Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Using the data from the Tri-State Leukemia Survey and a mathematical model, the hypothesis that low levels of diagnostic radiation produce severe genetic damage that is expressed in the child of the exposed person as leukemia and other diseases is tested. It is estimated that for about 1% of the exposed persons who are affected by radiation, there is a 50-fold increase in the risk of leukemia and a five-fold increase in certain other diseases.
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PMID:Genetic damage from diagnostic radiation. 57 41

The effect of chronic infection with the protozoan parasite Babesia rodhaini on the subsequent development of mouse leukemia was investigated in three different murine leukemia-lymphoma model systems: congenital lymphoma (in AKR mice), irradiation-induced lymphoma (in C57BL mice), and Rauscher-virus-induced leukemia in NMRI mice. Leukemia incidence was significantly greater than in controls in Babesia-infected (NMRI strain) mice that had been infected with an adjusted dose of Rauscher leukemia virus.
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PMID:The effect of chronic protozoan infection by Babesia rodhaini on leukemogenesis in mice. 59 Nov 32

The six cases of Preleukemia (or Preleukemic States) are described. The peripheral blood was characterised with Pancythopoenia in 5 and bicytopoenia in 1 patient. Morphological alterations of Erythrocytes were present in all cases. The Bone Marrow was hypercellular in 3 and hypocellular in 3 patients. Erythropoiesis was megaloblastic or partly megaloblastic in 5 cases, with "ring" sideroblasts present in all cases. The percentage of Leukemic blast cells was as follow: 0, 5, 6, 10, 30 and 33. The duration of the preleukemic phase varied from 3-53 months. With the manifestations of overt Acute Nonlymphatic Leukemia the agressive therapy was applied. The results were poor in 5 patients (the survival 1, 5-4 m.). Only one survived more than 60 months and is still in full remission.
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PMID:[Preleukemia]. 60 31

From the time of its inception in 1955, the Drug Development Program of the National Cancer Institute has relied primarily on transplanted rodent tumor systems in vivo for the evaluation and selection of potential antitumor agents. Although greater emphasis has been placed in recent years on rationally designed drugs, the major effort throughout the history of the program has involved the empirical screening of a wide variety of chemical structures and natural products of varying sources. The initial screening spectrum consisted of three mouse tumors, Sarcoma 180, Carcinoma 755 and Leukemia 1210, based on the retrospective analysis presented in the GELLHORN-HIRSCHBERG Report. As a result of further expermental studies and analyses, the screens changed successively to (1) L1210 plus a spectrum of mouse, rat and hamster tumors, (2) L1210 plus the rat tumor, WALKER 256, (3) L1210, plus P388 for natural products and B16 melanoma and LEWIS lung carcinoma for special studies, and finally (4) P388 as a pre-screen followed by a panel of transplanted tumors and xenografts representing the major tumor sites. The rationale underlying each of the successive changes, and results obtained with each approach, will be discussed.
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PMID:Antitumor screening procedures of the National Cancer Institute. 61 10

Among 2966 acute leukemia, 26 familial cases were reported. Leukemia occured mainly in the first relative individuals and particularly in the sibship. The relative risk for a sib of leukemic patient is four time more than for random people. Leukemia was often similar among patients of the same family and the onsets of the disease occured approximatly at the same age whatever the time between the dates of diagnosis. Twins with leukemia were often monozygotous. Relative risk of leukemia among twins, decreases according to the age: the probability of leukemia for a twin is: (a) 100 p. cent if the other twin is leukemic before 1 year old; (b) 15 p. cent between 1 to 4 years old and (c) similar to other sib after 4 years old. Among chronic leukemias, only chronic lymphocytic leukemia seems to have a genetic background for susceptibility. Some familial diseases (congenital aplastic anemia, Bloom's disease, Ataxia telangiectasia) or congenital diseases (Down's syndrome) increase the risk of leukemia.
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PMID:[Familial leukemia (author's transl)]. 66 77

Cell proliferation was investigated in normal and Rauscher Leukemia Virus-infected BALB/c mice. Five days after inoculation, islands of leukemic blasts arose in the red pulp, and proliferated as shown by autoradiographic analysis after a pulse of 3H-Thymidine. These cells subsequently infiltrated the whole spleen and 3 weeks after infection about 60% of the spleen consisted of large immature erythroblast-like cells. Repeated injections of 3H-Thymidine led to uniform labeling of 85% of the spleen cells. Cell cycle analysis showed that for bone marrow as well as for spleen cells the total duration of the cell cycle did not differ from the cell cycle times of normal erythroblasts. From the difference between the actual doubling time and the potential doubling time (estimated on the basis of the cell cycle time) it can be calculated that considerable cell loss must occur. This cell loss is only to a minor extent due to the release of blasts into the peripheral blood. Probably cell death and extrusion of nuclei during erythroid differentiation are the main factors involved.
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PMID:The effect of Rauscher murine leukemia virus infection on the hemopoietic system of BALB/c mice. Cell proliferation and cell loss. 66 30

