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PubMed1982

Report on the presence of a toxic substance, dimethyl formamide, in sodium fluorescein used for fluorescein angiography.

The revelation that intravenous sodium fluorescein is not all that it might seem to be may be a significant finding in the light of the adverse reactions to fluorescein that have been previously reported. Analysis of commercially prepared intravenous sodium fluorescein by mass spectroscopy and nuclear magnetic resonance has indicated that an industrial solvent used in the manufacturing process has not been eliminated. Dimethyl formamide is an industrial solvent with a maximum acceptable exposure level of 10 parts per million for dermal contact. It has been found in quantities of 5000 parts per million in the fluorescein for intravenous use. This investigation was prompted by a significant increase in the adverse reactions in patients receiving intravenous fluorescein in the retinal photographic unit at the Manchester Royal Eye Hospital.

Dimethylformamide↗
PubMed1987

Identification of inhibitory growth factors from a N-[4-(5-nitro-2-furyl)-2-thiazolyl]formamide-induced murine bladder cancer cell line.

The N-[4-(5-nitro-2-furyl)-2-thiazolyl]formamide (FANFT)-induced murine bladder carcinoma cell line MBT-683 contains growth-stimulating (TGF) and growth-inhibiting factors (GI). These activities coeluted on BioGel P-30 between molecular weights 6,000 and 29,000 daltons. They can be separated by high performance liquid chromatography. Both activities were destroyed by trypsin and dithiothreitol. However, they were resistant to acid and heat. Pool 1 (TGF) stimulated the growth of normal rat kidney cells, whereas pool 2 (GI) inhibited the colony formation of the cell lines MBT-683 and RBTCC-8.

Animals↗
PubMed1976

Enhancing effect of allopurinol on the induction of bladder cancer in rats by n-[4-(5-nitro-2-furyl)-2-thiazolyl]formamide.

The effects of allopurinol on the induction of bladder cancer by N-[4-(5-nitro-2-furyl)-2-thiazolyl]formamide (FANFT), excretion of urinary tryptophan metabolites, hepatic nitroreductase activity, and the acid-soluble thiol content of liver and blood in weanling female Fischer rats were investigated. Four groups of rats were given normal diet or normal diet supplemented with 0.005% allopurinol, 0.188% FANFT, or 0.005% allopurinol-0.188% FANFT. Transitional cell carcinomas appeared in 3 of 30 rats (10%) at 15 weeks and in 7 of 44 rats (16%) at 20 weeks in the FANFT-treated group; the carcinomas appeared in 14 of 35 rats (40%) at 15 weeks and in 27 of 50 rats (54%) at 20 weeks in the FANFT-allopurinol-treated group. Growth rate was not affected by allopurinol and FANFT. Allopurinol alone caused no morphological change in the epithelial cells of the urinary bladder but decreased hepatic cytosol nitroreductase activity. FANFT alone had no effect on hepatic cytosol or microsomal nitroreductase activity but increased hepatic and blood acid-soluble thiol content. FANFT increased the urinary excretion of anthranilic acid glucuronide, kynurenine, acetylkynurenine, and 3-hydroxykynurenine and decreased indican and o-aminohippurate excretion. Allopurinol did not alter the effects of FANFT on the acid-soluble thiol content of liver and blood or the excretion of urinary tryptophan metabolites.

Allopurinol↗
PubMed1991

H-ras mutations in rat urinary bladder carcinomas induced by N-[4-(5-nitro-2-furyl)-2-thiazolyl]formamide and sodium saccharin, sodium ascorbate, or related salts.

