Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0596263 (carcinogenesis)
 64,820 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The data on the changes in the isoenzyme spectrum of pepsinogen-pepsin inversely correlating with the development and retaining of the malignant condition of gastric mucosa in human and animals are reviewed. The results of the molecular-genetic studies of gastric carcinogenesis, in particular the role of protooncogenes--oncogenes in this process are presented.
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PMID:[Biochemical and molecular biology characteristics of gastric carcinogenesis in humans and animals]. 240 39

Pepsinogen mRNA is shown to be the major fraction of rat poly (A)+RNA. It codes polypeptide with molecular weight of about 45 kD. Changes in the pepsinogen mRNA content at the early stage of carcinogenesis are nonspecific and are due to the toxic effect of MNNG. Steady shifts in the quantity of pepsinogen mRNA are found between the 1st and 3d months. Pepsinogen mRNA content decreases down to the half of the normal one between the 3d and 6th months. A quantity of RNA capable to be a template for pepsinogen synthesis is reduced by more than 90% in the MNNG induced tumour. The pepsinogen production defect in gastric mucosa neoplasia is mainly due to pepsinogen mRNA synthesis damage.
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PMID:[Changes in the content of pepsinogen messenger RNA in the gastric mucosa of rats during N-methyl-N'-nitro-N-nitrosoguanidine-induced carcinogenesis]. 243 20

Epithelial cell differentiation was evaluated in 15 samples of duct-acinar dysplasia, a putative premalignant lesion of the prostate, through immunohistochemical staining for five differentiation markers. Prostate-specific antigen (PSA), prostatic acid phosphatase (PAP), Leu-7, pepsinogen II (PG II), and tissue plasminogen activator (t-PA) are all constituents of seminal fluid that are produced by prostatic epithelium. Dysplasia foci were classified into three grades of severity and their locations mapped by camera lucida drawings of each slide. The degree of abnormal staining with each antibody was recorded on the map, and its correlation with dysplasia grade was evaluated. PSA, PAP, and Leu-7 staining were reduced in dysplasia and often absent in severe dysplasia, indicating that reduced differentiation is an early change in prostatic carcinogenesis. PG II and t-PA stains were sometimes positive in a region where they are usually absent, suggesting that deregulation of differentiation markers may accompany reduction in differentiation in these preneoplastic lesions.
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PMID:Immunohistochemical evidence for impaired cell differentiation in the premalignant phase of prostate carcinogenesis. 245 43

The cell kinetics of pepsinogen isozyme 1 altered pyloric gland (PAPG) cells with low pepsinogen isozyme 1 (Pg 1) content were analysed using double immunohistochemical staining for bromodeoxyuridine (BrdU) incorporation and Pg 1 in male WKY/NCrj rats treated with N-methyl-N'-nitro-N-nitrosoguanidine (MNNG). After administration of 100 micrograms/ml MNNG for 10 weeks in the drinking water, carcinogenic insult was terminated and the animals killed two weeks later. BrdU was given either as a single i.p. injection (100 mg/kg b.w.) 1 h prior to death or continuously by osmotic minipump (120 micrograms/h) for 4, 7 and 10 days before killing. Immunogold-silver staining was used to detect BrdU and the avidin-biotin-peroxidase complex method adopted for demonstration of Pg 1. PAPG were found only in the MNNG treated group: their frequency was 4.1 +/- 0.6 per 100 pyloric glands. Almost no normal pyloric gland cells with high Pg 1 content demonstrated incorporation after BrdU flash labelling. However, a few pyloric gland cells in PAPG were labelled. The number of labelled cells in the pyloric columns containing PAPG was larger (P less than 0.05) than in normal pyloric columns. After continuous BrdU administration, the life span of cells comprising PAPG was estimated to be approximately 6-8 days while that of normal pyloric gland cells was approximately 11-13 days. Thus, the data indicate that PAPG cells demonstrate a degree of independence from surrounding pyloric glands with regard to proliferation kinetics, suggesting that PAPG is a preneoplastic lesion involved in gastric carcinogenesis.
Carcinogenesis 1989 May
PMID:Proliferation kinetics of pepsinogen altered pyloric gland cells in rats treated with N-methyl-N'-nitro-N-nitrosoguanidine. 270 44

