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PubMed1986

The failure of long-term feeding of raw soy flour, in the presence or absence of azaserine, to induce carcinogenic changes in the mouse pancreas.

The effects of feeding mice raw or heated soy flours or casein in the presence and absence of injected azaserine were investigated over a period of 18 months. Although the feeding of raw soy flour (compared with heated soy flour or casein) caused a significant inhibition of growth and an enlargement of the pancreas, there was no macroscopic evidence of pancreatic nodules in any of the six experimental groups. Microscopic examination of the pancreas revealed a somewhat higher (not significant) incidence of atypical acinar cell nodules in all animals injected with azaserine, but this difference was little influenced by the diets themselves. We concluded that raw soy flour itself has no carcinogenic effect on the mouse pancreas and does not enhance the sensitivity of the mouse pancreas to azaserine. Thus, it cannot be assumed that the appearance of pancreatic nodules constitutes an obligatory sequela of pancreatic hypertrophy and/or hyperplasia in all species of animals.

Animals↗

PubMed1997

Effects of dietary galactooligosaccharide on azaserine-induced acinar pancreatic carcinogenesis in male Wistar rats.

In the present study the effects of dietary galactooligosaccharide (GOS) on dietary fat-promoted pancreatic carcinogenesis in azaserine-treated rats were investigated. The aims of this study were to determine 1) whether GOS acts as an inhibitor of pancreatic carcinogenesis and 2) whether GOS interacts with dietary fat-promoted pancreatic tumor development. Four groups of 39 azaserine-treated rats were maintained on different experimental diets that were formulated as follows: 4.3 wt% fat-8.3 wt% GOS (low fat-low GOS), 3.5 wt% fat-27.4 wt% GOS (low fat-high GOS), 15.5 wt% fat-9.5 wt% GOS (high fat-low GOS), and 14.3 wt% fat-28.6 wt% GOS (high fat-high GOS). Autopsies were performed after 6 months (9 animals/group) and 12 months (30 animals/group). Five rats per group were treated with bromodeoxyuridine before autopsy. Parallel sections of the pancreas were stained with hematoxylin and eosin or with hematoxylin and a monoclonal antibody against bromodeoxyuridine and examined by light microscopy. A high-fat diet caused a significant decrease, whereas a diet high in GOS caused a significant increase, in absolute and relative weight of the cecum content. A high level of dietary fat caused a highly significant increase in multiplicity and incidence of pancreatic (pre)neoplastic lesions after 6 and 12 months of feeding. A high level of GOS in the diet did not influence the number of atypical acinar cell nodules or the tumor incidence in comparison with controls. Dietary fat and dietary GOS caused a significant increase in cell proliferation in atypical acinar cell nodules after six months. It was concluded that dietary GOS has no modulating effect on pancreatic carcinogenesis in azaserine-treated rats or on the tumor-promoting effect of a high-fat diet.

Animals↗

PubMed1987

Effect of castration and hormone replacement on azaserine-induced pancreatic carcinogenesis in male and female Fischer rats.

Previous reports have shown that pancreatic cancer was induced preferentially in male versus female azaserine-treated rats. This study was designed to determine the importance of estrogen and testosterone in this phenomenon. Fischer (F344) rats received a single injection of azaserine (30 mg/kg) at 21 days of age. At 28 days of age, they were weaned and divided into 12 groups of 9-10 rats as shown below. Surgery (castration or sham operation) was performed at 4 weeks of age. All drugs (estradiol, the antiestrogen tamoxifen, testosterone propionate and/or the antiandrogen flutamide) were administered, starting at weaning, in 3-week timed-release pellets until autopsy. Rats were killed 4 months after the administration of azaserine. The pancreas was weighed and prepared for quantitative histologic analysis of atypical acinar cell nodules (AACNs) which are putative preneoplastic lesions. Both number and size of AACNs were analyzed. In intact female rats, AACN burden was smaller than in intact males (P less than 0.05). Ovariectomy increased the AACN burden (P less than 0.05), while estradiol or tamoxifen treatments to ovariectomized females resorted the burden to control levels (P less than 0.05). Testosterone with tamoxifen treatment to ovariectomized females led to a significant increase in AACN burden over control values. In intact male rats, orchiectomy decreased the AACN burden (P less than 0.05). In orchiectomized rats, testosterone treatment slightly increased the AACN burden, flutamide treatment alone increased this parameter (P less than 0.05) but flutamide with estradiol decreased the AACN burden (P less than 0.01). These data strongly support the hypothesis that sex steroids play a major role in the higher incidence of pancreatic cancer in male versus female rats.