Male F344 rats were fed 0.2% N-[4-(5-nitro-2-furyl)-2-thiazoly]formamide for 6 weeks and then fed 3% or 5% sodium saccharin, 5% sodium ascorbate, 3.12% calcium saccharin, 1.34% sodium chloride, 5.2% calcium saccharin plus 1.34% sodium chloride, or basal diet alone for 72 weeks. Protein and DNA were extracted from 89 bladder tumors [87 transitional cell carcinomas (TCC), 1 papilloma, and 1 sarcoma] from 86 rats p21 expression was examined by Western blotting using a monoclonal antibody against p21 (NCC-RAS-004). H-ras mutations in exons 1 and 2 were examined by direct sequencing of DNA amplified by polymerase chain reaction. Sequencing results demonstrated mutations at codon 61 (CAA to CGA in 15 TCCs; CAA to CTA in 2 TCCs), at codon 12 (GGA to TGG in 1 TCC), and at codon 13 (GGC to GTC in 3 TCCs). Mutations at codon 61 were confirmed by faster mobility of the p21 band in Western blots. The level of p21 expression varied among samples, but many TCCs appeared to express more p21 than controls. The overall incidence of H-ras mutations was 24.4% (21 of 86 rats). The type of chemical used for the promoting phase had essentially no effect on H-ras mutation, suggesting that the effects observed were related to FANFT administration. The frequency of H-ras mutation in each group was negatively related to the incidence of carcinoma (r = -0.85; P less than 0.01). Two groups of tumors (with or without the mutated ras gene) were compared for tumor size (reflected by the bladder weight), histological grading, and the presence of invasion. The size of tumors with mutated ras was significantly smaller than those without mutated ras. There was no difference in the histological grading between the two groups. Although not statistically significant, histological invasion was more frequently observed in tumors with mutated ras (14.3%) than in tumors without mutation (3.1%).

Animals↗
PubMed1989

Effect of aspirin on urinary bladder carcinogenesis initiated with N-[4-(5-nitro-2-furyl)-2-thiazolyl]formamide in rats.

N-[4-(5-Nitro-2-furyl)-2-thiazolyl]formamide (FANFT), a potent urinary bladder carcinogen, is metabolically activated in vitro by a variety of enzyme systems including aerobic cooxidation by prostaglandin H synthase which is present in the rat bladder mucosa. In a previous experiment, aspirin coadministered with FANFT for 12 weeks inhibited FANFT-induced bladder carcinogenesis and enhanced forestomach carcinogenesis. To further evaluate the effects of aspirin on FANFT carcinogenesis, male F344 rats were fed either FANFT (0.2% of the diet) for 12 weeks (Group 4), aspirin (0.5% of the diet) simultaneously with FANFT for 12 weeks (Group 2), aspirin simultaneously with FANFT for 12 weeks and then subsequently to the end of the experiment (Group 1), or FANFT only followed by aspirin (Group 3). The incidence of bladder carcinoma was significantly higher when aspirin was fed after FANFT treatment (87%) compared to FANFT followed by control diet (48%) and was higher in rats given aspirin plus FANFT followed by aspirin (73%) compared to aspirin plus FANFT followed by control diet (47%). Aspirin alone given for 13 weeks (Group 6) or throughout the experiment (68 weeks) (Group 5) did not induce bladder cancer. However, in all groups administered aspirin long-term, renal papillary necrosis and renal pelvic hyperplasia and atypia were frequently observed. Only a single forestomach tumor was observed. In the present experiment, aspirin appeared to exhibit promoting activity for bladder carcinogenesis in the rat.

Animals↗
PubMed1979

Effect of dose on urinary bladder carcinogenesis induced in F344 rats by N-[4-(5-nitro-2-furyl)-2-thiazolyl]formamide.

Because of the utility of the N-[4-(5-nitro-2-furyl)-2-thiazolyl]formamide (FANFT) rat model in the study of bladder cancer, the effect of dose on FANFT-induced bladder carcinogenesis was evaluated. Weaning male F344 rats were given FANFT in the diet at doses of 0.1, 0.05, 0.01, 0.005, 0.001, and 0.0005% for 30 weeks and then a control diet for 22 weeks. A control group received only the control diet throughout the experiment. Papillary tumors were present at the higher doses, hyperplasia of various degrees of severly was present at the intermediate doses, and minimal hyperplasia was observed in 4 of 16 rats at the 0.005% dose; no mucosal abnormalities were observed at the two lower doses or in the control group. Bladder epithelium from selected animals was also examined by scanning electron microscopy (SEM) after 10 weeks and again at the end of the experiment. Hyperplastic mucosa with pleomorphic microvilli similar to that previously demonstrated for 0.2% FANFT was observed at 10 weeks in rats fed 0.1% FANFT. Hyperplastic mucosa with pleomorphic microvilli was also observed at 52 weeks in rats fed 0.1% and 0.05% FANFT. Hyperplastic mucosa without pleomorphic microvilli was observed in rats fed 0.01 and 0.005% FANFT. The bladder appeared normal by light microscopy and SEM at the two lower doses and in the control group at both the 10- and 52-week intervals. A dose relationship was thus demonstrated for FANFT-induced bladder carcinogenesis in male F344 rats, and more severe surface changes were observed by SEM as the dose increased.

