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PubMed1992

Condensation products of 2-amino-3-cyano-4,6-disubstituted pyridine with carbon disulfide, thiourea, urea & formamide and their antibacterial activity.

Some new 5,7-disubstituted pyrido[2,3-d]pyrimidine derivatives have been synthesized by the condensation of 2-amino-3-cyano-4,6-disubstituted pyridine with carbon disulfide, thiourea, urea and formamide. The structure of these products are supported by their IR and 1H-NMR spectra as well as by elemental analysis. The compounds have been tested for their antibacterial activity against E. coli and S. aureus.

Aminopyridines↗
PubMed1978

[Reaction of ortho-ortho-dimethylphenacyl-halides with formamide. Formation of 4(5)-(ortho-ortho-dimethylbenzoyl)imidazoles].

Reaction of 2,3,5,6-tetramethylphenacyl halides with formamide did not produce the expected 4(5)-(2,3,5,6-tetramethylphenyl)imidazole, but 4(5)-(2,3,5,6-tetramethylbenzoyl)imidazole (VII) was isolated as the major product together with 5-(2,3,5,6-tetramethylphenyl)oxazole (III), alpha-formylamino-2,3,5,6-tetramethylacetophenone (IV) and alpha-chloro-beta-amino-vinyl 2,3,5,6-tetramethylphenyl ketone (IX) as by-products. The corresponding mesitylene derivatives gave analogous results, whereas 4(5)-(2-methylphenyl)imidazole was obtained from 2-methylphenacyl bromide as expected according to the Bredereck's reaction. The structure of the isolated compounds were elucidated by element analysis, mass, I.R., U.V. and N.M.R. spectra, and by chemical reactivity.

Acetophenones↗
PubMed1977

Summation effect of N-butyl-n-(4-hydroxybutyl)nitrosamine, N-(4-(5-nitro-2-furyl)-2-thiazoly)formamide, N-2-fluoroenylacetamide, and 3,3'-dichlorobenzidine on urinary bladder carcinogenesis in rats.

The effects of the sequential administration of 0.01% N-butyl-N-(4-hydroxybutyl)nitrosamine (BBN), 0.15% N-(4-(5-nitro-2-furyl)-2-thiazoly)formamide (FANFT), 0.025% N-2-fluorenylacetamide (2-FAA), and 0.3% 3.3'-dichlorobenzidine (3,3'-DCB) on urinary bladder carcinogenesis were examined in male Wistar rats. Each chemical was administered for 4 weeks in various combinations. BBN for 4 weeks resulted in no histopathological changes, mild diffuse cell growth, and/or focal hyperplasia after 4, 8, 12, or 16 weeks of observation. No bladder carcinomas were present in rats given only BBN or any one of the other 3 chemicals. Statistically significant incidences of bladder carcinomas occurred with the sequential administration of all 4 chemicals or the first 3 chemicals without 3,3'-DCB. Bladder cancer was also present in rats administered the sequence of FANFT, 2-FAA, and 3,3'-DCB. No antagonistic effects between chemicals were observed.

2-Acetylaminofluorene↗
PubMed1982

Growth characteristics of N-[4-(5-nitro-2-furyl)-2-thiazolyl]-formamide (FANFT)-induced mouse bladder tumor lines in a human tumor stem cell assay.

Four N-[4-(5-nitro-2-furyl)-2-thiazolyl]-Formamide (FANFT)-induced mouse bladder tumor (MBT) lines were tested for their ability to form colonies in a tumor stem cell assay. Anticancer drug testing was done using this assay to determine whether reproducible colony survival curves could be be produced. All four cell lines produced colonies at 10--14 days, whether taken from culture or murine tumor. Cloning efficiencies ranged from 0.29% to 1.93% from culture and from 0.005% to 0.05% from the murine source. Growth characteristics were described. Cells from colonies were histologically similar to the original cells plated. A linear relationship existed between the number of cells plated and the number of colonies produced. In vitro drug studies were reproducible and correlated with in vivo data. Therefore, MBT lines can be used for in vitro drug testing in a tumor stem cell assay and may be useful in selecting active chemotherapeutic agents in the murine tumor model.

Animals↗
PubMed1990

Point mutation in codons 12 and 61 of the Ha-ras gene in rat urinary bladder carcinomas induced by N-[4-(5-nitro-2-furyl)-2-thiazolyl]formamide.