Animals↗

PubMed1988

Stimulation of the growth of azaserine-induced nodules in the rat pancreas by dietary camostate (FOY-305).

The effects of dietary camostate (FOY-305), a synthetic trypsin inhibitor, on the early stages of pancreatic carcinogenesis in the rat were studied because of earlier reports that feeding soy bean trypsin inhibitor stimulated growth and promoted carcinogenesis in the pancreas of rats. These effects are attributed to excess secretion of cholecystokinin, a trophic hormone for pancreatic acinar cells. Camostate has been shown to induce pancreatic enlargement in rats by the same mechanism. In preliminary experiments, pancreatic growth was studied in adult Fischer 344 (F344) and Lewis rats fed camostate mixed in the diet to define a level that induced pancreatic hypertrophy and hyperplasia. As little as 0.02% fed 3 days per week was effective. In a second experiment, F344 rats were injected with azaserine and thereafter were given camostate by gavage 5 days a week until autopsy 18 weeks later. In a third experiment, azaserine-treated Lewis rats were fed camostate in the diet 3 days a week for 8 or 16 weeks until autopsy. In the latter two experiments the number and size of atypical acinar cell foci and nodules (AACN) were measured in pancreas sections. Growth of acidophilic AACN was stimulated in camostate-fed groups; both the number and the size were increased in comparison with the control groups. The data suggest a promoting effect of dietary camostate on the growth of azaserine-induced preneoplastic lesions in the pancreas of both rat strains. The number of basophilic AACN was decreased in camostate-fed Lewis rats suggesting that the camostate diet also affected the phenotype of the carcinogen-induced AACN.

Animals↗

PubMed1977

Species and rat strain variation in pancreatic nodule induction by azaserine.

Subtoxic doses of azaserine induced atypical acinar cell nodules (AACN) in the pancreases of outbred Wistar rats, inbred W/LEW and F344 rats, and outbred Charles River CD-1 albino mice 4-6 months after initiation of treatment in the growing animal. These AACN apparently represented preneoplastic lesions, some of which have the potential to develop into adenomas or adenocarcinomas. Wistar and W/LEW rats were highly responsive to nodule induction; AACN developed in about 90% of the outbred Wistar rats and in all of the W/LEW rats tested. F344 rats were less susceptible and developed about 10% as many AACN as the Wistar rats. Female rats developed approximately half as many AACN as males. The mouse was intermediate in response between the F344 and the two Wistar rats. Syrian golden hamsters and strain 13 guinea pigs were relatively unresponsive. These studies of azaserine-induced AACN provided a basis for selection of carcinogenic azaserine regimens and suggested that the young male W/LEW rat was the most sensitive of the animals studied.

Animals↗

PubMed1993

Effects of pancreaticobiliary diversion and gastric fundectomy on azaserine-induced pancreatic carcinogenesis in the rat.

The effects of pancreaticobiliary diversion (PBD) and gastric fundectomy on the pancreas in azaserine-treated rats were studied over 14 months. Sham-operated azaserine-treated animals served as controls. A significant increase in pancreatic weight and total DNA and protein content was found in PBD-operated and fundectomized animals. DNA flow cytometry showed a significantly increased ratio of tetraploid to diploid cells in pancreatic tissue in both experimental groups. Mean values of all these variables were significantly higher after PBD than after fundectomy. Acidophilic atypical acinar cell foci of the pancreas were observed in all of the experimental and 75% of the control animals. The volume density of these foci was significantly higher in each experimental group than in the controls. The volume density, radioactive thymidine labeling index, and mitotic index of the foci were significantly higher after PBD than after fundectomy. Changes consistent with pancreatic adenoma were diagnosed in the PBD group only. It is concluded that not only PBD with endogenous hypercholecystokininemia, but also fundectomy with endogenous hypergastrinemia lasting about half of the life span in rats, induces pancreatic hypertrophy and enhances the development of precancerous pancreatic changes after azaserine treatment. In comparison with PBD, fundectomy caused less pronounced changes and no observable neoplasia.

Animals↗

PubMed1980

Azaserine resistance in Escherichia coli: chromosomal location of multiple genes.