Animals↗
PubMed1978

The influence of N-[4-(5-nitro-2-Furyl)-2-thiazolyl]formamide and phenacetin on the immune status in male Fischer rats.

The effect of N-[4-(5-nitro-2-furyl)-2-thiazolyl]formamide (FANTF) and phenacetin on the immune status of Fischer rats was determined utilizing the spleen plaque and phytohemagglutinin blastogenesis assays 6, 10, and 15 weeks after administration at doses of 0.2 per cent and 0.535 per cent, respectively. Azathioprine (0.02 per cent of the diet) was tested as a known immunosuppressive chemical for comparison, and a negative control group, fed a control diet without added chemicals, was also tested. Immunosuppression was shown in the rats receiving azathioprine at all times by both assays, whereas in FANFT-fed rats immunosuppression was greater than in the control group (not statistically significant). Results from rats fed phenacetin were not significantly different than those of the control group. These results show that immunosuppression does not occur in rats administered phenacetin for up to 15 weeks, nor in FANFT-induced bladder carcinogenesis at the time of reversible bladder mucosal hyperplasia (6 weeks), or when the mucosal lesions have become irreversible, non-invasive carcinomas (10 and 15 weeks).

Animals↗
PubMed1987

Enhancement of N-[4-(5-nitro-2-furyl)-2-thiazolyl]formamide-induced carcinogenesis by urinary tract infection in rats.

Epidemiological studies suggest that urinary tract infection is an important risk factor in the development of bladder cancer. Chronic urinary tract infection in rats is associated with urothelial hyperplasia and papillomatosis. In the Sprague-Dawley strain, exposure to the 5-nitrofuran, N-[4-(5-nitro-2-furyl)-2-thiazolyl]formamide (FANFT), is associated in particular with the development of renal pelvic tumors. The present study was designed to evaluate whether chronic urinary tract infection could enhance tumor development in FANFT-induced urinary tract carcinogenesis. One hundred forty-four female Sprague-Dawley rats were divided into the following groups. Group 1 received 0.2% FANFT in the diet for 7 wk followed by control diet. Group 2 received 0.2% FANFT in the diet for 7 wk followed by control diet. One wk after completion of FANFT administration, the suspension of 0.5 ml of Escherichia coli (06K13H1) was injected into the bladder through the urethra. Group 3 received 0.2% FANFT in the diet for 7 wk followed by control diet. One wk after completion of FANFT administration, a suspension of heat-killed E. coli (06K13H1) was injected into the bladder through the urethra. Group 4 received a suspension of 0.5 ml of E. coli (06K13H1) through the urethra and received control diet throughout the experiment. Group 5 was fed control diet only. The experiment continued for 104 wk. A significantly higher number of urinary tract tumors, particularly of the renal pelvis, was recorded in Group 2 compared to Groups 1, 3, 4, and 5. The majority of the rats in Groups 2 and 4 had morphological signs of urinary tract infections, particularly pyelitis and/or pyelonephritis. Thus, a single injection of E. coli (06K13H1) into the bladder results in an enhancement of FANFT-induced urinary tract carcinogenesis in the Sprague-Dawley rat, especially for renal pelvic tumors. The formation of dimethylnitrosamine or other nitroso compounds from nitrates in the urine or increased cell proliferation due to chronic inflammation or both may be important pathogenetic factors in the tumor development.

