Immunohistochemical Demonstration of Intestinal‐type Alkaline Phosphatase in Stomach Tumors Induced by N‐Methyl‐N′‐nitro‐N‐nitrosoguanidine in Rats

Yuasa, Hirofumi; Hirano, Kazuyuki; Kodama, Hirohiko; Nakanishi, Hayao; Imai, Toshio; Tsuda, Hiroyuki; Imaida, Katsumi; Tatematsu, Masae

doi:10.1111/j.1349-7006.1994.tb02966.x

Cited by 23 publications

(19 citation statements)

References 16 publications

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“…[29][30][31][32][33] By sequential observation of rat glandular stomach carcinomas and comparisons of phenotypic expression of human gastric carcinoma cells between early and advanced cases, a phenotypic shift from gastric to intestinal epithelial cell type expression has been recognized with progression of each histological type of gastric carcinomas. [33][34][35][36] The present results regarding phenotypic expression of tumor cells showed that mouse glandular stomach adenomas and carcinomas consist solely of tumor cells of gastric epithelial cell type, without any intestinal metaplasia in the mucosa surrounding carcinomas.…”

Section: Discussionmentioning

confidence: 99%

N‐Methyl‐N‐nitrosourea Concentration‐dependent, Rather than Total Intake‐dependent, Induction of Adenocarcinomas in the Glandular Stomach of BALB/c Mice

Yamachika

Nakanishi

Inada

et al. 1998

Japanese Journal of Cancer Research

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The influence of the level of carcinogen exposure on histopathological types and cellular differentiation of the induced tumors was examined in 100 male BALB/c mice given N-methyl-Nnitrosourea (MNU) in their drinking water at 240 ppm on alternate weeks (total exposure: five weeks) (group 1), at 120 ppm similarly (total exposure: ten weeks) (group 2), at 60 ppm for 20 weeks continuously (group 3), or at 30 ppm for 40 weeks continuously (group 4). Forty-three differentiated and 17 undifferentiated type adenocarcinomas were induced. Glandular stomach carcinomas and undifferentiated type lesions were more common in mice treated with a high concentration of MNU for a short period than with a low concentration of MNU for a long period, even though total measured intake of MNU was smaller (P< < < <0.01). All the induced glandular stomach carcinomas, independent of the treatment schedule, consisted entirely of gastric phenotype cells. In conclusion, the induction of glandular stomach cancers and the proportion of undifferentiated type lesions depend not on the total quantity, but rather on the concentration of the carcinogen, while the phenotypic expression of tumor cells is not affected by the differences in the administration protocol.

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Section: Discussionmentioning

confidence: 99%

N‐Methyl‐N‐nitrosourea Concentration‐dependent, Rather than Total Intake‐dependent, Induction of Adenocarcinomas in the Glandular Stomach of BALB/c Mice

Yamachika

Nakanishi

Inada

et al. 1998

Japanese Journal of Cancer Research

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“…We have proposed [27][28][29][30][31] that, in humans, intestinal metaplasia and the appearance of the intestinal epithelial cell phenotype in gastric carcinomas during carcinogenesis are independent phenomena, although it had earlier been suggested 9) that the intestinal-type carcinomas might develop from intestinal metaplasia and that diffuse-type carcinomas might originate from nonmetaplastic mucosa.…”

Section: Discussionmentioning

confidence: 99%

“…(Received July 22, 1997/Revised October 6, 1997 Revised November 27, 1997/Accepted November 27, 1997) …”

Section: Acknowledgmentsmentioning

confidence: 99%

Increased Expression of Sucrase and Intestinal‐type Alkaline Phosphatase in Human Gastric Carcinomas with Progression

Nakamura

Inada

Hirano

et al. 1998

Japanese Journal of Cancer Research

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The activities of sucrase, total alkaline phosphatase (total ALP) and intestinal-type alkaline phosphatase (I-ALP) were assayed in gastric carcinomas and in their surrounding mucosae from 57 patients with advanced cancers, and the localization of sucrase in 203 carcinomas, including 86 early cancers, was examined immunohistochemically using polyclonal anti-sucrase antibody. All three enzymes were active in the 57 carcinomas as well as in their surrounding mucosae, but the levels were fairly low as compared to those in normal jejunum mucosa. A considerable part of the total ALP activity in tumor specimens was assumed to be due to I-ALP itself. Increased sucrase and I-ALP were found with greater depth of invasion by undifferentiated-type carcinomas. The pattern of immunohistochemical localization of sucrase in the 203 carcinomas also clearly indicated increased expression with greater depth of invasion even in differentiated-type carcinomas.