Resistance to azaserine in Escherichia coli is the result of mutations in at least three different loci. All spontaneously arising azaserine-resistant mutants harbor a lesion in the aroP gene. However, a lesion in this gene is not solely responsible for resistance. All spontaneously arising intermediate-level azaserine-resistant mutants also harbor a lesion in a gene designated azaA, which lies near min 43 on the chromosome. High-level resistant mutants harbor lesions in the aroP and azaA genes and in a third gene designated azaB, which lies near min 69 on the chromosome. Transport studies demonstrate that mutants harboring lesions in the azaA gene are not defective in the transport of the aromatic amino acids, but that mutants which harbor lesions in the azaB gene are defective in phenylalanine transport but not in tyrosine or tryptophan transport.

Amino Acids↗

PubMed2003

Effects of a diet high in fish oil (MaxEPA) on the formation of micronucleated erythrocytes in blood and on the number of atypical acinar cell foci Induced in rat pancreas by azaserine.

The present study was performed to investigate the influence of fish oil on the genotoxic effects of azaserine, using the formation of micronucleated erythrocytes as a measure for the degree of initiating potency and the number and size of putative preneoplastic pancreatic atypical acinar cell foci (AACF) as a measure for the actual number of initiated cells. Male Wistar rats were treated twice i.p. with 30 mg azaserine per kg body weight to induce AACF. During the initiation/early promotion phase the rats were maintained on diets containing 5 wt% vegetable oil (safflower and high-oleic sunflower oil), 25 wt% vegetable oil, 25 wt% fat (15% vegetable oil + 10 wt% fish oil), or 25 wt% fat (5% vegetable oil + 20 wt% fish oil), respectively. One day after carcinogen treatment, the numbers of micronucleated polychromatic erythrocytes were determined in blood smears obtained from 10 animals per group. Each high-fat diet resulted in higher percentages of micronucleated polychromatic erythrocytes than the low-fat diet. Dietary fish oil did not significantly influence the number of micronucleated cells. Two weeks after carcinogen treatment, the diets containing fish oil were replaced by the diet containing 25% vegetable oil, and the animals were further maintained for about 14 wk. Pancreatic tissue slides were microscopically evaluated for the number and size of AACF. Dietary fish oil caused an increase in the number and size of AACF, although a clear dose-effect relationship was absent. It was concluded that a high level of dietary fish oil, when given during the induction/early promotion phase, enhances azaserine-induced pancreatic carcinogenesis in rats.

Animals↗

PubMed1984

Lesions induced in rodent pancreas by azaserine and other pancreatic carcinogens.

Focal proliferative changes in the acinar cells of the pancreas of rats have been induced by several systemically administered carcinogens including azaserine, N-nitrosobis(2-oxopropyl)amine, N-nitroso-(2-hydroxypropyl) (2-oxopropyl)amine, and N delta-(N-methyl-N-nitrosocarbamoyl)-L-ornithine (MNCO). Foci, nodules, and adenomas induced by these carcinogens are usually made up of atypical-appearing acinar cells that maintain a high degree of differentiation, but a minority of these lesions exhibit anaplastic cellular changes that suggest the development of malignant potential. Such anaplasia may occupy the whole of smaller lesions or may occur as a secondary focal change within larger nodules or adenomas. Many foci and nodules per pancreas have been induced by single or multiple exposures to these known genotoxic carcinogens, but relatively few of them develop into carcinomas. Azaserine and MNCO have induced acinar cell carcinomas in rats. Those induced by azaserine have exhibited a broad spectrum of histologic variants, including ductlike cystic, and undifferentiated patterns. Higher doses of MNCO have induced a second pattern of change in the pancreatic lobules of rats, which includes cystic and tubular ductlike structures that have been called cystic and tubular ductal complexes. MNCO has also induced focal acinar cell lesions, cystic and tubular ductal complexes, and adenocarcinomas in the pancreas of Syrain golden hamsters. In this species, ductal complexes are much more numerous than are proliferative lesions of acinar cells, and the histologic appearance of the carcinomas is ductlike. Hyperplasia and atypical changes were also seen in the epithelium of the intralobular ducts of hamsters.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed2001

Quantitative microvascular changes during azaserine-initiated pancreatic carcinogenesis.