Three groups of male Fischer rats were given single doses of N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) at 160 mg (group 1), 80 mg (group 2) and 40 mg (group 3)/kg body weight by gastric intubation. A fourth group was given drinking water containing 100 micrograms/ml of MNNG for 2 weeks, and a fifth group served as a control. Rats were killed in weeks 5, 8 and 12. Serial sections of the pyloric mucosa were examined by paradoxical concanavalin A (Con A) staining and pepsinogen isozyme 1 (Pg 1) immunostaining. All pyloric glands contained class III mucin as detected by paradoxical Con A staining. Most pyloric glands had a high Pg 1 content, but a few stained only weakly if at all. The percentage and number (No./500 normal-looking pyloric glands) of pyloric glands with a low Pg 1 content were 50.0 and 0.2 +/- 0.4 (week 5), 87.5 and 0.5 +/- 0.4 (week 8) and 100.0 and 1.2 +/- 1.0 (week 12) in group 1, 50.0 and 0.2 +/- 0.3 (week 8) and 87.5 and 0.5 +/- 0.4 (week 12) in group 2, and 30.0 and 0.2 +/- 0.4 (week 12) in group 4. No pyloric glands with a low Pg 1 content were found in groups 3 and 5. Thus the results showed significant dose-dependent induction (P less than 0.05-0.01) of altered pyloric glands demonstrating reduced Pg 1 content and their earlier appearance in groups given higher doses of MNNG. The results suggest that the appearance of pyloric glands with a low Pg 1 content may be a preneoplastic change in gastric carcinogenesis.
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PMID:Immunohistochemical demonstration of induction of pyloric glands with low pepsinogen 1 (Pg 1) content in rat stomach by N-methyl-N'-nitro-N-nitrosoguanidine. 308 14

Sequential changes of numbers of pepsinogen 1 (Pg 1)-decreased pyloric glands (PDPG) detected by immunohistochemistry and of the incidence of gastric carcinomas were examined in five different strains of rats treated with N-methyl-N'-nitro-N-nitrosoguanidine (MNNG;CAS:70-25-7). Male SD (Crj:CD), WKY (WKY/NCrj), Lewis (LEW/Crj), Wistar (Crj:Wistar) and F344 (F344/DuCrj) rats (40 per strain), were given drinking water containing 100 micrograms/ml MNNG for 30 weeks and then normal tap water, and were killed at week 10, 30 and 50 of the experiment. Adenocarcinomas of the glandular stomach were found in nine of 15 SD rats (60%), in eight of 12 WKY rats (67%), in eight of 15 Lewis rats (53%), in three of 13 Wistar rats (23%) and in one of 18 F344 rats (6%) at week 50. These incidences of carcinomas in SD, WKY and Lewis were significantly higher (P less than 0.01) than that in F344 rats. From week 10, the numbers of PDPG in SD, WKY and Lewis rats were significantly greater (P less than 0.01) than that in F344 rats. From week 30, the numbers of PDPG in Wistar rats were also significantly greater (P less than 0.05-0.01) than that of F344. The susceptibility of rats to induction of gastric carcinoma by MNNG correlated with the susceptibility to induction of PDPG by MNNG in each strain, suggesting that induction of PDPG is a preneoplastic change in chemical gastric carcinogenesis.
Carcinogenesis 1988 Mar
PMID:Coefficient induction of pepsinogen 1-decreased pyloric glands and gastric cancers in five different strains of rats treated with N-methyl-N'-nitro-N-nitrosoguanidine. 334 88

