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)

13 patients with extrahepatic bile duct carcinoma treated in our institute from 1960 to 1986 are reported. All were proven by pathology. There were 10 moderately differentiated or mucin adenocarcinomas, 2 poorly differentiated and 1 undifferentiated cancers. There were 9 males and 4 females with an average age of 60.6 years. Progressive obstructive jaundice was the most common presenting symptom (11/13). Hepatomegaly was found in 7 patients, distended gallbladder in 4 and gallstone in 2. Before operation, 10 patients were misdiagnosed as hepatitis, cholecystitis or cholelithiasis. During operation, regional lymph node metastasis was observed in the majority of patients. Palliative operation was performed in 10 patients and radical surgery in 3. Three received operation plus postoperative radiotherapy. None survived more than two years. The lesions occurred frequently in the upper bile duct (8 patients). The middle bile duct and diffuse type carcinomas comprised 2 each. One was not recorded clearly. The prognosis is related to the gross type of the tumor and differentiation degree. Finally, carcinogenesis is discussed briefly.
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PMID:[Carcinoma of the extrahepatic bile duct--report of 13 patients]. 285 Jan 47

Two new epithelial cell lines from sporadic human colorectal adenomas designated S/AN and S/RG are reported. S/AN was from a villous adenoma and S/RG from a tubular adenoma. Both cell lines have extended growth capacities in vitro reaching passages 18 and 15, respectively, so far and show no signs of senescence. S/AN and S/RG have retained in vitro the ability to form mucin-producing goblet-like cells. Every cell of S/AN has a deletion on the short arm of chromosome 1 and one normal copy of chromosome 1. S/AN is also monosomic for chromosome 18. The majority of cells of S/RG only have one normal copy of chromosomes 6, 7, 14, 17, 18, and 22. S/RG also has several marker chromosomes. Although aneuploid S/AN and S/RG are nontumorigenic in athymic nude mice, these cytogenetic abnormalities are insufficient for the fully tumorigenic phenotype. The common abnormality for S/AN and S/RG is monosomy for chromosome 18, indicating that this is a central and important step in colorectal carcinogenesis. Our cytogenetic analysis of the adenoma cell lines suggests at least two possible routes by which premalignant colonic cells can develop and progress to malignancy. S/RG, unlike most other adenoma cell lines, is clonogenic. Aneuploidy, clonogenicity, and extended in vitro growth capacity may therefore be useful in vitro markers for adenoma cell lines with a relatively high malignant potential.
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PMID:Specific cytogenetic abnormalities in two new human colorectal adenoma-derived epithelial cell lines. 291 57

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

Preneoplastic mucosal changes were studied at six different time-points during dimethylhydrazine (DMH)-induced colorectal carcinogenesis in the rat. After 40 weeks of treatment, seven of 10 animals were bearing a total of 11 colorectal adenocarcinomas. The crypt cell production rate in the normal mucosa of DMH-treated animals was greatly increased in the left colon and rectum and further rose with the duration of the experiment. Focal disturbances of the mucosal architecture could be detected as early as 4 weeks after the initiation of DMH-treatment using a stereomicroscope. Their incidence was greatest in the left colon and rectum and increased strongly with the duration of carcinogen exposure. Characterization of these mucosal alterations, by means of conventional histology, morphometry after microdissection, cell kinetics, mucin histochemistry and quantitative enzyme histochemistry performed with serial sections, revealed mild epithelial dysplasia, a considerable elongation and dilatation of the crypts and a marked increase of the crypt cell production, including a shift of the main proliferative compartment from the basal to the medial crypt segment as well as the occurrence of mitotic figures in the luminal epithelium. In affected crypts, the goblet cells completely lacked sulphomucins and exclusively contained sialomucins. The activities of the enzymes diaminopeptidase IV (brush-border), succinate dehydrogenase (mitochondria) and acid beta-galactosidase (lysosomes) were markedly reduced. We conclude that these early mucosal alterations are indeed preneoplastic lesions and indicate the existence of the adenoma-carcinoma sequence in this animal model.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Characterization of stereomicroscopically identified preneoplastic lesions during dimethylhydrazine-induced colonic carcinogenesis. 314 93

The expression of large and small intestinal mucin antigens (LIMA and SIMA) was investigated in 30 gastrectomy specimens of carcinoma and in 11 controls resected for various pathologic conditions. One hundred eighty-five samples of normal mucosa, hyperplasia, intestinal metaplasia (types I, II, and III), dysplasia, and tumor were studied to identify phenotypes indicative of premalignant change. Our results showed LIMA and SIMA were not detected in normal gastric epithelium from either control or carcinoma specimens. SIMA characterized goblet cell mucin in all types of intestinal metaplasia and was not discriminatory between controls and carcinoma groups. On the other hand, LIMA was extensively expressed in columnar and goblet cells in carcinoma-bearing stomachs (97 per cent) but was absent in controls. There was a crescendo intensity and frequency of LIMA staining in an inverse relation to the degree of cell maturation and differentiation from type I intestinal metaplasia (60 per cent) to type II (85 per cent), type III (100 per cent), and dysplasia (100 per cent). In contrast, intestinal metaplasia of any type in controls did not show LIMA. The distribution of LIMA seemed to be intimately related to cell differentiation in the proliferative zone at the base of metaplastic glands. Carcinomas revealed antigenic phenotype heterogenicity. Our data indicate that LIMA sharpens the diagnosis of dysplasia, discriminates between reactive and preneoplastic epithelium (particularly within intestinal metaplasia), and detects abnormal phenotypes that may represent early stages in carcinogenesis.
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PMID:Expression of intestinal mucin antigens in the gastric epithelium and its relationship with malignancy. 327 79