Although angiogenesis is considered to be indispensable for continuous tumour growth, only very few studies have been published performing microvessel quantification during tumour progression. We measured the tumour vascularity in different stages of rat pancreatic carcinogenesis induced by azaserine and promoted by raw soya flour-containing pancreatotrophic diet. Besides the tumour samples taken at 6 (atypical acinar cell nodules), 15 (adenomas) and 20 (localised adenocarcinomas) months after carcinogen initiation, we also investigated 3 control groups: tumour-bearing host tissue of azaserine-treated rats and normal tissue of untreated rats kept on standard or pancreatotrophic diet. In contrast with the usual microvessel counting on hot spots, we determined microvascular surface density (Sv) and volume density (Vv) by electron microscopic morphometry. There was no significant difference in these respect between the control groups. At month 6 after the azaserine induction Sv and Vv showed slight, nonsignificant decrease as compared to the host control. Both values remained unchanged until the 15th month and increased significantly by the 20th month. These results may indicate comparable growth rate of tumour and new microvessels in the premalignant stages of carcinogenesis while a more intense angiogenesis than tumour growth afterwards.

Adenocarcinoma↗

PubMed1992

Overexpression of cholecystokinin receptors in azaserine-induced neoplasms of the rat pancreas.

Cholecystokinin (CCK) is a growth factor for normal pancreas. Numerous studies also suggest that CCK promotes pancreatic carcinogenesis in the rat. Our previous studies suggested that growth of preneoplastic pancreatic foci was stimulated by CCK more than that of normal pancreas. We hypothesized that such differential growth might be due to increased numbers of CCK receptors in neoplastic tissue. Azaserine-induced pancreatic carcinoma (DSL6) had an increased high-affinity CCK receptor binding capacity of 122 +/- 23 (SD) fmol/mg protein compared to 12 +/- 2 fmol/mg protein in normal pancreas (P less than 0.001). The Kd of the high-affinity site was 0.33 +/- 0.04 nM for carcinoma and 0.46 +/- 0.08 nM for normal pancreas (P less than 0.01). The amount of cholecystokinin octapeptide (CCK-8) bound to high-affinity receptor was 8.6 +/- 1.9 fmol/mg protein for DSL6 compared to 0.6 +/- 0.2 fmol/mg protein in normal pancreas (P less than 0.001). Azaserine-induced premalignant nodules were compared to remaining internodular pancreas. Nodules demonstrated a mean high-affinity CCK receptor binding capacity of 38 +/- 9 fmol/mg protein compared to 6 +/- 3 fmol/mg protein in internodular pancreas (P less than 0.001). The amount of CCK-8 bound to high-affinity receptor was 3.1 +/- 0.8 fmol/mg protein in nodules compared to 0.6 +/- 0.3 fmol/mg protein in internodular pancreas (P less than 0.001). Overexpression of high-affinity CCK-8 receptor in premalignant and malignant azaserine-induced tumors may result in a growth advantage relative to normal pancreas.

Animals↗

PubMed1989

Modulation by CR-1409 (lorglumide), a cholecystokinin receptor antagonist, of trypsin inhibitor-enhanced growth of azaserine-induced putative preneoplastic lesions in rat pancreas.

Feeding of raw soya flour or other trypsin inhibitors such as camostate is a well-established method for promoting growth of (pre)neoplastic foci induced in the exocrine pancreas of rats by azaserine. The effect of trypsin inhibitors is thought to be mediated through an increased release of cholecystokinin. Using the specific cholecystokinin receptor antagonist lorglumide (CR-1409), we performed a 16-wk study to investigate the potential of this drug in inhibiting growth of putative preneoplastic foci and to determine whether and to what extent cholecystokinin is responsible for the effect of trypsin inhibitors on pancreatic growth. After initiation with 30 mg/kg of azaserine at 19 days of age, six groups of 15 rats each received one of the following treatments: camostate, cholecystokinin-8, or gelatin control, either or not in combination with CR-1409, once daily, 3 days wk for 16 wk. Plasma cholecystokinin levels, measured 30 min after the stimulus, were similar after camostate and cholecystokinin octapeptide administration. After 16 wk the pancreata were removed, weighted, and quantitatively analyzed for the number and size of putative preneoplastic foci by light microscopy. Both camostate and cholecystokinin octapeptide stimulated pancreatic growth and development of acidophilic putative preneoplastic foci, whereas growth of basophilic putative preneoplastic foci was inhibited by camostate but stimulated by cholecystokinin. CR-1409 almost completely abolished the effect of cholecystokinin and was found to cause a significant decrease in the effects of camostate. It is concluded that (a) cholecystokinin plays a significant role in camostate-stimulated growth of acidophilic putative preneoplastic foci in rat pancreas and (b) CR-1409 inhibits growth of putative preneoplastic foci induced in rat pancreas by azaserine and hence may be of potential value for the treatment of pancreatic cancer in humans.

