 33

The mortality of all 14,282 workers employed at the Sellafield plant of British Nuclear Fuels between 1947 and 1975 was studied up to the end of 1988 and cancer incidence was examined from 1971 to 1986. This updates a previous report on mortality only up to the end of 1983. Ninety-nine per cent of the workers were traced satisfactorily. Cancer mortality was 4% less than that of England and Wales [standardised mortality ratio (SMR) = 96; 95% confidence interval (CI) = 90,103] and the same as that of Cumbria (SMR = 100: Cl = 94,107). Cancer incidence was 10% less than that of England and Wales [standardised registration ratio (SRR) = 90; Cl = 83.97] and 18% less than that of Northern Region (SRR = 82; Cl = 75.88). Cancer mortality rates were significantly in excess of national rates for cancers of the pleura (nine observed, 2.6 expected; P = 0.001), thyroid (six observed, 1.8 expected; P = 0.01) and ill defined and secondary sites (53 observed, 39.2 expected; P = 0.02). There were significant deficits of cancers of the liver and gall bladder, larynx and lung. Among radiation workers there were significant positive correlations between accumulated radiation dose and mortality from cancers of ill-defined and secondary sites (10 year lag: P = 0.01) and for leukaemia (2 year lag: P = 0.009), but not for cancers of the pleura and thyroid cancer. Previous findings of such associations with multiple myeloma and bladder cancer were less strong. There was a significant excess of incident cases of cancer of the oesophagus (P = 0.01), but this was not associated with accumulated radiation dose. For cancers other than leukaemia, the dose-response risk estimates were below those of the adult atomic bomb survivors, but the 90% confidence interval included risks of zero and of 2-3 times higher. For leukaemia (12 deaths, excluding CLL), under an excess relative risk model, the risk estimate derived for the Sellafield workers was about four times higher than that for the adult atomic bomb survivors with a confidence interval ranging from a half to nearly 20 times that of the atomic bomb survivors. Overall, however, there was no excess of leukaemia among the workers compared with national rates.
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PMID:Cancer mortality and morbidity among workers at the Sellafield plant of British Nuclear Fuels. 798 Oct 83

We previously reported a strong positive association between vasectomy and the risk of prostatic cancer that arose in multiple comparisons made within data collected from 1976 to 1988 in an ongoing hospital-based surveillance study of many exposures and diseases. We have reassessed this association with data collected in the surveillance study during 1988-1992 from a new set of patients (355 cases of prostatic cancer and 2,048 controls with nonmalignant conditions). Because some studies have reported increased relative risks of lung cancer and testicular cancer in vasectomized men, we also used the surveillance database (4,126 men with various cancers, 7,027 men with nonmalignant conditions) to assess the relation of vasectomy to the risk of these and other cancers. In the newly collected data, the multivariate relative risk estimate for prostatic cancer in vasectomized men was 1.2 (95% confidence interval (CI) 0.6-2.7). For lung cancer and testicular cancer, the relative risk estimates were 1.3 (95% CI 0.8-2.1) and 0.8 (95% CI 0.4-1.9), respectively; for lung cancer occurring > or = 15 years after vasectomy, the relative risk estimate was 1.9 but it was not statistically significant (95% CI 0.7-5.0). For pancreatic cancer, the relative risk estimate was 1.8 (95% CI 1.0-3.1). For each of the other cancers considered--malignant melanoma, large bowel cancer, bladder cancer, kidney cancer, lymphoma, leukemia, and other cancers--the relative risk estimate was 1.3 or less and compatible with a value of 1.0. The present data provide little support for an association of vasectomy with the risk of prostatic cancer or other cancers. In addition, the data from two sets of cases of prostatic cancer and controls interviewed consecutively illustrate that increased relative risks detected in screening for statistically significant associations may tend to have an upward bias and to be lower in subsequent data.
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PMID:The relation of vasectomy to the risk of cancer. 806 35

Mortality to January 1, 1991, has been studied in 2,067 women in Scotland given X-ray therapy for metropathia haemorrhagica during the period 1940-1960. Average follow-up was 28 years. Overall, 1,313 deaths were observed compared with 1,297.01 expected from Scottish rates [standardized mortality ratio (SMR): 1.01]. Mortality was increased for cancers of heavily irradiated pelvic sites (SMR 5+ years after irradiation: 1.46) following mean doses to organs in the vicinity of the pelvis in the range 2.6-5.3 Gy. For these cancers the SMR was higher 30+ years after irradiation than at 5-29 years, indicating that the effects of exposure last for over 30 years, and in this period bladder cancer mortality was exceptionally high (SMR = 4.91). Mortality was also raised for leukaemia (SMR 2+ years after irradiation: 2.05), following a mean bone-marrow dose of 1.3 Gy, and for multiple myeloma (SMR 5+ years after irradiation: 2.59). For leukaemia the SMR was lower 30+ years after irradiation than at earlier periods, but remained greater than unity. For other cancers mortality was similar to Scottish rates, except for breast cancer for which mortality was low (SMR 5+ years after irradiation: 0.53), even in women aged over 50 at irradiation (SMR 5+ years after irradiation: 0.14). The deficit was principally due to a large deficit of breast cancer in women with ovarian doses of at least 5 Gy.
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PMID:Mortality in a cohort of women given X-ray therapy for metropathia haemorrhagica. 811 68

A population-based case-control study was used to evaluate the relationship between cases of bladder cancer (n = 61), kidney cancer (n = 35), and leukemia (n = 34) and exposure to tetrachloroethylene from public drinking water. Subjects were exposed to tetrachloroethylene when it leached from the plastic lining of drinking water distribution pipes. Relative delivered dose of tetrachloroethylene was estimated, using an algorithm that accounted for (1) residential history and duration, (2) whether lined pipe served the neighborhood, (3) distribution system flow characteristics, and (4) pipe age and dimensions. Whether or not latency was considered, an elevated relative risk of leukemia was observed among ever exposed subjects (adjusted OR = 1.96, 95% CI = 0.71-5.37, with latency; adjusted OR = 2.13, 95% CI = 0.88-5.19, without latency) that increased further among subjects whose exposure level was over the 90th percentile (adjusted OR = 5.84, 95% CI = 1.37-24.91, with latency; adjusted OR = 8.33, 95% CI = 1.53-45.29, without latency). When latency was ignored, there was also an increased relative risk of bladder cancer among subjects whose exposure level was over the 90th percentile (adjusted OR = 4.03, 95% CI = 0.65-25.10). Given that tetrachloroethylene is a common environmental and workplace contaminant in the United States, its carcinogenic potential is a matter of public health concern.
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PMID:Cancer risk and tetrachloroethylene-contaminated drinking water in Massachusetts. 778 54


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