Disease relevance of Dimethylformamide

• Dimethylformamide, metal dyes, and testicular cancer [1].
• CONCLUSIONS: an outbreak of toxic liver disease has been associated with exposure to dimethylformamide in the workplace [2].
• The human acute promyelocytic leukemia cell line HL-60 is induced by retinoic acid (RA) and N,N-dimethylformamide (DMF) to differentiate into cells having many of the functional and morphologic characteristics of mature granulocytes [3].
• The responses of unfed plateau-phase cultures of two clonal subpopulations of cells (clones A and D) from a human colon adenocarcinoma (DLD-1) to X-irradiation were examined in detail either as control cultures or after growth in medium containing the differentiating agent N,N-dimethylformamide (DMF, 0.8%, three passages) [4].
• N,N-Dimethylformamide-induced morphological differentiation and reduction of tumorigenicity in cultured mouse rhabdomyosarcoma cells [5].

Psychiatry related information on Dimethylformamide

• The degree of sulfation was easily controlled by changing the amount of DMF/SO3 complex added and reaction time [6].

High impact information on Dimethylformamide

• Expression of YBB 3/10 antigen in human tumor colon cell lines and its induction by N,N-dimethylformamide [7].
• Expression of the YBB 3/10 antigen could be induced in the only negative colon tumor cell line (DLD-1 cells) by treatment with N,N-dimethylformamide (CAS: 68-12-2) [7].
• Cultured human colon carcinoma cells were induced by the polar solvent N,N-dimethylformamide (DMF) to express a more differentiated phenotype as indicated by three types of antigen markers [8].
• Dimethylformamide and testicular cancer [9].
• Clinical and pathological characteristics of hepatotoxicity associated with occupational exposure to dimethylformamide [10].

Chemical compound and disease context of Dimethylformamide

• The effects of N,N-dimethylformamide (DMF) and N-methyl-formamide (NMF) on the growth of two human colon cancer cell lines xenografted in nude mice were assessed [11].
• Three clonal subpopulations (A, B, C) isolated from the same rhabdomyosarcoma of the rat were tested and compared for their susceptibility to differentiation induction using retinoic acid (RA), dimethylformamide (DMF), and N-monomethylformamide (NMF) [12].
• Mesylation of these alcohols and refluxing with imidazole in dimethylformamide furnished title compounds, which were active in vitro against dermatophytes, yeasts, other fungi, and gram-positive bacteria and in vivo as well as in vitro against Candida albicans [13].
• It was concluded that occlusive hydration and lack of thermodynamic control may have obscured the enhancing abilities of the solvents, 2-P, NMP, EP, DMF, and DEET induced erythema in some volunteers, although this was usually short-lived [14].
• Therefore dexamethasone and N,N-dimethylformamide, both causing a decreased growth rate, showed opposing actions on myogenic differentiation and on c-myc proto-oncogene expression of human rhabdomyosarcoma cells [15].

Biological context of Dimethylformamide

• Disulfiram effect from inhalation of dimethylformamide [16].
• Tuning the activity of an enzyme for unusual environments: sequential random mutagenesis of subtilisin E for catalysis in dimethylformamide [17].
• PC3 subtilisin E and other variants containing different combinations of amino acid substitutions are effective catalysts for transesterification and peptide synthesis in dimethylformamide and other organic media [17].
• Chemotactic function first appears between 48 and 96 hr of DMF induction and is associated not only with the coincidental development of deformability, spontaneous motility, greatly increased binding of fMet-Leu-Phe, and orientation but also with decreasing cell size and pleomorphism of nuclei [18].
• Competitive binding experiments showed a preference order dimethylformamide > ethanol > MeCN for L binding at the single exchangeable metal site [19].