A non-tumorigenic epithelial cell line designated PC/AA, derived from a large pre-malignant colorectal adenoma from a patient with familial polyposis coli (also referred to as hereditary adenomatosis of the colon and rectum) has become immortal in vitro. PC/AA has been passaged in vitro continuously for over 4 years and shows no signs of senescence. At early passage, PC/AA has a normal diploid karyotype but with late passage is showing signs of progression, becoming aneuploid and displaying signs of morphological transformation. Every cell examined of late-passage PC/AA has an isochromosome (1q), and one other marker chromosome which is probably derived from an additional chromosome 8. The majority of cells examined have 48 chromosomes. Despite showing signs of progression in vitro, late-passage PC/AA has remained non-tumorigenic in athymic nude mice and retained morphological differentiation characteristics of colonic cells, in particular the ability to synthesize and secrete mucin. Two other cell lines derived from small adenomas did not become immortal in vitro and were also non-tumorigenic in athymic nude mice. The isolation of an immortal pre-malignant human epithelial cell line could prove invaluable in studies on human carcinogenesis and tumour progression. Our results, showing that only a large adenoma and no small adenomas have given rise to immortal cell lines, raise the possibility that the acquisition of in vitro immortality is associated with a relatively late stage in the adenoma-carcinoma sequence. The possible involvement of chromosome 1 in tumour progression is discussed.
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PMID:Immortalization of a human colorectal adenoma cell line by continuous in vitro passage: possible involvement of chromosome 1 in tumour progression. 337 63

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 integrity of the colonic mucin layer has been reported to be altered during carcinogenesis in both humans and rodents. Prior to attempting scanning microscopic techniques on colonic mucosa of patients at high risk to develop colorectal cancer, these procedures were performed on colonic mucosa from rats with chemically induced colon cancers. Substantial technical difficulties in preparation and serious subjectivity in interpretation of the scanning micrographs were encountered. The major technical problem was the unpredictable retention of the mucin layer upon both normal and cancerous mucosae. Visual interpretation of the integrity or disruption of the mucin layer with the scanning electron microscope revealed variable fenestration and fraying of the mucin in both normal and cancerous colons. Our findings suggest that scanning electron microscopy of colonic mucin may not be a reliable screening procedure for (pre)cancerous changes in human colonic mucosae.
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PMID:Scanning microscopy of colonic mucin during carcinogenesis: is it clinically applicable? 361 29

The effects of combined administration of propranolol and tetragastrin on gastric acid secretion and the incidence and histological types of gastric adenocarcinomas induced by N-methyl-N'-nitro-N-nitrosoguanidine were investigated in inbred Wistar rats. Prolonged administration of tetragastrin, 1 but not 0.2 mg/kg body weight in depot form after treatment with N-methyl-N'-nitro-N-nitrosoguanidine significantly reduced the incidence of adenocarcinoma of the glandular stomach. The adenocarcinomas that did develop in rats treated with the higher dose of tetragastrin had high mucin-producing activity and showed little or no typical glandular structure. A combination of propranolol (2 mg/kg) and tetragastrin (1 mg/kg) did not influence the inhibitory effect of gastrin on gastric carcinogenesis. However, concomitant administration of propranolol (2 mg/kg) and tetragastrin (0.2 mg/kg) caused a significant increase in gastric acid secretion and a reduction in the incidence of gastric carcinomas. With this treatment, the incidence of adenocarcinoma was similar to that of treatment with tetragastrin (1 mg/kg). Histological examinations showed that like the cancers in control rats, the adenocarcinomas induced in these rats were all highly differentiated.
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PMID:Enhancement by propranolol of the inhibitory effect of tetragastrin on gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine in Wistar rats. 379 Nov 97

Twenty eight patients with colonic cancer, who were asymptomatic after intestinal resection and anastomosis, underwent colonoscopy as part of their routine follow up, and biopsies were obtained from the anastomosis and several other sites. Sections were stained by haematoxylin and eosin, several methods for mucin, and by the peroxidase-antiperoxidase method for carcinoembryonic antigen. Non-specific inflammatory changes were seen at the anastomosis in 11 of the 28 cases, apparent in several two years after operation; focal surface ulceration was seen in over half these samples. Neither dysplastic nor adenomatous change was detected, but at seven anastomoses the so called transitional change, which has been regarded as a preneoplastic change, was apparent. There was no consistent alteration in carcinoembryonic antigen reactivity. It is concluded that there is morphological evidence of a continued stimulus to regenerative activity at some anastomoses and that this may represent a promoting factor enhancing further carcinogenesis.
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PMID:Mucosal abnormalities at the anastomosis site in patients who have had intestinal resection for colonic cancer. 398 51


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