Animals↗

PubMed1985

Effect of raw soy flour, feeding regime, and azaserine on rat pancreas.

The combined effects of feeding rats increasing amounts of raw soy four, feeding regime (ad libitum vs one meal per day), and injection of azaserine on the incidence of pancreatic nodules were investigated over a period of 12 months. Food consumption and body weights of meal-fed rats were lower than those of their ad libitum counterparts. The difference in body weight between the ad libitum and meal-fed rats became greater as the level of raw soy flour in the diet increased. Azaserine injections did not affect food consumption or body weight. The weights of the pancreas (gm/100 gm BW) increased parallel to the level of raw soy flour in the diet. The survival rate of rats on diets containing 19% and 42% raw soy flour was greater on the meal-fed regime than in the ad libitum group, but the converse was true when the diet contained 80% raw soy flour. The number and severity of pancreatic nodules observed in azaserine-injected animals surviving at the end of 12 months increased in relation to the level of raw soy flour in the diet and was enhanced at each level by meal feeding.

Animals↗

PubMed1984

Characterization of two populations of pancreatic atypical acinar cell foci induced by azaserine in the rat.

Multiple and single intraperitoneal injections of azaserine in male Wistar/Lewis rats induced a 100% incidence of atypical acinar cell foci. The foci were histologically classified into one of two populations, basophilic or acidophilic. The number and size of transections of the foci in tissue sections were determined. By means of known mathematical relationships, focal transectional data were transformed into three-dimensional data (i.e., foci/unit volume, foci/pancreas, mean diameter and volume of foci, and focal volume as percentage of pancreas volume). In general, initiation with azaserine resulted in more acidophilic than basophilic foci. An increase in the azaserine dose from 10 to 30 mg/kg resulted in the initiation of more acidophilic and basophilic foci. Over a 6-month period following initiation, basophilic foci showed a small increase in number and no increase in size. In these same pancreases, acidophilic foci significantly increased in both number and size. A promoter of pancreatic carcinogenesis (20% unsaturated fat diet) enhanced the number and percentage of the pancreas volume occupied by acidophilic foci. This modulator of the postinitiation phase of pancreatic carcinogenesis did not have a significant effect on the basophilic foci. Unlike the basophilic foci, the acidophilic foci show considerable growth potential and appear to be responsive to modulators of carcinogenesis. Further study of this population of carcinogen-induced pancreatic foci is warranted.

Animals↗

PubMed1993

Stimulation of growth of azaserine-induced putative preneoplastic lesions in rat pancreas is mediated specifically by way of cholecystokinin-A receptors.

Cholecystokinin (CCK) has been shown to stimulate the growth of both normal pancreas and azaserine-induced putative preneoplastic pancreatic lesions in the rat. The present study was performed to determine whether these effects are mediated by way of CCK-A receptors, CCK-B receptors, or both. Sixteen-day-old male Lewis rats were given i.p. injections of azaserine at 30 mg/kg body weight. Starting on day 21, rats were given s.c. injections, 5 days/week for 16 consecutive weeks, of either (a) CCK octapeptide (nonselective CCK agonist) (2.50 micrograms/kg body weight, n = 17), (b) tert-butyloxycarbonyl-Trp-Lys(epsilon-N-2-methylphenylaminocarbonyl++ +)-Asp- (N-methyl)-Phe-NH2 (highly selective CCK-A agonist) (1.84 micrograms/kg body weight, n = 18), (c) [(2R,3S)-beta-MePhe28,N-MeNle31]CCK26-33 (highly selective CCK-B agonist) (2.40 micrograms/kg body weight, n = 18), or (d) normal saline solution (control, n = 17). Rats were subsequently sacrificed, pancreatic weights were determined, and quantitative morphometric analysis of atypical acinar cell foci and nodules was performed. Both CCK octapeptide and the selective CCK-A agonist tert-butyloxycarbonyl-Trp-Lys(epsilon-N-2- methylphenylaminocarbonyl)-Asp-(N-methyl)-Phe-NH2 stimulated pancreatic growth and the development of acidophilic atypical acinar cell foci and nodules. Furthermore, the effect produced by the selective CCK-A agonist tert-butyloxycarbonyl-Trp-Lys(epsilon-N-2- methylphenylaminocarbonyl)-Asp-(N-methyl)-Phe-NH2 was greater than that produced by CCK octapeptide. In contrast, the selective CCK-B agonist [(2R,3S)-beta-MePhe28,N-MeNle31]CCK26-33 had no effect. These findings suggest that the growth of putative preneoplastic lesions (acidophilic atypical acinar cell foci and nodules) in the rat pancreas during the early stages of azaserine-induced pancreatic carcinogenesis is mediated specifically by way of CCK-A receptors.