Male F344 rats were fed N-[4-(5-nitro-2-furyl)-2-thiazolyl]formamide (FANFT) for up to 4 wk, then were given the basal diets (Prolab 3200 or AIN-76A) with or without 5% sodium saccharin for up to 100 wk. Eleven transitional cell carcinomas (TCCs), one undifferentiated carcinoma, and two sarcomas of the urinary bladder were examined for the expression of ras gene product, p21, by immunohistochemical staining and western blot analysis. Point mutation in codons 12 or 61 of the Ha-ras genes amplified by polymerase chain reaction was examined by a slot-blot screening procedure using allele-specific oligonucleotide probes. Immunohistochemical staining showed enhanced immunoreactivity with the antibody to ras p21 in seven TCCs and one undifferentiated carcinoma. Western blot analysis showed faster migration of the p21 band in 6 of 11 TCCs. Oligonucleotide hybridization revealed the point mutation in codon 12 of Ha-ras gene (GGA----GTA in 1 TCC) and in codon 61 (CAA----CGA in 5 TCCs and CAA----CTA in 1 TCC). Two mutations in codons 12 and 61 coexisted in one tumor, which were found to be present in different Ha-ras alleles. The incidence of Ha-ras gene mutations were similar in groups treated with (3 of 6) or without (3 of 8) sodium saccharin. These results suggest the involvement of activated Ha-ras gene in rat urinary bladder carcinogenesis induced by FANFT.

Animals↗
PubMed1990

Activating missense mutations in Ha-ras-1 genes in a malignant subset of bladder lesions induced by N-butyl-N-(4-hydroxybutyl)nitrosamine or N-[4-(5-nitro-2-furanyl)-2-thiazolyl]formamide.

Urothelial cell cultures generated from urinary bladders from a series of N-butyl-N-(4-hydroxybutyl)nitrosamine (BBN)- or N-[4-(5-nitro-2-furanyl)-2-thiazolyl]formamide (FANFT)-treated Fischer 344 rats were examined for activating missense mutations in Ha-ras-1 genes. Our overall objective was to identify oncogene-activating mutations in this system and to determine what altered biological properties correlate with such genetic changes. The urinary bladders from the treated animals showed a spectrum of histopathologies, from simple hyperplasia to transitional cell carcinoma (TCC). Using restriction analysis, oligonucleotide hybridization, and DNA sequencing, we found that approximately 20% (3/14) of the bladder cell cultures had acquired oncogenic single-base substitutions in codon 61 of Ha-ras-1 genes (CAA----AAA or CGA). The donor bladder lesions for these three cultures, which also harbored the same ras-activating mutations, were all classified as stage A or B TCCs. However, four other TCCs also arising in this series were found to have normal Ha-ras genes. Whereas approximately half of the bladder cultures derived from the carcinogen-treated rats were nontumorigenic in athymic mice, the three cultures containing ras oncogenes were all highly tumorigenic (forming tumors within 5 wk of injection into athymic mice). These cultures also displayed a high degree of anchorage-independent growth and NIH 3T3-transforming activity in gene transfer assays. The nontumorigenic cultures were derived from bladder lesions that included three hyperplasias and three stage A TCCs. We conclude that ras-activating missense mutations were present in a malignant subset of bladder lesions induced by BBN or FANFT, but most of the lesions in this system appeared to involve genetic alterations elsewhere. Thus other oncogenes besides activated Ha-ras may apparently be associated with the same bladder histopathologies and transformation markers.

Animals↗
PubMed1993

Sequencing analysis of Ha-, Ki-, and N-ras genes in rat urinary bladder tumors induced by N-[4-(5-nitro-2-furyl)-2-thiazolyl]formamide (FANFT) and sodium saccharin.

Male F344 rats were fed N[4-(5-nitro-2-furyl)-2-thiazolyl]formamide (FANFT) for up to 4 wk, then given the basal diet with or without 5% sodium saccharin for up to 100 wk. In a previous study, we demonstrated point mutations in codons 12 and 61 of Ha-ras gene among eleven transitional cell carcinomas (TCC), one undifferentiated carcinoma, and two sarcomas of the urinary bladder (Mol Carcinogen 3:210-215, 1990). In this study, Ha-ras, Ki-ras, and N-ras sequences were examined by polymerase chain reaction (PCR) and direct DNA sequencing. The results confirm the point mutation in codon 61 (CAA to CGA in 5 TCCs and to CTA in one TCC) of the Ha-ras gene. Mutation at codon 12 was not confirmed. No mutation was found in the Ki-ras gene. Sequences of the N-ras gene exons 1 and 2 were determined, and no mutations was detected. These results suggest the involvement of activated Ha-ras gene, but not Ki-N or N-ras gene, in rat urinary bladder carcinogenesis induced by FANFT. Subsequent sodium saccharin administration did not affect the changes in Ha-ras gene.

Amino Acid Sequence↗
PubMed1978

Induction of transitional cell carcinoma of the urinary bladder in rats by feeding N-[4-(5-nitro-2-furyl)-2-thiazolyl] formamide. Histological and ultrastructural findings.