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“…Anti-rat Pg1 20 and anti-rat I-ALP antibodies were prepared 16 for immunohistochemical analyses. The avidinbiotin complex method with a Vectastain ABC kit (Vector Laboratories Inc., Burlingame, CA) was used for detection.…”

Section: Immunohistochemical Enzyme Histochemical and Mucin Histochementioning

confidence: 99%

“…However, there are differences with regard to intestinal change in the stomach between the human and mouse cases. We have examined carcinogenesis with MNU in six strains of mice (BALB/cA, C57BL/6N, CBA/JN, C3H/HeN, DBA/2N, and CD-1) and the typical intestinal metaplasia and intestinal type gastric tumors which appear in the rat 15,16 were not observed, despite the fact that the lesions positive for intestinal alkaline phosphatase (I-ALP), a marker of intestinal absorptive cells, could be detected with immuno-and enzyme-techniques 17 . Since intestinal metaplasia is commonly observed in the human stomach of old individuals, it could be considered as an age-related change.…”

Section: Introductionmentioning

confidence: 99%

Gastric Carcinogenesis and Intestinalization Induced by N-methyl-N-nitrosourea in the Senescence-Accelerated Mouse(SAMP3).

et al. 2003

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Abstract:The relationship between gastric neoplasia and intestinal metaplasia, a process whose incidence increases with age, remains controversial. In the present experiment, we therefore investigated induction of both intestinal metaplasia and gastric cancers in the Senescence-accelerated mouse (SAMP3/Aicc) treated with N-methyl-N-nitrosourea (MNU). Seven-week-old animals of both sexes received the carcinogen in their drinking water at 120 or 60 ppm on alternative weeks for 10 weeks, or continuously at 30 ppm for the same period, then maintained without further treatment until sacrificed at week 50. The incidences of adenocarcinomas in the 120, 60, and 30 ppm MNU treated and control groups were 6/10 (60%), 5/16 (31.3%), 1/17 (5.9%), and 0/6 (0%) in males, and 2/7 (28.6%), 3/13 (23.1%), 1/6 (16.7%), and 0/9 (0%) in females, respectively. All neoplasms were of well-differentiated type, mainly consisting of gastric epithelial type cells. With immuno-and enzyme-histochemistry, intestinal alkaline phosphatase (I-ALP) positive intestinal absorptive cell-like elements were observed in regions of hyperplasia, adenomas, and adenocarcinomas of MNU treated mice, but no phenotypic expression of goblet or Paneth cells was found. In the control mice, gastric mucosa showed no intestinal epithelium phenotype. Since the degree of appearance of I-ALP positive cells in the lesions in SAMP3/Aicc mice was not different from that found for six other strains mice in our previous work, the results suggest that Senescence-acceleration may not influence intestinalization in the gastric mucosa or induction of gastric carcinomas. (J Toxicol Pathol 2003; 16: 33-39)

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Immunohistochemical Demonstration of Intestinal‐type Alkaline Phosphatase in Stomach Tumors Induced by N‐Methyl‐N′‐nitro‐N‐nitrosoguanidine in Rats

Cited by 23 publications

References 16 publications

N‐Methyl‐N‐nitrosourea Concentration‐dependent, Rather than Total Intake‐dependent, Induction of Adenocarcinomas in the Glandular Stomach of BALB/c Mice

N‐Methyl‐N‐nitrosourea Concentration‐dependent, Rather than Total Intake‐dependent, Induction of Adenocarcinomas in the Glandular Stomach of BALB/c Mice

Increased Expression of Sucrase and Intestinal‐type Alkaline Phosphatase in Human Gastric Carcinomas with Progression

Gastric Carcinogenesis and Intestinalization Induced by N-methyl-N-nitrosourea in the Senescence-Accelerated Mouse(SAMP3).

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