Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: DrugBank:APRD00249 (Mutagen)
 5,946 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Normal mouse sera contain naturally occurring antibodies that are cytotoxic in the presence of rabbit complement for NB1, a cell line derived from a neuroblastoma adrenal metastasis of a spontaneous ovarian teratoma. The anti-NB1 antibodies can be specifically removed from normal mouse sera by absorption of the sera with homogenized brain tissue of mouse, rat, guinea pig, chicken, and man and by homogenized kidney tissue of mouse and man. The antigen recognized by anti-NB1 naturally occurring autoantibodies, designated mouse brain antigen-2 (MBA-2), is not present on other normal tissues or tumor cell lines tested. MBA-2 is distinct from previously described mouse brain antigens.
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PMID:Interspecies brain antigen detected by naturally occurring mouse anti-brain autoantibody. 4 48

The radioprotective drug, WR-2721 (S,2-[3-aminopropylamino]ethyl-phosphorothioic acid), has been studied in terms of its ability to (a) protect mice against mechlorethamine (HN2)-induced hematopoietic death, and (b) alter the ability of HN2 injections to induce growth delay in a solid tumor, the Line 1 lung carcinoma. When WR-2721 was injected ip 15 minutes before iv injections of HN2, it increased resistance to hematopoietic death by a factor of 2, and the protection declined with a half-life of 1.5-2.0 hours. Similar administration of both drugs failed to alter the responsiveness of the Line 1 lung carcinoma to HN2-induced growth delays, except when the HN2 was given within 15 minutes after WR-2721. This interaction of the two drugs, when given within 5-15 minutes of each other, does not appear to be true protection at the tumor site, but rather appears to result from HN2 inactivation in the blood. When HN2 is given 30-60 minutes after WR-2721, it is possible to obtain a twofold increase in the tumor delay without risking increased hematopoietic injury.
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PMID:Differential protection of normal and malignant tissues against the cytotoxic effects of mechlorethamine. 22 59

Mycosis fungoides is a T-cell lymphoma which is often localized to the skin in the early stages. Untreated, the process eventually progresses through eczematous, plaque, and tumor stages to systemic involvement. Its course, however, is unpredictable. Topical chemotherapy is effective in early stages of mycosis fungoides. Possibly prognostic benefits can occur from the early use of these agents. Nitrogen mustard and BCNU, both alkylating agents, have been used topically to control the disease. A dermatitis may develop in persons treated with nitrogen mustard but systemic side-effects are rare. However, BCNU may rarely lead to marrow depression when used topically. The use of these agents in mycosis fungoides is discussed herein.
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PMID:Topical chemotherapy of mycosis fungoides. 52 32

In vivo treatment of sensitive tumor cells with nitrogen mustard (HN2) results in marked inhibitions of protein and nucleic acid synthesis by mitochondria subsequently isolated from these cells. This inhibition occurs at doses of drug which produce no apparent inhibition of total RNA synthesis. The inhibition gradually reverses itself in sensitive cells and is less severe and more rapidly reversed in resistant cells. The in vivo sensitivity of the mitochondria is in striking contrast to their in vitro behavior; isolated mitochondria resist 50 times the in vivo ID50 level of the drug. The sensitivity of protein and RNA synthesis in mitochondria is presumed to be related to the differences in organization between the nucleocytoplasmic processes and the mitochondrial. But the data also suggest that the in vivo effects on mitochondria are indirect, either acting via the cytoplasm or nucleus or via a carrier mechanism having mitochondrial affinity.
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PMID:Comparison of the effects of nitrogen mustard on the functional properties of mitochondria from sensitive and resistant strains of Ehrlich ascites tumors. 97 18

Immediate and delayed effects of nitrogen mustard (HN2) (0.1 mg/kg/day for 4 days) on the growth and cell proliferation patterns of the 3-methylcholanthrene-induced autogenous rat sarcoma were studied. Tumor cells were labeled continuously with 0.5 muCi tritiated thymidine/g for 24 hours. The labeling index fell from 36.4 to 14.0% and the mitotic index from 0.88 to 0.67% after two treatments with HN2. At that time, tumor growth stopped and remained arrested during HN2 administration. After four injections of HN2, the labeling index was reduced further to 0.73% and the mitotic index to 0.36%. After the drug was withdrawn, tumor growth resumed at the pretreatment rate, even though the labeling index on day 3 was only 15.5% (or 40% of the control). The percent labeled mitosis curves and DNA contents, before and 4 days after HN2 was given, were similar. It was concluded that a subpopulation of cells of predominantly short intermitotic times caused tumor growth before and after drug treatment.
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PMID:Growth and regrowth of an autogenous rat sarcoma: effects of nitrogen mustard. 115 48

Thy-1 antigen is one of the widespread cell surface antigens. The antigen is expressed in the cells of a wide variety of different tissues and species and its pattern varies considerably during development and among species. Although the Thy-1 is one of the members of Ig-superfamily its function(s) remain unknown. Here we show that monoclonal antibodies to mouse Thy-1.2 antigen prevent adhesion of Thy-1.2-positive mouse T-leukemic cells 127 to monolayers of two mouse bone marrow stromal cell lines (14F1.1 and MBA-15). The same antibodies do not prevent adhesion of cell 127 to monolayers of two other mouse bone marrow stromal cell lines (MBA-2.1 and MBA-1.1.1) and to a wide spectrum of different normal and tumor mouse cell lines. A characteristic of the cell line 14F1.1 is the ability to support growth of mouse haemopoietic stem-cells. This data suggest that cells of stromal lines 14F1.1 and MBA-15 contain on their surface a specific ligand for the Thy-1 molecule. Cell-cell interaction via this ligand and the molecule on the cell surface may be an important step for development of certain lineages of cells.
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PMID:Thy-1 antigen-mediated adhesion of mouse lymphoid cells to stromal cells of haemopoietic origin. 135 19