Animals↗
PubMed1986

Inhibition by aspirin of N-[4-(5-nitro-2-furyl)-2-thiazolyl]formamide initiation and sodium saccharin promotion of urinary bladder carcinogenesis in male F344 rats.

N-[4-(5-Nitro-2-furyl)-2-thiazolyl]formamide (FANFT) is metabolically activated by several enzyme systems, including prostaglandin H synthase. Aspirin is an inhibitor of prostaglandin H synthase and has been shown to inhibit FANFT-induced bladder carcinogenesis when coadministered in the diet. To further evaluate the effects of aspirin on bladder carcinogenesis in the rat, we have coadministered aspirin with FANFT during the initiation phase and with sodium saccharin during the promotion phase of carcinogenesis. FANFT was administered in the diet at a level of 0.2% for 6 weeks as the initiator and sodium saccharin was administered in the diet at a level of 5% for 61 weeks as promoting stimulus. Aspirin was administered at a level of 0.5% with FANFT or with sodium saccharin, and appropriate control groups were included. Weanling male Fischer 344 rats were utilized and the chemicals were added to Agway Prolab 3000 rat chow. A 1-week interval was included between the FANFT and sodium saccharin administration during which the rats received either aspirin containing diet or control chow, depending on the treatment regimen of the group. Thirty rats were included in each group at the beginning of the experiment, except for the control group which contained 40. Rats given FANFT followed by saccharin had a bladder carcinoma incidence of 83%. Rats given aspirin with FANFT but not with saccharin had a carcinoma incidence of 20% and the rats fed aspirin with the saccharin but not with the FANFT had an incidence of 28%. FANFT followed by control diet resulted in a bladder carcinoma incidence of 10%, as was true for the rats given FANFT plus aspirin followed by control diet. However, the hyperplastic effects induced in the bladder epithelium by saccharin without prior FANFT administration were inhibited by coadministration with aspirin. These results indicate that aspirin inhibits both FANFT initiation and sodium saccharin promotion of bladder carcinogenesis, but the mechanisms involved would most probably be different for each.

Animals↗
PubMed1986

Effect of sodium phenobarbital and sodium saccharin in AIN-76A diet on carcinogenesis initiated with N-[4-(5-nitro-2-furyl)-2-thiazolyl]formamide and N,N-dibutylnitrosamine in male F344 rats.

Promoting activities of sodium phenobarbital (PB) and sodium saccharin (SS), incorporated in a semisynthetic diet (AIN-76A), on 2-stage carcinogenesis initiated with N-[4-(5-nitro-2-furyl)-2-thiazolyl]formamide (FANFT) or N,N-dibutylnitrosamine (DBN) in male F344 rats were investigated. For the first 4 weeks of the experiment, weanling male Fischer rats were fed Wayne diet containing 0.2% FANFT or drinking water containing 0.005% DBN. The control rats were given the basal diet and normal drinking water. Beginning at the fifth week, the rats were given the AIN-76A diet or this diet containing 0.05 or 0.15% PB or 5% SS. The experiment was terminated at the end of 100 weeks. PB significantly increased the incidence of transitional cell carcinoma of the bladder of the rats that had been treated with FANFT (P = 0.027). PB also increased the incidence of bladder carcinoma of the rats that had been treated with DBN, but the increase was not significant (P = 0.081). SS in the AIN-76A diet increased the incidence of bladder carcinoma in the rats which had been treated with FANFT or DBN, but the increase was not significant (P = 0.059 and 0.327, respectively). Both high and low doses of PB, but not SS, significantly increased the incidence of hepatocellular carcinoma in the rats that had been treated with DBN. None of the control rats that had been fed the basal diet or the basal diet containing low or high PB or 5% SS developed either bladder or liver carcinoma. These results demonstrate that PB promotes urinary bladder carcinogenesis of rats initiated with FANFT but not with DBN. In contrast to incorporation in commercial rat chows, SS incorporated in the AIN-76A diet is very weak in promoting bladder carcinogenesis. On the other hand, PB, but not SS, promotes hepatocarcinogenesis initiated with DBN. Neither PB nor SS promoted DBN-induced carcinogenesis of esophagus or forestomach.