After feeding with 0.188% N-[4-(5-nitro-2 furyl)-2-thiazolyl] formamide (FANFT), transitional cell carcinoma of the urinary bladder was induced in all female Wistar rats tested. Histological changes of the urothelium consisted of various degrees of hyperplasia and dysplasia. An infiltrating transitional cell carcinoma first appeared after 8 months. These results are compared with the findings of other authors, and divergencies of the tumour induction rates are discussed with respect to strain, sex and weight of experimental animals as well as concentration and amount of ingested carcinogen. Electron microscopy shows microvillous transformation of the luminal plasma membrane and appearance of a thick fluffy cell coat (glycocalyx). These changes are explained by an altered function of the Golgi complex occurring during malignancy and leading to a loss of the specific discoid vesicles of the urothelial cells.

Animals↗
PubMed1978

Biological behavior of N-[4-(5-nitro-2-furyl)-2-thiazolyl]-formamide induced carcinoma of the transitional epithelium in the rat.

30 female Wistar rats weighing between 70 and 90 g were fed for 8 months with 0,188% N-[4-(5-nitro-2-furyl)-2-thiazolyl] Formamide (FANFT). After this period a papillary tumor of the urinary bladder was demonstrable in each animal. Histological examination always revealed a transitional cell carcinoma with prevailing medium tumor stages; no distant metastases were found. The grade of malignancy was classified as medium and high. No significant statistical relationship could be ascertained between tumor stage and grade or between grade and weight, but a correlation was established between tumor stage and weight. After 12 months, 36/60 kidneys were found to be normal, whereas in 20/60 dysplasias and in 2/60 transitional cell carcinomas of the renal pelvis were observed; secondary hydronephrosis due to bladder tumors occured 4 times. Other organ changes were not noticeable.

Animals↗
PubMed1996

Dimethyl formamide (DMFA) and ethylene glycol (EG) are estrogenic in rainbow trout.

During our studies on the effects of environmental estrogenic chemicals on vitellogenin gene expression in fish, dimethyl formamide (DMFA) and ethylene glycol (EG) were used as solvents to dissolve and deliver hydrophobic beta-estradiol or nonylphenol. Control groups were injected with water only. It was surprising to find that in certain doses, Vg mRNA from control fish can be induced by DMFA or EG alone. This suggested that DMFA and EG are weak estrogens.

Animals↗
PubMed1989

Effects of sodium salts of phenobarbital and barbital on development of bladder tumors in male F344/NCr rats pretreated with either N-[4-(5-nitro-2-furyl)-2-thiazolyl]formamide or N-nitrosobutyl-4-hydroxybutylamine.

Promoting effects of sodium salts of phenobarbital (NaPB) and barbital (NaBB) on the development of bladder tumors were investigated in F344 male rats initiated with N-[4-(5-nitro-2-furyl)-2-thiazolyl]formamide (FANFT) or N-nitrosobutyl-4-hydroxybutylamine (BBN). To initiate with FANFT, rats were fed 0.2% FANFT mixed in diet for either 2 or 6 weeks and 2 weeks later were offered diet containing 1000 ppm of NaPB or NaBB. Rats were killed either at 52 or 68 weeks of age. To initiate with BBN, rats were given 0.05% BBN in drinking water for 4 weeks and beginning 1 day later were fed NaBB mixed in diet at 1000 ppm for up to 52 weeks. NaBB promoted bladder carcinogenesis initiated by either FANFT or BBN; the incidence and average number of simple or preneoplastic nodular (PN) hyperplasias, papillomas, and carcinomas per 10 cm of urothelium were significantly increased in the groups receiving NaBB following exposure to FANFT for 6 weeks (p less than 0.05) or BBN for 4 weeks (p less than 0.01). No such effect was seen in rats fed FANFT for only 2 weeks. NaPB also significantly increased (p less than 0.05) the frequency of preneoplastic PN hyperplasias but not the average number of papillomas and carcinomas per 10 cm of urothelium in rats fed FANFT for 6 weeks. NaBB was an effective promoter of bladder carcinogenesis under these experimental conditions, as expected from its known promoting effect on transitional epithelium of the renal pelvis, but NaPB in contrast did not affect the incidence or multiplicity of bladder papillomas or carcinomas under these conditions. NaPB could be considered a promoter for bladder urothelium only by the less rigorous criterion that it increased the frequency of preneoplastic PN hyperplasia.

Animals↗
PubMed1984

Mutagenicity of urine of various species fed N-[4-(5-nitro-2-furyl)-2-thiazolyl]formamide or 2-amino-4-(5-nitro-2-furyl)thiazole.

