Host Resistance to Gastric Adenocarcinomatosis in Three Strains of Rats Ingesting N-Methyl-N′-Nitro-N-Nitrosoguanidine

Bralow, S. P.; Gruenstein, Margot; Meranze, David R.

doi:10.1159/000224732

Cited by 40 publications

(6 citation statements)

References 10 publications

(15 reference statements)

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“…The increased tumour incidence, reduced induction time and potent hyperplastic activity of MSS (Tudor et al, 1983) are all characteristic of the action of skin promoters (Boutwell et al, 1982) and in an operational sense, MMS clearly acts as a promoter of carcinogenesis in the rat urinary bladder. In the present experiment, however, as in many other bladder promotion studies (see Hicks, 1983b) (Severs et al, 1982 (Bralow et al, 1973;Martin et al, 1974).…”

Section: Pathology Of Other Organssupporting

confidence: 64%

The “promoting” activity of methyl methanesulphonate in rat bladder carcinogenesis

Tudor¹,

Severs²,

Hicks³

1984

Br J Cancer

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Summary The carcinogenic activity of the alkylating agent methyl methanesulphonate (MMS) was investigated in the F344 rat bladder, both untreated and pretreated with a single threshold dose of N-methyl-N-nitrosourea (MNU). On its own, 6 doses of 2.5mg MMS produced a 7% incidence of bladder cancer. After a single intravesical instillation of MNU, the same MMS treatment produced a bladder cancer incidence of 56%. This was significantly higher than the incidence (24%) observed after treatment with MNU alone, and greater than the sum of the lesions produced by either treatment alone. By reference to the mouse skin multistage carcinogenesis model, it is argued that MMS is a complete, albeit weak carcinogen with little initiating but powerful late-stage activity. Its promoting activity is most probably attributable to its potent mitogenic action and in this model it is analogous to a stage 2, rather than a stage 1 skin promoter.

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Section: Pathology Of Other Organssupporting

confidence: 64%

The “promoting” activity of methyl methanesulphonate in rat bladder carcinogenesis

Tudor¹,

Severs²,

Hicks³

1984

Br J Cancer

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“…MNNG is a nitrosamide with mutagenic and carcinogenic properties. In the extremely sensitive Wistar rats adenocarcinomas were obtained in 73% at the 83 mg/l dose within 1 year [2]. In contrast, the mouse is relatively resistant to the carcinogenic actions of MNNG.…”

Section: Discussionmentioning

confidence: 99%

Effects of Helicobacter pylori and bile on N-methyl-N′-nitro-N′-nitrosoguanidine exposed antral mucosa of C57BL/6 mice

et al. 2001

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The aim of this study was to evaluate the early influence of Helicobacter pylori infection on cell kinetics in the antral mucosa of mice exposed to N-methyl-N'-nitro-N'-nitrosoguanidine (MNNG) and bile alone or in combinations. Four hundred and one C57BL/6 male and female mice were assigned into seven treatment groups and one non-treated control group. The gastric antrums were assessed by histology and immunohistochemistry for studies of cell proliferation and apoptosis at 32 and 44 weeks. One female and one male mouse had developed dysplastic adenomas in the pylorus mucosa and one male animal had dysplastic proliferation in the antrum. Only one of these lesions occurred in a H. pylori colonized animal. H. pylori infection significantly increased the cell proliferation at 32 weeks and promoted the cell proliferation in the MNNG and bile group at 44 weeks. Female mice showed less increase in cell proliferation than did the males. No change in apoptosis was seen in any of the groups. Bile had no promotional effect on cell proliferation. These results indicate that H. pylori infection has the potential to alter epithelial cell kinetics as well as antrum mucosa of an animal species that is regarded as resistant to MNNG. However, this change is not sufficient to promote the early development of neoplastic lesions.