Animals↗
PubMed1985

Evaluation of the effects of cotinine and nicotine-N'-oxides on the development of tumors in rats initiated with N-[4-(5-nitro-2-furyl)-2-thiazolyl]formamide.

The effects of cotinine and nicotine-N'-oxides on tumor development in F344 rats initiated with N-[4-(5-nitro-2-furyl)-2-thiazolyl]formamide [(FANFT) CAS: 24554-26-5] were evaluated. When rats were 6 weeks old, FANFT in an agar diet was administered for a 6-week period. Subsequently, cotinine, trans-nicotine-N'-oxide, and a mixture of cis-nicotine-N'-oxide and trans-nicotine-N'-oxide in drinking water were given as promoters in concentrations of 0.1, 0.02, and 0.02%, respectively. These nicotine metabolites were offered ad libitum for 78 weeks. Control groups consisted of rats that received tap water with or without prior administration of FANFT. Cotinine, trans-nicotine-N'-oxide, and the mixture of cis- and trans-nicotine-N'-oxides were neither carcinogens nor promoters of urinary bladder tumors in rats initiated with FANFT. A reduced incidence of urinary bladder tumors was observed in FANFT-pretreated animals that also received a mixture of cis- and trans-nicotine-N'-oxides. FANFT administration increased the incidences of mesothelioma of the peritoneum and thyroid tumors. Tumor formation in the tongue and palate observed in FANFT-treated rats was not affected by administration of these nicotine metabolites. There was, however, a significant increase in the incidence of forestomach tumors in rats that were initiated with FANFT and subsequently received either trans-nicotine-N'-oxide or a mixture of cis- and trans-nicotine-N'-oxides.

Animals↗
PubMed1985

Low susceptibility of analbuminemic rats to induction of bladder cancer by N-[4-(5-nitro-2-furyl)-2-thiazolyl]formamide.

The susceptibility of analbuminemic rats (Nagase analbuminemic rats; NAR) to induction of bladder cancer by oral N-[4-(5-nitro-2-furyl)-2-thiazolyl]formamide (FANFT) was studied. Male NAR and Sprague-Dawley rats (SD) were fed normal diet or normal diet supplemented with 0.2% FANFT for 10 weeks and killed in week 52. Bladder cancer was found in 5 of 24 SD (21%) but not in 18 NAR (0%). Proliferative lesions of the bladder epithelium, which are considered to be precancerous or more advanced than precancerous changes, were found in 16 of 24 SD (67%), but in only 4 of 18 NAR (22%). NAR showed lower susceptibility than control SD to induction of bladder cancer by FANFT.

Animals↗
PubMed1983

Enhanced macromolecular binding of N-[4-(5-nitro-2-furyl)-2-thiazolyl]- formamide in germfree versus conventional rats.

To investigate the binding of a nitrofuran to tissue macromolecules in vivo, the urinary bladder carcinogen N-[4-(5-nitro-2-furyl)- 2-[35S]thiazolyl]formamide [[35S]FANFT; 94 mCi/mmol] was given p.o. to conventional [n = 4; 115 +/- 8 g (S.D.)] and germfree [n = 4; 105 + 5 g] female CD rats [1.23 mCi/rat]. After 18 hr, organs were removed, and macromolecules were then isolated from individual livers and kidneys and from pooled urinary bladders. A hydroxylapatite isolation procedure was followed (Beland et al., J. Chromatogr., 174: 177-186, 1979), and the nucleic acids obtained were further purified by digestion with appropriate nucleases and/or centrifugation (105,000 X g). The results are as follows and are given in pairs (conventional/germ-free) expressed as pmol FANFT bound per mg macromolecule. Protein binding levels were: liver, 165 +/- 40/307 +/- 31; kidney, 72 +/- 19/88 +/- 24; bladder, 272/322. RNA levels were: liver, 217 +/- 184/413 +/- 196; kidney, 219 +/- 60/617 +/- 196; bladder, 448/1373. DNA levels were: liver, 9.8 +/- 7.5/17.0 +/- 7.5; kidney, 0.69 +/- 0.38/4.5 +/- 1.0. The quantity of bladder DNA was insufficient for accurate measurement. Diethylaminoethyl cellulose chromatography of liver RNA from a germfree rat, either before or after RNase digestion, showed that the majority of the radioactivity was associated with a polynucleotide fraction that appeared to be RNase resistant and accounted for only a small portion of the total RNA but that also permitted the intercalation of ethidium bromide. The deformylated FANFT metabolite, 2-amino-4-(5-nitro-2-fury)thiazole, reacted with transfer RNA upon reduction with sodium dithionite in vitro to give adduct(s) that also appeared to be RNase resistant. Thus, these results show that the urinary bladder carcinogen FANFT or its metabolites react in vivo with protein and nucleic acid of both target and nontarget organs and that binding levels are elevated in germfree rats.

