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 carcinogenicities of 1-nitropyrene and 1,3-, 1,6- and 1,8-dinitropyrene were assessed in weanling female CD rats. The animals were administered one of the compounds at 10 mumol/kg body wt through intraperitoneal or intragastric administration three times a week for 4 weeks. The total cumulative dose averaged 16 mumol/animal. The experiment was ended 78 weeks following the first administration. The average survival period for the animals in the 1,6- and 1,8-dinitropyrene i.p. treated groups, due to the occurrence of life-threatening peritoneal malignant fibrous histiocytomas (MFHs) in nearly all of the animals, were 19 and 38 weeks respectively. 1,3-Dinitropyrene induced only a few MFHs. 1,8-Dinitropyrene also induced a significant incidence of leukemia. A significant increase of the incidence of mammary tumors was observed in the groups of rats treated i.p. with 1-nitropyrene, or 1,3- or 1,8-dinitropyrene, and those treated i.g. with 1,8-dinitropyrene. These results demonstrate that nitropyrenes are capable of inducing MFH, mammary tumors and leukemia in the rat.
Carcinogenesis 1991 Jul
PMID:Carcinogenicity of dinitropyrenes in the weanling female CD rat. 164 14

Pleural implant experiments using Sprague-Dawley rats have shown that those injected with the carcinogen 15,16-dihydro-11-methylcyclopenta[a]phenenthren-17-one (11-methyl-17-ketone) intraperitoneally followed by silica fibres intrapleurally develop mesotheliomas. These tumours were histologically similar to those induced by crocidolite alone. The intraperitoneal injection of 11-methyl-17-ketone also induced leukaemia.
Carcinogenesis 1991 Oct
PMID:Tumours of mesothelial origin in rats following inoculation with biogenic silica fibres. 165 31

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

We demonstrate in this study that infection with Moloney murine leukemia virus (M-MLV) and exposure to 3-methylcholanthrene (3-MC) can cooperate to transform NIH/3T3 mouse fibroblasts. M-MLV seems to stimulate the expression of c-myc and of a certain major histocompatibility complex (MHC) class I gene. Yet M-MLV infection by itself is insufficient to transform these cells. However, exposure of the infected cells to 3-MC resulted in a rapid cell transformation with concomitant enhancement of c-Ha-ras and H-2K class I MHC gene expression in the transformed cells. No such transformation was observed when uninfected NIH/3T3 cells were similarly treated with this carcinogen. Clones of cells transformed by this combined effect of M-MLV and 3-MC were found to be highly tumorigenic in fully immunocompetent allogeneic BALB/c mice. We provide evidence to suggest that the enhanced expression of the H-2K gene in these transformed cells plays an important role in overcoming the BALB/c allogeneic barrier and allowing tumor growth in these mice.
Carcinogenesis 1990 Dec
PMID:Chemical-retroviral cooperative carcinogenesis and its molecular basis in NIH/3T3 cells. 170 67

The first of case of adult T-cell prolymphocytic lymphosarcoma is reported which according to the natural course, cell composition of tumor, cell surface markers as well as expressed immune response to a wide spectrum of HTLV-1 gag an env encoded proteins can be classified as HTLV-associated adult T-cell leukemia. Diagnosis of the tumor alongside with identification of HTLV-1-infected individuals in the USSR emphasizes the need to stimulate research in HTLV-1-associated carcinogenesis in this country.
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PMID:[The 1st case of adult T-cell leukemia (ATL) with expressed immune response to HTLV in the USSR]. 176 11

Studies in humans and animals have shown that gasoline contains a number of cancer-causing and toxic chemicals such as 1,3-butadiene, benzene, toluene, ethylbenzene, xylenes, isoparaffins, methyltert-butylether, and others. The International Agency for Research on Cancer (IARC) in its Monograph Supplement 7 (1987) concludes that "in the absence of adequate data on humans, it is biologically plausible and prudent to regard agents for which there is sufficient evidence of carcinogenicity in experimental animals as if they present a carcinogenic risk to humans." Epidemiological studies in humans provide important evidence of potential increased risk of leukemia, lymphatic tissue cancers, cancers of the brain, liver, and other organs and tissues. Recently (July, 1990) the American Conference of Governmental Industrial Hygiene (ACGIH) recommended that the TLV-TWA for benzene be reduced from 1 ppm to 0.1 ppm (ACGIH, 1990). The Collegium Ramazzini and others have also recommended that the exposure level for 1,3-Butadiene be reduced from 1,000 ppm to below 0.2 ppm. This recommendation is based on the findings that were presented at the Symposium on Toxicology, Carcinogenesis, and Human Health Aspects of 1,3-Butadiene (Environ. Health Perspec., 1990). Thus, studies on health effects resulting from very low levels of benzene, 1,3-butadiene, and other cancer-causing chemicals--components of gasoline--necessitate that all avoidable exposure to gasoline or gasoline vapors be avoided.
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PMID:Dangerous and cancer-causing properties of products and chemicals in the oil refining and petrochemical industry: Part I. Carcinogenicity of motor fuels: gasoline. 178 Aug 52