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“…However, an active gastric ulcer was lacking in any of our cases with phenotype B: one patient had a pyloric channel ulcer and one a scar after a healed gastric ulcer. The phenotype B has also been related to gastric carcinoma (60,61,62). Indeed our own experience (63) and that of others (60)(61)(62)(64)(65)(66) suggest that in gastric cancer the antral mucosa is, in general, more often and more severely affected than the body and, in addition, the antral area is probably the predilection site of GC.…”

Section: Discussionmentioning

confidence: 99%

“…The phenotype B has also been related to gastric carcinoma (60,61,62). Indeed our own experience (63) and that of others (60)(61)(62)(64)(65)(66) suggest that in gastric cancer the antral mucosa is, in general, more often and more severely affected than the body and, in addition, the antral area is probably the predilection site of GC. Moreover, our statistical calculation (67) shows that a subject with severely affected antral mucosa carries about a 20 times higher than expected risk to get GC.…”

Section: Discussionmentioning

confidence: 99%

Abstract

1987

Scandinavian Journal of Gastroenterology

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Kekki M, Siurala M, Varis K, Sipponen P, Sistonen P, Nevanlinna H R. Classification principles and genetics of chronic gastritis. Scand J Gastroenterol 1987,22 (suppl. 141) 1-28.Two family samples, (i) a sample considered to represent the population at large (431 subjects) and (ii) a sample of first-degree relatives of index subjects (IS) with overt pernicious anaemia (183 subjects) were analyzed in order to evaluate the onset and course of chronic gastritis (CG) and the pathogenetic factors involved with special reference to the effects of genetic variation.The analysis was based on data obtained from two generations: first generation (sibs of the IS) and second (children of the IS). Formulae derived from Poisson process were used for age-correction of the gastritic changes. Otherwise, conventional statistical methods were used in the genetic analysis and the calculation of prevalences of CG. This approach enabled us to achieve a classification of gastritis into more spesific subgroups and to evaluate the natural course of the disease. The progression of gastritis in the second generation (children; mean age 35 years) was roughly similar in antrum and body, indicating that gastritis starts as a diffuse process affecting both areas of the stomach to a rather similar degree. The start of CG and its progression is at least to some degree influenced by genetic factors and probably regulated by the male sex. Thus nearly all children of male IS'S with a non-atrophic mucosa (normal mucosa or superficial gastritis) showed a normal mucosa suggesting the existence of a particular sex-bound, genetic mechanisms. These mechanisms may prevent or delay the progression of gastritis up to middle age, when a change in dynamics occurs leading to formation of more spesific subtypes of CG. In the first generation (mean age 60 years) CG dispersed into more spesific subtypes (corresponding to types A and B of Strickland and McKay and type AB of Glass) and to more advanced stages, which were connected with a higher than expected prevalence of advanced stages also in the relatives. The families of Is's with type A atrophic gastritis (AG) (severe AG in the body but no AG in antrum), type B (AG in antrum but no AG in body) and type AB AG (AG in both antrum and body) showed typical dynamic patterns of the age-spesific prevalences of AG. Genetic calculations showed that the type A of AG found in pernicious anaemia patients and their relatives is inherited by a simple dominant gene, while this type of inheritance is statistically unlikely in the type B of AG. The type B, on the other hand, exhibited characteristics that indicate a recessive Mendelian inheritance. However. more data are needed for clarification of the genetic background of the type B.As a whole the analyses indicate that genetic factors participate on different levels in the onset and progression of CG, i.e., at the start and early progression of CG and at the formation of the spesific subtypes of CG. The onset and progression of CG can be expressed in simple morphological te...

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Host Resistance to Gastric Adenocarcinomatosis in Three Strains of Rats Ingesting N-Methyl-N′-Nitro-N-Nitrosoguanidine

Cited by 40 publications

References 10 publications

The “promoting” activity of methyl methanesulphonate in rat bladder carcinogenesis

The “promoting” activity of methyl methanesulphonate in rat bladder carcinogenesis

Effects of Helicobacter pylori and bile on N-methyl-N′-nitro-N′-nitrosoguanidine exposed antral mucosa of C57BL/6 mice

Abstract

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