The appearance of pyloric gland-type cells with a low pepsinogen isozyme 1 (Pg 1) content in the stomach mucosa of F344/Du rats during stomach carcinogenesis was examined by a combination of paradoxical concanavalin A (Con A) staining and immunohistochemical staining for Pg 1. Male F344 rats were given drinking water containing 100 micrograms N-methyl-N'-nitro-N-nitrosoguanidine [(MNNG) CAS: 70-25-7]/ml for 30 weeks and then normal tap water and were killed in week 10, 20, 30, 40, 50, or 70. Untreated rats were killed in week 30 or 70. Serial sections of pyloric mucosa were stained by paradoxical Con A staining and Pg 1 immunostaining. After MNNG treatment, tissues showing changes were classified into normal-looking pyloric mucosa with a low Pg 1 content, mucosa showing atrophic or hyperplastic changes, adenomatous hyperplasia, and adenocarcinoma. From the results of paradoxical Con A staining and Pg 1 immunostaining, the cells in lesions were classified into gastric types (surface mucous cell type and pyloric gland cell type) and intestinal types (intestinal-absorptive cell type and goblet cell type). In this experiment, the cells in lesions were mainly of the gastric cell types. All pyloric glands of control rats in weeks 30 and 70 contained class III mucins and had a high Pg 1 content demonstrated immunohistochemically. After MNNG treatment, class III mucin-positive pyloric glands with a low Pg 1 content in normal-looking pyloric mucosa were found from week 10; subsequently, their number increased with time. Changed mucosa was found from week 20, and the area of cells of the pyloric gland cell type with little or no Pg 1 in changed mucosa was about 30% of the area of cells of the pyloric gland cell type. Adenomatous hyperplasias were found from week 30; adenocarcinomas were found from week 50. Almost all cells of the pyloric gland cell type (greater than 95%) in areas of adenomatous hyperplasia and adenocarcinomas had little or no Pg 1 content. The present results suggested that the appearance of pyloric glands with a low Pg 1 content in normal-looking mucosa might be an immunohistochemically detectable preneoplastic change preceding morphologically detectable preneoplastic changes in stomach carcinogenesis.
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PMID:Immunohistochemical demonstration of pyloric gland-type cells with low-pepsinogen isozyme 1 in preneoplastic and neoplastic tissues of rat stomachs treated with N-methyl-N'-nitro-N-nitrosoguanidine. 347 May 52

The paper discusses changes occurring in the enzymatic activity of pepsin in rat's gastric mucosa at early stages of carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine treatment with drinking water. All doses (5, 15, 45, 75 and 150 mg/l) proved to be effective and inhibited pepsinogen biosynthesis considerably. Particularly sharp drops in the enzyme activity were observed with the concentrations of 45, 75 and 150 mg/l. The effect was reversible at early stages, particularly, at low concentrations of the agent. It is suggested that the critical point reached by pepsinogen synthesis in gastric mucosa carcinogenesis, which is manifested by the enzyme synthesis resumption on treatment being suspended, may be regarded as the check point in the course of neoplastic development.
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PMID:[Changes in the pepsin activity of the gastric mucosa of rats in the early stages of carcinogenesis]. 393 73

A model of gastric tumour induced by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) in rats made it possible to detect essential alterations of chromatin-DNA-protein complexes, that is a weakening of the DNA-protein linkage. The changes appear at early stages of carcinogenesis and persist in induced adenocarcinomas of the stomach. Simultaneously an inhibition was established in pepsinogen synthesis during MNNG carcinogenesis, which reflects a damage in expression of functionally important genetic information. This fact shows a molecular-genetic connection between the process of the gastric mucosa malignization and a disturbance of physiologically important tissue-specific gene functions.
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PMID:[Changes in the supramolecular structure of chromatin and pepsinogen synthesis in the gastric mucosa of rats undergoing N-methyl-N'-nitro-N-nitrosoguanidine-induced carcinogenesis]. 394 55

Biochemical changes in the stomach mucous membrane of rats treated with N-methyl-N-nitro-N-nitrosoguanidine (MNNG) were studied. Carcinogenesis was shown to involve considerable changes in gastric mucous membrane, e. g. disorders in biosynthesis of isoforms of pepsinogen-pepsin. Their level and proteolytic activity are gradually declined. This effect can be reversed at an early stage of treatment and is persistent in advanced tumors of glandular part of rat stomach.
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PMID:[Biochemical changes in the glandular part of the rat stomach as affected by N-methyl-N'-nitro-N-nitrosoguanidine]. 679 54


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