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)

The published studies of cancer of United States Jews are reviewed. Despite the lack of religious designation on death certificates, case reports, and census returns, a number of indirect methods for measuring the problem have been devised, which produce fairly consistent findings. In general, for American Jews, these show deficits in cancer mortality, among males, for the buccal cavity and pharynx and prostate and, among females, for the breast, uterine cervix and corpus, and bladder. Excesses in mortality, noted for both sexes, are esophagus, stomach, colon, pancreas, lymphomas, and leukemia and, in females, the lung and the ovary. The standardized mortality ratios for cancer of selected sites for Russian-born residents of upstate New York, 1969 through 1971, are presented as an indirect measure of the problem in the United States Jews. Statistically significant excesses were found in males for stomach and colon, with a striking deficit in cancer of the buccal cavity and pharynx. Among females, excesses were noted for stomach, pancreas, and lung with a sharp deficit in the uterine cervix. On the basis of the religious affiliation of the cemetery of burial, estimates of the Jewish and non-Jewish components of the 800 deaths in Russian-born residents were determined. Expected deaths in these two subgroups by sex, for each cancer site, were then calculated by use of the site-specific proportionate mortality of upstate New York for these years. This revealed a significant excess among Jewish males for colon cancer, with a deficit in lung cancer, while among the non-Jewish male components stomach cancer mortality was the only site significantly in excess. Among Jewish females, stomach and lung cancers were in excess, with a deficit in cancers of the breast and cervix uteri. In non-Jewish Russian-born females, the only site significantly in excess was stomach, with breast cancer showing a deficit.
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PMID:Cancer in United States Jews. 119 15

The cytotoxicities of 2 derivatives of artemisinin B and 2 derivatives of artemisic acid (designated as Compound A, B, C, and D) were investigated, using trypan blue dye exclusion test and colony-forming units assay. At the concentration of 5 micrograms.ml-1, the inhibition rates of these 4 compounds against murine leukemia cell line P388 were > 85%. When tested against human hepatoma cell line SMMC-7721 at 25 micrograms.ml-1, the inhibition rates of Compound A, B, C, and D were found to be 92.3%, 96.9%, 84%, and 82.1%, respectively, and 27%, 8%, 37.8%, 1.7% against normal human embryonic lung cell line WI-38, respectively. These 4 compounds all showed an inhibition rate of 100% against human gastric cancer cell line SGC-7901 at 50 micrograms.ml-1.
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PMID:[Antitumor activities of 4 derivatives of artemisic acid and artemisinin B in vitro]. 130 44

We recently reported the isolation of the K-sam complementary DNA (cDNA), which was amplified preferentially in poorly differentiated types of stomach cancer and codes for one of the heparin-binding growth factor or fibroblast growth factor (FGF) receptor families. The K-sam-related gene, N-sam (NCC-IT-cell-derived sam), was isolated by screening of the cDNA libraries of human immature teratoma cells, NCC-IT. Sequence analysis of the N-sam cDNAs showed that N-sam encodes a human FGF receptor, the FLG protein. N-sam was expressed in lymphocytic leukemia/lymphoma cells, predominantly in the thymic T-cell phenotype. In a T-cell leukemia line, MOLT3, N-sam mRNA expression was markedly enhanced by 12-O-tetradecanoylphorbol-13-acetate treatment and was also up-regulated by basic FGF exposure. These results indicate that N-sam expression is regulated during T-cell ontogeny and modulated by its putative ligand exposure. The results also suggested that interaction between immature T-cell and marrow or thymic interstitial cells might be mediated by N-sam and basic FGF stored in the extracellular matrix of stromal cells.
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PMID:K-sam-related gene, N-sam, encodes fibroblast growth factor receptor and is expressed in T-lymphocytic tumors. 131 50