Animals↗
PubMedDate not supplied

Adjuvant immunotherapy of N-[4(5-nitro-2-furyl)-2-thiazolyl]-formamide-induced bladder tumors.

The prophylactic effect of maltose tetrapalmitate (MTP), a newly developed non specific immunoadjuvant in preventing or delaying bladder cancer induction by N-[4(5-nitro-2-furyl)-2-thiazolyl] formamide (FANFT) or in reducing the growth rate of the induced tumor was compared to other well-known immunoadjuvants (BCG, C. parvum, levamisole and pyran copolymer). The evaluation of the prophylactic role of immunoadjuvants demonstrated that MTP, levamisole and C. parvum were the most effective in prolonging animal survival. MTP was found superior to either of them in reducing the tumor size. The development of lung metastasis was lower in the group receiving MTP or C. parvum. Next, MTP was studied for its therapeutic effect against primary FANFT induced tumor. The subcutaneous (s.c.) and oral routes of MTP administration and their combination with intravesical route were tried. Combinations of intravesical with s.c. or oral MTP were most effective in reducing tumor size, obtaining lower metastases along with greater mononuclear lymphocyte infiltration in the primary tumor.

Adjuvants, Immunologic↗
PubMed1980

Metabolism of N-[4-(5-nitro-2-furyl)-2-thiazolyl]formamide by prostaglandin endoperoxide synthetase.

Cooxidative metabolism of the urinary bladder carcinogen N-[4-(5-nitro-2-furyl)-2-thiazolyl]formamide (FANFT) was examined using solubilized and particulate microsomal preparations from the rabbit renal inner medulla and the ram seminal vesicle. Metabolism was measured by the rate of decrease in absorbance at 400 nm. In these soluble and particulate preparations, FANFT metabolism was observed only in the presence of specific fatty acids. These fatty acids are substrates for prostaglandin endoperoxide synthetase. Structurally dissimilar inhibitors of prostaglandin endoperoxide synthetase such as indomethacin, aspirin, 5,8,11,14-eicosatetraynoic acid, ethoxyquin, and meclofenamic acid specifically inhibited FANFT metabolism. Other inhibitor and substrate specificity studies suggest that FANFT was not metabolized by nitroreductase, xanthine oxidase, lipoxygenase, lipid peroxidation, or mixed-function oxidases. In addition, the lack of detectable 2-amino-4-(5-nitro-2-furyl)thiazole formation suggests that arylformamidase was not participating in FANFT metabolism measured in these experiments. The data indicate that prostaglandin endoperoxide synthetase can mediate FANFT metabolism by a cooxidative process.

Animals↗
PubMed1981

Aspirin inhibition of N-[4-(5-nitro-2-furyl)-2-thiazolyl]formamide-induced lesions of the urinary bladder correlated with inhibition of metabolism by bladder prostaglandin endoperoxide synthetase.