4-isothiocyanate-2,2,6,6-tetramethyl-piperidine-1-oxyl has the strongest effects on the DNA synthesis and viability of isolated leukemia 7712 cells. This compound is a very potent inhibitor of DNA synthesis with 50% inhibition of cell DNA synthesis occurring at 2.2 micrograms/ml, while the LD50 for white mice is 277 mg/kg. During the concentration of 50 micrograms/ml, the inhibition of DNA synthesis is 99.7%, which is unable to damage the DNA replicate template. The inhibition of this compound, a combination of nitroxide and isothiocyanate, appears to be stronger than that of the sum of the two separate actions. Much more moderate effects are seen for all the other nitroxide radicals. After reducing nitroxide to hydroxylamine, there is no inhibition for DNA synthesis. The free radical mechanism of carcinogenesis and antitumor action has been discussed.
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PMID:DNA synthesis inhibition of nitroxide radicals on leukemia cells. 182 Nov 28

Dichlorvos (dichlorovinyl dimethyl phosphoric acid ester) is a cholinesterase inhibitor used widely as a contact and stomach insecticide for control of internal and external parasites. Carcinogenesis studies were conducted by administering dichlorvos in corn oil by gavage 5 times a week for 103 weeks to groups of 50 male and 50 female Fischer rats at 0, 4, or 8 mg/kg body weight, to groups of 50 male B6C3F1 mice at 0, 10, or 20 mg/kg, and to groups of 50 female B6C3F1 mice at 0, 20, or 40 mg/kg. During the course of the studies, body weights and survival rates of the male and female rats and mice were not different from those of their respective controls; females of both species appeared to gain more weight than controls. Neoplasms induced by dichlorvos included adenomas of the exocrine pancreas (male rats), mononuclear cell leukemia (male rats), and squamous cell papilloma of the forestomach (male and female mice; two other female mice had squamous cell carcinomas). Lesions observed in female rats that may have been due to dichlorvos administration included adenomas of the exocrine pancreas and fibroadenomas of the mammary gland. The results demonstrated that dichlorvos is carcinogenic for Fischer rats and B6C3F1 mice.
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PMID:Carcinogenesis studies of dichlorvos in Fischer rats and B6C3F1 mice. 190 Aug 19

The carcinogenic effect of 7,12-dimethylbenz[a]anthracene (DMBA) was examined in the virgin female Japanese house musk shrew, Suncus murinus (family: Soricidae, order: Insectivora). Leukemia, musk gland tumors, pilosebaceous tumors and sarcomas were induced in the DMBA-treated shrews, whereas none of the controls developed any tumors up to 50 weeks of age. DMBA emulsion was administered i.p. at a dose of 1.25 or 2.5 mg once a week, with either four or eight doses being given from 8 weeks of age. Leukemia developed in 100% (9/9), 50% (5/10), 56% (5/9) and 0% (0/10) of the animals treated with a total dose of 20 mg (8 x 2.5 mg), 10 mg (8 x 1.25 mg), 10 mg (4 x 2.5 mg) and 5 mg (4 x 1.25 mg) of DMBA respectively. Leukemia was of the lymphatic and/or mast cell type, and the spleen was the organ invariably involved. A dose-dependent effect of DMBA was not observed for pilosebaceous and musk gland tumors. When 1 mg of DMBA powder was dusted into the subcutaneous tissue at 4 weeks of age, sarcomas developed at the dusted site (69%; 9/13).
Carcinogenesis 1991 Aug
PMID:Induction of tumors in the Japanese house musk shrew, Suncus murinus (Insectivora), by dimethylbenz[a]anthracene. 190 23

Previous studies have demonstrated that BR-931, a hepatic peroxisome proliferator, can induce liver tumours in mice and rats. Since alterations in gene expression may play a critical role in multistage hepatocarcinogenesis, the present studies examined the expression of the c-myc, c-H-ras, epidermal growth factor (EGF) receptor and ODC (ornithine decarboxylase) genes, as well as endogenous retrovirus-like sequences, in F344 rat liver during the first 8 weeks of feeding a 0.16% Br931 diet and in liver tumours induced by chronic feeding of this diet. Northern blot analysis of poly A + liver RNA samples showed an increase in the level of RNAs homologous to rat leukaemia virus (RaLV) but no significant change in the level of 30S-retrovirus related RNAs in the liver RNA samples obtained from rats during the first 8 weeks of feeding the diet containing BR931. An increase in the levels of c-myc, c-H-ras and ODC transcripts was also seen in the liver RNA samples from the treated rats. Of particular interest was a decrease in the abundance of EGF receptor transcripts in the liver RNA samples from rats fed the BR931 diet. Increased levels of RaLV, c-myc, and ODC RNAs were also seen in the tumours induced by BR931, but this was not the case for 30S and c-H-ras. The liver tumour samples also showed a decrease in EGF receptor RNA. These changes in cellular levels of specific RNAs resemble, in several respect, those we previously described in rodent liver during regeneration and tumour promotion, and also those seen in rodent hepatomas induced by other agents. Therefore, they may reflect a common profile of gene expression relevant to liver proliferation and carcinogenesis.
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PMID:Changes in expression of cellular oncogenes and endogenous retrovirus-like sequences during hepatocarcinogenesis induced by a peroxisome proliferator. 193


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