We evaluated the occurrence and type of malignant tumors in 148 patients with sarcoidosis followed at the Okayama University Hospital. Nine patients had malignancies; in 2 of 9 patients the development of malignancy preceded that of sarcoidosis, and one patient presented with sarcoidosis and malignancy at the same time. Six patients developed six types of malignancy following the development sarcoidosis; one case each of stomach cancer, lung cancer, breast cancer, thyroid cancer, testicular tumor, laryngeal cancer, and chronic lymphocytic leukemia. There was no significant difference between sexes (3 males and 3 females). The mean age of the cancer group at the onset of sarcoidosis was 56 years, which was significantly higher (p less than 0.05) than that of the control group. In these 6 patients, the mean interval from onset of sarcoidosis to detection of cancer was 11.7 years (range 1.5 to 30.2 years). The relative risk of malignancy was calculated based on the data for 148 patients with sarcoidosis with a total of 1371 person-years. The expected incidences of cancer for all sites and specific sites were estimated by applying age- and sex-adjusted person-years. The observed incidence of cancer was significantly (p less than 0.05) greater than the expected incidence for thyroid cancer, laryngeal cancer, and leukemia. No significant difference in incidence was found for all sites or for the other sites of cancer. The increased cancer incidence in sarcoidosis may be secondary to immunological abnormalities associated with this disease.
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PMID:[Malignancies in patients with sarcoidosis]. 140 74

A study was carried out to analyse trends in cancer mortality sex differentials. This study compared age-standardized sex ratio values for mortality from 18 cancers (or groups of cancers), and total cancer mortality over the period 1950-1989 in 24 European countries, for 4 age groups (all ages, 20-44 years, 45-64 years, and 65 years and over). For lung cancer and other tobacco-related neoplasms, appreciable rises in sex ratio values were observed until the late 1970s, particularly in Southern and Eastern Europe, before levelling off in recent years, particularly among the younger age groups. In the late 1980s, the range of variation in overall age-standardized sex ratios for lung cancer was between 2 and 3 in the United Kingdom and in Nordic countries, and around or over 10 in Southern Europe. In young adults, the decline in sex ratio values observed in Denmark and Sweden (unity), and in other Nordic countries and in the United Kingdom (around or below 2) reflects a levelling of lung cancer in young males and an increase in young females. This clearly indicates that young women are a priority target group for smoking control interventions in Europe. Appreciable cohort effects were also observed for stomach cancer: rises in sex ratio values were greater in, or restricted to, middle- and older age groups, whereas in the young there was some tendency towards a levelling in sex differentials. The overall sex ratio values for stomach cancer were around 2 in most areas of Europe in the late 1980s. For intestinal cancer, sex ratio values showed some tendency to rise, reaching a level of 1.3-1.7 in the late 1980s; steady rises were also registered in sex ratio values for melanoma (skin cancer), reaching 1.5-1.8 in the late 1980s in most countries. These upward trends which were minor or inconsistent at younger ages in several countries became progressively stronger with advancing age. Sex ratio values were below unity for cancers of the gallbladder and the thyroid. Sex ratio values tended to rise also for leukaemia (from 1.2-1.5 to 1.5-1.7), but showed no noticeable trend for lymphomas or myeloma. The overall sex ratio values for total cancer mortality in the 1950s were between 1.2 and 1.4 in most European countries. Thereafter, they rose appreciably in several countries, reaching 1.9 in Czechoslovakia, Italy and Poland, and 2.3 in France.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Trends in cancer mortality sex ratios in Europe, 1950-1989. 141 53

Ethylene oxide is a colorless gas that can cause neoplastic disease (leukemia, stomach cancer) in animals and humans. Its mutagenic potential is expressed by chromosome aberrations and sister chromatid exchange, as has been shown in numerous studies of groups exposed to ethylene oxide. The results of our pilot study on the effects of exposure to high levels of ethylene oxide show chromosome breakage in exposed individuals at twice the frequency of the normal population. Although these are preliminary findings, they justify urgent, specific protection from further exposure.
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PMID:Cytogenetic changes in ethylene oxide-exposed workers: a challenge to occupational medicine. 142 15

In this study, the intensity of exposure to asbestos was evaluated in the residents of Kure City, the site of the Japanese naval shipyard, Kure. The number of asbestos bodies was counted in 728 autopsied cases from those treated surgically in Kure Kyosai Hospital. Five grams of lung tissue was lysed, and the number of asbestos bodies was counted with the use of light microscopic examination. By this method, the number of asbestos bodies detected in men was significantly higher than that in women. There was a peak between 60 and 70 years of age. The number of asbestos bodies in exposed cadavers in Kure City exceeded greatly that found in other districts of Japan. By this criterion, 58 of 109 patients with lung cancer had asbestos exposure, and 39 had a high exposure to asbestos. All 13 patients with malignant mesothelioma had a high exposure to asbestos. Excess asbestos exposure also was found in a large proportion of patients with gastric cancer, colon cancer, and acute leukemia. The crocidolite type of asbestos was detected frequently in patients of malignant mesothelioma or leukemia, and the chrysotile form was found in those with lung cancer.
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PMID:Intensity of exposure to asbestos in metropolitan Kure City as estimated by autopsied cases. 156 84