The effects of aspirin on N-[4-(5-nitro-2-furyl)-2-thiazolyl]-formamide (FANFT) -induced urinary bladder lesions, endogenous bladder prostaglandin E2 synthesis, and the metabolism of FANFT by bladder epithelial microsomes were examined. Rats were fed 0.5% aspirin and/or a diet containing 0.1% or 0.2% FANFT. Bladder lesions were observed with light and scanning electron microscopy, and the prostaglandin E2 content of rat bladder was measured by radioimmunoassay. Metabolism of FANFT was measured by decreased absorbance at 400 nm. Aspirin inhibited the appearance of hyperplastic lesions induced by feeding 0.1% or 0.2% FANFT for 6 or 12 weeks. Aspirin reduced bladder prostaglandin E2 content at 1, 2, 6, and 13 weeks compared to corresponding control values. Rat and rabbit microsomal metabolism of FANFT were dependent upon specific fatty acid substrate and prevented by specific inhibitors (including aspirin) of prostaglandin endoperoxide synthetase. Other inhibitor and substrate specificity studies suggest that FANFT was not metabolized by xanthine oxidase, lipoxygenase, lipid peroxidation, or mixed-function oxidases. These results suggest that the metabolism of FANFT by prostaglandin endoperoxide synthetase may be involved in the metabolic activation of FANFT necessary for the induction of bladder cancer in rats.

Animals↗
PubMed1983

Orthotopic implantation of primary N-[4-(5-Nitro-2-furyl)-2-thiazolyl]formamide-induced bladder cancer in bladder submucosa: an animal model for bladder cancer study.

Primary bladder tumors induced in Fischer 344 inbred rats by N-[4-(5-nitro-2-furyl)-2-thiazolyl]formamide were transplanted in syngeneic rats by the intravesical, s.c., i.v., and orthotopic routes. Attempts were made to establish bladder cancer cell lines in vitro. No success was achieved in transplantation by either the s.c., i.v., or intravesical routes when primary tumor cells were transplanted as cell suspensions. Cell suspensions of primary tumors also failed to grow in culture. However, orthotopic implantation into the bladder submucosa gave 45% success. Tumor fragments obtained from either the primary tumor or its lung metastases resulted in 10.6 and 36% tumor takes, respectively, when implanted s.c. However, after one orthotopic passage in the bladder submucosa, the tumor cells injected as cell suspension grew s.c. in 14% and orthotopically in 79% of the animals. Tumor fragments obtained from orthotopic tumors and implanted s.c. resulted in 15% tumor takes. After the second orthotopic passage, tumor cells could be grown in cultures and orthotopically in 100% of animals. The technique of orthotopic implantation as well as the usefulness of this tumor model for bladder cancer studies are described.

Animals↗
PubMed1980

Neovascularization in rats during urinary bladder carcinogenesis induced by N-[4-(5-Nitro-2-furyl)-2-thiazolyl]formamide.

Neovascularization in inbred F344 rats during urinary bladder carcinogenesis induced by N-[4-(5-nitro-2-furyl)-2-thiazolyl]formamide (FANFT) was examined by scanning electron microscopic observation of vascular casts. FANFT was fed to rats at a level of 0.2% of the diet for 6, 10, or 20 weeks, and vascular casts were examined in these rats at those times and after various times on control diets. Similar foci of vascular proliferation (types I and III) were observed after the use of FANFT as previously reported during bladder carcinogenesis induced by N-butyl-N-(4-hydroxybutyl)nitrosamine. However, the vascular proliferations were observed to regress as the FANFT-induced epithelial proliferations regressed, similar to the observation of reversible hyperplasias induced by cyclophosphamide or ulceration. Type I vascular foci were present after 6 and 10 weeks, but no vascular lesions were seen through week 20 after these groups of rats were fed the control diet for 4 or more weeks. The epithelial lesions present after 6 and 10 weeks of FANFT feeding also regressed and the mucosa returned to normal as observed by light microscopy. Type III foci were present after 12 weeks and were observed through week 20 when epithelial tumors appeared. Rats fed FANFT for 10 weeks and then the control diet developed hyperplastic epithelial lesions and carcinomas by week 52, whereas those fed FANFT for 6 weeks had normal bladders through 52 weeks.

Animals↗