The present experiment was undertaken to investigate possible synergism in induction of rat prostate tumor. F344 rats were repeatedly administered the prostate carcinogens 3,2'-dimethyl-4-aminobiphenyl (DMAB),N-nitrosobis(2-oxopropyl)amine(BOP), and N-methylnitrosourea (MNU) sequentially or together at times of hormonal castration induced regenerative cell proliferation of prostate epithelial cells. Group 1 animals received two 100 mg/kg doses of DMAB, two 20 mg/kg applications of BOP, and two times 15 mg/kg of MNU. Groups 2, 3, and 4, respectively, received each of the carcinogen treatment alone. Group 5 was given 6 applications of all three in combination, each at one-third the dose administered to the other groups. The results showed a clear synergism in enhanced tumor development in the colon but not in the prostate, in which the incidence of lesions induced by the three carcinogens was similar to that with DMAB alone.
Teratog Carcinog Mutagen 1992
PMID:Lack of synergism among DMAB, BOP, and MNU in induction of carcinomas of the rat ventral prostate. 135 64

Sister-chromatid exchange (SCE) induction and cell cycle kinetics alterations by ethyl carbamate in bone marrow of non-gravid murine Swiss Webster, ICR/Jcl, and C57Bl/6J dams were evaluated, and data from non-gravid females were compared with those previously reported for pregnant dams of the same strains. In addition, lung adenoma induction by ethyl carbamate in gravid Swiss Webster dams, their offspring, and in non-pregnant Swiss Webster females was also determined. Relative cytogenetic and tumor responses in non-gravid and gravid Swiss Webster females and their offspring were compared. In contrast to the increased sensitivity reported for gravid Swiss Webster dams versus ICR/Jcl and C57Bl/6J dams, SCE responses to 1.1, 2.2, or 3.3 mmol/kg of ethyl carbamate in non-gravid females were approximately equivalent among strains. In Swiss Webster and C57Bl/6J (but not ICR/Jcl) strains, SCE responses in non-gravid females at 2.2 and 3.3 were significantly lower than those of their pregnant counterparts. Tumor induction by 3.3 mmol/kg ethyl carbamate paralleled relative SCE induction with Swiss Webster dams, demonstrating a 5-fold increase in the number of tumors relative to their offspring and a 4-fold enhancement of tumor induction relative to their non-pregnant counterparts.
Teratog Carcinog Mutagen 1992
PMID:Tumor formation and sister chromatid exchange induction by ethyl carbamate: relationships among non-pregnant murine females, gravid dams, and transplacentally exposed offspring. 136 58

Acyl derivatives of 4,4,4-trifluoro-1-phenyl-1,3-butanedione (TFPB), 1-benzoyl-2-trifluoromethyl-2-acetoxyethene (BTAE), and 1-benzoyl-2-trifluoromethyl-2-(4-methylthio)benzoyloxyethene (BTME), were synthesized and investigated for inhibition of tRNA binding by N-acetoxy-2-acetylaminofluorene (N-AcO-AAF), and induction of glutathione S-transferase placental form (GST-P) positive foci in the rat liver by 2-acetylaminofluorene (2-AAF). Male F344 rats were given BTAE or BTME intraperitoneally and 2-AAF by intragastric intubation. Two weeks following the treatment, the rats were maintained on the diet containing 0.05% phenobarbital for an additional 6 weeks and then killed. Development of GST-P positive foci was not affected by concomitant treatment with BTAE or BTME. These two compounds inhibited the in vitro binding of N-AcO-AAF to tRNA. Thus, although these diacylmethane derivatives had the in vitro inhibitory activity, they did not inhibit tumor-initiating activity of 2-AAF in the rat liver.
Teratog Carcinog Mutagen 1992
PMID:Effect of acyl derivatives of 4,4,4-trifluoro-1-phenyl-1,3-butanedione on 2-acetylaminofluorene-induced glutathione S-transferase positive foci in the rat liver. 136 64

The familial occurrence of head and neck cancers supports the role of heredity in this disease group. The roles of environmental and genetic factors are difficult to separate. There are several well-characterized entities, however, that are associated with risk and prognosis of head and neck cancer, including Lynch-II syndrome, Bloom syndrome, Fanconi's anemia, xeroderma pigmentosum, ataxia telangiectasia, and Li-Fraumeni syndrome. Mutagen-induced chromosomal damage is associated with an increased risk of multiple primary neoplasms and upper aerodigestive tract cancers. A possible reduction of genotoxicity, mediated by micronutrients, was demonstrated in vitro. Sister chromatid exchanges and micronuclei are useful exposure and disease markers. Metabolic changes (acetylation, DBQ phenotype, and the AH locus polymorphism) have been found to be associated with cancer of the upper aerodigestive tract. Most associations between histocompatibility antigens and solid tumors are relatively weak, probably because of the masking effects of environmental factors. Infections by HPV, EBV, and HSV have a causative or predisposing role in several types of head and neck cancer. Amplification and rearrangement of oncogenes may also play a role in carcinogenesis, and oncogene amplification may be associated with aggressive tumor behavior and unfavorable clinical prognosis. Ploidy of tumors seems to be an important determinant of survival and response to therapy.
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PMID:Hereditary and environmental factors associated with risk and progression of head and neck cancer. 140 93


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