The treatment of any malignant disease requires appropriate criteria for diagnosis of the disease, appropriate methods for study, and techniques for evaluating response to treatment. In the past five years, there have been a number of proposed guidelines for studies in chronic lymphocytic leukemia (CLL). These submitted guidelines represent a further re-evaluation of concepts in CLL, and are currently in use by Cancer and Leukemia Group B for protocol studies. It is clear that revisions will continue to be make as new knowledge accumulates. In the meantime, these are submitted for publication for use by other investigators.
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PMID:Guidelines for protocol studies in chronic lymphocytic leukemia. 71 96

Carcinogenic effect of a single oral administration of 300 or 200 mg/kg body weight of 1-butyl-1-nitrosourea (BNU) and continuous oral administration of 400 ppm solution of BNU in the drinking water for 5, 10, 15, and 20 weeks to female SD rats was studied. In addition, the number of spleen cells capable of forming plaques (PFC) against primary immunization with sheep red blood cells was investigated in various stages of the animal experiments. With a single oral administration of BNU, tumors developed in 31/50 (62%) rats between the 25th and 75th week. They were most frequently seen in the mammary gland (40%), followed by the stomach (10%), kidneys (8%), and ovary (8%). Leukemia was found in 8%. No dose-effect relationship was observed in these 2 experimental groups. On the other hand, tumors developed in 67/77 (88%) of the rats that received BNU in their drinking water. The incidence of tumors was highest in leukemia (61%), followed by mammary tumors (26%), intestinal tumors (12%), and ear duct tumors (8%). There was a dose-effect relationship among the 4 groups in the latent period and target organs for tumor development. Although the PFC count of the rats receiving BNU for 5 weeks recovered gradually to about 50% of the control level at the end of the 25th experimental week, it remained less than 10% of the control level for the whole experimental period in those receiving BNU longer than 10 weeks. Therefore, it was apparent that the tumors developed, proliferated, and finally killed the host rats in highly immunosuppressive state.
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PMID:Carcinogenic effect of 1-butyl-1-nitrosourea on female Sprague-Dawley rats. 77 31

Female Sprague-Dawley rats, 36 days old, were pretreated for 2 weeks either with 100 ppm 1,1,1-trichloro-2,2-bis(p-chlorophenyl)ethane (DDT) or 250 ppm S-(1,2-dicarbeth-oxyethyl)OO-dimethyldithiophosphate (Malathion) in the diet. From day 50 they were given, via stomach tube, 21 consecutive daily doses of 0.714 mg 7,12-dimethylbenz[a]anthracene (DMBA). Pesticide diets and observation of the animals for mammary tumors continued until necropsy, 230 days after the start of DMBA administration. DDT-treated rats had a significantly lower mammary tumor incidence, prolonged tumor latency period, and fewer tumors per rat than did the control group. Animals given Malathion (an organophosphate pesticide) had a higher mammary tumor incidence, shortened latency period, more tumors per rat, and more actively growing tumors than did the control group (DMBA only). Leukemia incidence in rats surviving to necropsy (230 days after the start of DMBA administration) was 11/20 for control, 2/29 for DDT, and 8/12 for Malathion-treated rats. Leukemia was primarily myelogenous. DDT may inhibit DMBA-induced mammary tumors and leukemia by stimulating hepatic metabolism and excretion of DMBA so that less carcinogen is available to peripheral tissues. Malathion may potentiate DMBA induction of mammary tumors and leukemia by inhibiting the same enzyme systems induced by DDT.
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PMID:Protection by 1,1,1-trichloro-2,2-bis(p-chlorophenyl)ethane (DDT) against mammary tumors and leukemia during prolonged feeding of 7,12-dimethylbenz(a)anthracene to female rats. 80 43

Leukemia virus transmission was studied during an outbreak of leukemia among the baboons of the Sukhumi monkey colony. First, the possibility of "vertical" transmission of the virus was examined, as the Papio stock in Sukhumi was genetically homogeneous. "Vertical" transmission of the virus from a common ancestor seems unlikely, since cases of leukemia were registered in animals descending from different families. However, there were cases of innate leukemia, when babies born from leukemic parents displayed pronounced signs of leukemia immediately after birth. "Horizontal" transmission of the virus also seems indisputable, because special experiments have shown that imported baboons, even of other species, caged together with leukemic animals, may develop leukemia due to close contact. It was established earlier that the leukemia virus was excreted with urine. Kidneys, lungs, and salivary glands are the possible routes of infection. Thus, the present report aknowledges the possibility of both "horizontal" and "vertical" transmission of leukemia oncornaviruses in primates.
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PMID:Possible ways viral leukemia spreads among the hamadryas baboons of the Sukhumi monkey colony. 80 37


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