Rats, mice and hamsters, which are susceptible to the bladder carcinogenesis by N-[4-(5-nitro-2-furyl)-2-thiazolyl]formamide (FANFT), and guinea pigs, which are not, were fed a diet containing 0.188% FANFT or 0.188% 2-amino-4-(5-nitro-2-furyl)thiazole (ANFT) for 1 week and their urine was then examined for mutagenicity for S. typhimurium TA100. The mutagenicities of the urine of these species fed FANFT were approximately equal. Similarly, that of the urine of these species fed ANFT were also approximately equal. However, the urine from FANFT-fed animals was approximately 10 times as mutagenic as that from ANFT-fed animals. ANFT was detected only in the urine of rats, mice or hamsters fed FANFT. A positive correlation between the susceptibility toward bladder carcinogenesis by FANFT and urinary ANFT excretion was demonstrated, although the correlation between this susceptibility and urine mutagenicity was lacking.

Animals↗
PubMed1981

13-cis-retinoic acid: effect on urinary bladder carcinogenesis by N-[4-(5-nitro-2-furyl)-2-thiazolyl]-formamide in Fischer rats.

The failure of 13-cis-retinoic acid to inhibit either the incidence or severity of bladder carcinoma in female Fischer rate initiated with N-[4-(5-nitro-2-furyl)-2-thiazolyl]formamide (FANFT) suggests that inhibition of bladder carcinogenesis by natural and synthetic retinoids is carcinogen-class specific, and adds an element of complexity to approaches in chemoprevention.

Animals↗
PubMed1983

Effect of phenobarbital on the carcinogenesis of N-[4-(5-nitro-2-furyl)-2-thiazolyl]formamide in rats.

Male Fischer rats were fed a N-[4-(5-nitro-2-furyl]-2-thiazolyl]formamide (FANFT) diet for 6 weeks followed by a phenobarbital (PB) diet for an additional 86 weeks. PB significantly increased the incidence of bladder tumors, but not the incidence of hepatic foci and areas of cellular alterations caused by FANFT. The results suggest that PB may be a weak promoter for bladder carcinogenesis, and that FANFT may not be an initiator for hepatocarcinogenesis.

Animals↗
PubMed1983

Long term dose response study of N-[4-(5-nitro-2-furyl)-2-thiazolyl] formamide-induced urinary bladder carcinogenesis.

The effect of dose was evaluated for the bladder carcinogenicity of N-[4-(5-nitro-2-furyl)-2-thiazolyl] formamide (FANFT). The chemical was fed to male weanling F344 rats for 30 weeks followed by 74 weeks of control diet. The incidences of bladder carcinoma were 100, 100, 87, 0, 0 and 0% for doses of 0.2, 0.1, 0.05, 0.01, 0.005 and 0.001%, respectively. There was an inverse relationship between dose and latency period. There was no increased incidence of tumors of other tissues.

Animals↗
PubMed1984

Effect of aspirin on N-[4-(5-nitro-2-furyl)-2-thiazolyl]-formamide-induced epithelial proliferation in the urinary bladder and forestomach of the rat.

The co-administration of aspirin with N-[4-(5-nitro-2-furyl)-2-thiazolyl]-formamide (FANFT) to rats resulted in a reduced incidence of FANFT-induced bladder carcinomas but a concomitant induction of forestomach tumors. An autoradiographic study was performed on male F-344 rats fed diet containing FANFT at a level of 0.2% and/or aspirin at a level of 0.5% to evaluate the effect of aspirin on the increased cell proliferation induced by FANFT in the forestomach and bladder. FANFT-induced cell proliferation in the bladder was significantly suppressed by aspirin co-administration after 4 weeks but not after 12 weeks. In the forestomach, and also in the liver, aspirin did not affect the FANFT-induced increase in labeling index. The present results are consistent with the carcinogenicity experiment suggesting that different mechanisms are involved in FANFT carcinogenesis in the bladder and forestomach, and that aspirin's effect on FANFT in the forestomach is not due to an irritant effect associated with increased cell proliferation. Also, there appears to be an adaptation by the rats to the chronic ingestion of aspirin.

Animals↗
PubMed1984

Enhancement by phenothiazine and 2,5-di-O-acetyl-D-glucosaccharo-(1,4)(6,3)-dilactone of bladder carcinogenicity of N-[4-(5-nitro-2-furyl)-2-thiazolyl]-formamide in rats.

Rats concomitantly fed N-[4-(5-nitro-2-furyl)-2-thiazolyl] formamide (FANFT) and phenothiazine, or concomitantly fed FANFT and Glucaron then fed Glucaron alone had significantly greater incidences of transitional cell carcinomas of the bladder than rats fed FANFT alone. Caffeine and cysteamine did not affect FANFT bladder carcinogenesis. Phenothiazine induced nitroreductase activity of hepatic microsomes.

Animals↗