Animals↗

PubMed1990

Effect of tetragastrin on azaserine-induced carcinogenesis in rat pancreas.

The effect of tetragastrin on pancreatic tumors induced by azaserine was investigated in Wistar rats. Rats were given 25 weekly injections of 10 mg/kg body weight of azaserine and 1 mg/kg body weight of tetragastrin as a suspension in olive oil every other day. Carcinogen-induced pancreatic lesions were examined by histochemical techniques, and were classified as ATPase-positive or ATPase-negative. In week 62, quantitative histological analysis showed that prolonged administration of tetragastrin had little or no influence on the number and size of the carcinogen-induced pancreatic lesions, although it caused significantly increased cell proliferation, indicated by a greater labelling index of the pancreatic acinar cells.

Adenosine Triphosphatases↗

PubMed1991

Inhibition by neurotensin of azaserine-induced carcinogenesis in rat pancreas.

The effect of neurotensin on pancreatic carcinogenesis induced by azaserine was investigated in Wistar rats. Rats were given weekly injections of 10 mg/kg body weight of azaserine for 25 weeks and 200 micrograms/kg body weight of neurotensin in depot form every other day for 62 weeks. Carcinogen-induced pancreatic lesions were examined by histochemical techniques, and were classified as ATPase-positive or ATPase-negative. In week 62, quantitative histological analysis showed that prolonged administration of neurotensin significantly reduced the volume (as percent of parenchyma) of ATPase-positive pancreatic lesions, which are closely correlated with the ultimate development of pancreatic cancer. Histologically, pancreatic adenocarcinomas occurred at a significantly lower rate in rats treated with neurotensin than in untreated rats. Administration of neurotensin also significantly decreased the labelling indices of carcinogen-induced pancreatic lesions, but not of the surrounding acinar cells. These findings indicate that neurotensin inhibits pancreatic carcinogenesis, and that this may be related to the reduction of ATPase-positive lesions and to the inhibition of cell proliferation in neoplastic lesions of the pancreas.

Animals↗

PubMed1990

Azaserine-induced pancreatic carcinogenesis in rats: promotion by a diet rich in saturated fat and inhibition by a standard laboratory chow.

Dietary fat has been shown to enhance pancreatic carcinogenesis. Uncertainty still exists whether the amount of linoleic acid or the amount of fat is the main determining factor. In the present study the effects of a high lard, a low lard, a linoleic acid supplemented low lard and a laboratory chow diet were investigated on the development of (pre)neoplastic pancreatic lesions in rats treated with azaserine. The rats were killed 15 months after carcinogen treatment and the pancreata were examined for the number and size of putative preneoplastic lesions and for the occurrence of neoplasms. The linoleic acid supplemented low lard group showed a significantly increased number of basophilic foci as compared to the low lard group. Rats maintained on the linoleic acid supplemented diet or the laboratory chow developed significantly less atypical acinar cell nodules larger than 1.0 mm in diameter and adenocarcinomas as compared to the high lard group. Animals maintained on the low lard diet developed significantly less adenocarcinomas than rats on the high lard diet did. Overall, the number of benign and malignant pancreatic tumours was consistently higher in the high lard group and consistently lower in the linoleic acid supplemented low lard group than the number of these types of tumours in the low lard group, with the exception of the number of carcinomas in situ, which was lower in the high lard group. The laboratory chow group showed a significant lower number of atypical acinar cell nodules with a diameter over 1.0 mm and a lower number of adenocarcinomas as compared to both the high lard and the low lard group. It is concluded that a diet high in saturated fat has a promoting and that laboratory chow has an inhibitory effect on pancreatic carcinogenesis in azaserine-treated rats.

Animals↗