Cancer risk for farmers in Denmark and Italy was studied by linking occupational census data with incidence of cancer in Denmark and with cancer mortality in Italy. Farmers in the two countries had a consistent risk reduction for cancer of the lung, bladder, small intestine, colon, rectum, and prostate. No excess of stomach cancer was found among farmers in the two countries, which is in agreement with the most recent data from other surveys. The risk of oesophageal cancer was reduced among the Danish and increased among the Italian male farmers. This can probably be explained by differences in alcohol consumption between the Danish and Italian farmers compared with the general population. The risk of brain cancer was significantly reduced among Italian farmers. There was a significant risk reduction for Hodgkin's disease and no excess for non-Hodgkin's lymphoma in Denmark, whereas in Italy a statistically significant excess risk was found for the first and a slight excess risk for the second of these diseases. The per capita consumption of phenoxy-herbicides between 1950 and 1970 was lower in Italy than in Denmark but treatments were performed mainly by professional applicators in Denmark and by the farmers themselves in Italy. Risk of leukaemia among Italian female farmers was increased. In Denmark, this increase was limited to women who were themselves owners of a farm. Specific occupations in agriculture showing a high risk for cancers of the lymphopoietic system in Denmark mostly entailed contact with animals.
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PMID:Cancer risk among Danish and Italian farmers. 157 Dec 91

Transgenic animal technology has been useful for the direct demonstration of the tumorigenic potential of oncogenes in vivo. Over the past eight years a wide variety of oncogenes and proto-oncogenes from viral and cellular sources have been inserted into the germline of mice with subsequent development of neoplasia. Many of the published reports describe similarities between morphologic features of the transgenic mice tumors and those occurring naturally in humans. We discuss the morphologic features of selected transgenic models carrying viral genes and review their applicability to investigations directed toward understanding cancer in general and specifically gastric cancer, neurofibromatosis and leukemia. Examples of the impact of nutrition, interaction with growth factors and initiation with chemical carcinogens are presented. In one of the models functional similarities to the mechanism of oncogenesis in human T-cell leukemia virus type-1 (HTLV-1) lymphoma may exist with activation of cytokine production and subsequent autocrine stimulation. The transgenic model of proximal gastric cancer demonstrates features similar to those seen in carcinogen-induced neoplasia. These studies underscore the vast potential of transgenic models for inquiry into the genetic and epigenetic basis of human carcinogenesis. However, many features of transgenic cancer models differ from cancer in humans and the specific criteria for judging the value of transgenic models remain unclarified. For example, although the tumors arising in the HTLV-1 Tax transgenic mice show numerous similarities to human neurofibromatosis including development of lesions of the iris, the similarities do not necessarily extend to the molecular involvement of neurofibromatosis-1 (NF-1), a gene with structural and functional homology to GTPase activating proteins. Transgenic experiments of the future will ask questions beyond whether a particular gene is capable of initiating the neoplastic process. The ability to construct systems in vivo with a defined starting point that facilitate further controlled manipulation of events resulting in cancer provide great opportunities to dissect the various molecular pathways involved in such a process. Therefore, gene knockout experiments and disruption of gene function will further enhance our ability to understand the multi-factorial process of tumor development.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Transgenic models of human cancer. 166 87

This study is to calculate a risk of lung cancer in a cohort of 1411 sarcoidosis cases which were followed for a 3 year period from 1984 to 1987. The physicians were requested to answer the questionnaire about progress of the disease by mail. Excess death was investigated using standardized mortality ratio (SMR). The expected number of deaths was calculated from Japanese sex-age specific mortality rate in 1985, using person-year method. Death from all causes and cancers did not show any excess. SMR being 0.98 and 0.97 respectively. The SMR of lung cancer was 3.26 (male: 5.56, female: 3.03), being statistically significant. The SMR of lung infection was 4.2, with statistical significance. The SMR of other main causes of death in Japan i.e., cerebrovascular accident, ischemic heart diseases and heart failure was less than 0.88. It is probably that sarcoidosis is a risk factor of lung cancer. The SMR of leukemia and uterine cancer was 5.88 and 8.70, respectively, though the observed number of leukemia was too small to conclude how high the cancer risk is among sarcoidosis patients. Gastric cancer, hepatic cancer and colon cancers were not observed.
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PMID:Excess death of lung cancer among sarcoidosis patients. 166 41


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