Anatomical context of Dimethylformamide

• Nonstimulated cells induced to differentiate with dimethylformamide had no change in the degree of actin polymerization but exhibited a mean (m) ROL similar to normal human polymorphonuclear leukocytes (PMN) (8.6 +/- 1.4 micron/min [HL-60 cells] v 7.8 +/- 1.8 microns/min [PMN] [20].
• Cell surface features associated with differentiation-induction of methylcholanthrene-transformed AKR-2B fibroblasts by N,N-dimethylformamide [21].
• Membranes from hepatocytes incubated with PMA (1 microgram/ml) for 1 h exhibited a 40% decrease in alpha 1-adrenergic receptors (481 +/- 10 fmol/mg of protein; mean +/- S.E.M. for three separate experiments) relative to vehicle-treated (dimethylformamide) hepatocytes (802 +/- 91 fmol/mg of protein; n = 3), with no significant effect on the KD [22].
• Repression of c-myc expression by DMF was observed in MOSER and HCT 116 cells, whether it was added to proliferating or late log phase cultures, and was associated with a corresponding reduction in cellular proliferation [23].
• N,N-Dimethylformamide (DMF) is reported to cause testicular germ-cell tumors in exposed workers [24].

Associations of Dimethylformamide with other chemical compounds

• The expression of antigens on HL-60 cells recognized by the granulocyte-specified monoclonal antibodies PMN 6 and PMN 29 decreased after treatment of HL-60 cells with PMA, but remained constant after treatment with DMF, DMSO, cis-retinoic acid, PHA-LCM, or MLC [25].
• Dexamethasone at a concentration of 500 nM was markedly synergistic with dimethylformamide and dimethylsulfoxide, but not with trans-retinoic acid, in inducing f-met-leu-phe binding by HL-60 cells [26].
• Effects of N,N-dimethylformamide and retinoic acid on transforming growth factor-beta induced mitogenesis in AKR-2B mouse embryo fibroblasts [27].
• Role of glutathione depletion in the mechanism of action of N-methylformamide and N,N-dimethylformamide in a cultured human colon carcinoma cell line [28].
• Whereas tumor cell proliferation was significantly inhibited (P less than 0.001) in all three subpopulations, the effects of RA, DMF, and NMF on tumor cell differentiation were strikingly heterogeneous [12].

Gene context of Dimethylformamide

• Treatment of Rat-1 fibroblasts with 75 and 130 mM DMF induced IGF-1R mRNA as determined by reverse transcription-PCR analysis [29].
• Furthermore, 95-99% of cells were protected from DMF-induced apoptosis if cells were pretreated with platelet-derived growth factor (5 ng/ml) for 16 h before treatment with DMF in the presence of IGF-1 [29].
• Alterations in the binding of transforming growth factor-beta (TGF-beta) to the MOSER human colon carcinoma cell line caused by N,N-dimethylformamide (DMF) or extracellular matrix (ECM) were examined [30].
• Therefore, TGF-beta 2 acted as a negative autocrine inhibitory factor for MOSER cells and the growth inhibitory effects of DMF were mediated by the increased secretion of active TGF-beta 2 [31].
• Investigation of the mechanistic basis of N,N-dimethylformamide toxicity. Metabolism of N,N-dimethylformamide and its deuterated isotopomers by cytochrome P450 2E1 [32].

Analytical, diagnostic and therapeutic context of Dimethylformamide

• Results indicate that some human cancer xenografts respond to the polar solvent DMF and to its metabolite NMF and that DMF may be acting at least in part by its metabolism to NMF [11].
• N,N-dimethylformamide-induced alteration of cell culture characteristics and loss of tumorigenicity in cultured human colon carcinoma cells [33].
• The mechanism of the antitumor action of N-methylformamide (NMF), an agent currently undergoing clinical trials, and its congener, N,N-dimethylformamide (DMF), was examined in the DLD-1 Clone A human colon carcinoma cell line in vitro [28].
• For a system with 0.2 wt % copolymer concentration and 4.5 wt % water concentration in DMF/water, the micelle morphology observed in transmission electron microscopy changed from vesicles at room temperature to worm-like cylinders and then to spheres with increasing temperature [34].
• At ambient temperatures, only ligation by imidazole and pyridine occurs spontaneously while DeltaG degrees becomes positive for ligation by acetone and dimethylformamide, due to a relatively large entropic effect, which is dominating when the energetic effects of ligation are small [35].

References