Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0001430 (adenoma)
 21,222 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The p 21 product of ras oncogene has been detected immunohistochemically in normal, inflammatory, benign and malignant human thyroid tissues. With the monoclonal antibody SCI-oncogene I and an avidin-biotin-peroxidase complex (ABC), the expression of ras p 21 was evaluated in paraffin-embedded sections. The results showed that papillary and follicular adenocarcinomas of the thyroid had moderate to intense staining for ras p 21 in most cases. Cytoplasmic and apical surface staining were the most common patterns of immunoreactivity. Adenomas showed slight positive or negative staining in cytoplasm. Normal thyroid tissues and thyroiditis were uniformly negative. Grave's disease revealed slight to moderate staining in some cases. These findings suggest that ras oncogene is involved in carcinogenesis of thyroid carcinomas. Enhanced expression of ras p 21 may be useful in differentiation of thyroid adenocarcinomas from adenomas and may be a valuable parameter in evaluating biological behavior of tumors.
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PMID:[Expression of ras oncogene product P21 in thyroid tumors: an immunohistochemical study]. 216 39

Remarkable advances in the understanding of specific inherited and acquired genetic events that are important in colonic carcinogenesis have occurred in the last several years. Studies of the population genetics of colon cancer have determined that the gene responsible for familial adenomatous polyposis (FAP), and Gardner's syndrome has been localized on the long arm of chromosome 5 and have more clearly defined the importance of genetic influences in 'sporadic' colon cancer. Studies of the molecular genetics of colon cancer have identified acquired alterations in oncogenes such as the K-ras gene and in putative tumor suppressor genes such as the FAP gene on chromosome 5, the p53 gene on chromosome 17, and the DCC gene on chromosome 18, which appear to mediate important steps in the adenoma-dysplasia-carcinoma sequence. Some of these research advances (FAP gene carriage) are already being used clinically to identify individuals at risk for colon cancer, and they offer great promise for the future of both prevention and therapeutic programs.
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PMID:Lessons from the genetics of colon cancer. 217 30

The biochemical events that make colonic epithelial cells proceed along the adenoma-carcinoma sequence are not well understood. The phosphoinositol signal transduction pathway is involved in the regulation of cell growth and differentiation. To determine its role in colonic neoplasias we performed mass measurements of its second messenger sn-1,2-diacylglycerol in biopsy specimens from normal mucosa and neoplasias of the colon. Normal colonic mucosa was also investigated in patients without colonic abnormalities (n = 10). Compared with pooled diacylglycerol values from five colonic sites (100%), values in patients with a normal colon were highest in the ascending colon (120 (5)%, p less than 0.05) and lowest in the rectum (81 (5)%, p less than 0.01). Absolute diacylglycerol values in patients with normal colons (2.62 (0.16) nmol/mg protein) were not significantly different from those found in the normal mucosa of patients with colorectal neoplasias (2.45 (0.17) nmol/mg protein). Both colonic adenomas (n = 15) and colorectal carcinomas (n = 14) showed significantly decreased diacylglycerol values compared with the adjacent normal mucosa of each patient (72 (4)%, p less than 0.001, and 71 (4)%, p less than 0.001 respectively). The appreciable decrease in mass diacylglycerol values clearly distinguishes adenomas and carcinomas of the colon from the surrounding normal mucosa. This finding suggests that profound metabolic changes of the phosphoinositol signal transduction pathway occur early in the adenoma-carcinoma sequence and may be important in colonic carcinogenesis.
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PMID:Low diacylglycerol values in colonic adenomas and colorectal cancer. 221 Apr 51

Abnormalities in oncogenes, which are broadly classified into viral and cellular oncogenes, and suppressor genes appear critical for the development of colon cancer. Cellular oncogenes contribute to malignant transformation when they become activated by point mutation, translocation, amplification, or loss of regulator sequences. The properties of the oncoproteins, the proteins encoded by oncogenes which are essential for carcinogenesis, are unclear. Suppressor genes normally suppress the tumorigenic phenotype by keeping the growth of cells in check; it is their inactivation that contributes to malignant transformation. Development of colon cancer appears to take place by stepwise accumulation of multiple genetic alterations during the progression from normal colon to adenoma and carcinoma. Activation of ras, an early event in this sequence, is found in 50% of colon cancers; overexpression of c-myc is found in approximately 80%. Inactivation of suppressor genes, which occurs during later stages, is noted in greater than 70% of tumors. A current model of colonic tumorigenesis is presented.
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PMID:Oncogenes and suppressor genes: their involvement in colon cancer. 222 91

The development of colorectal cancer is an excellent example of the complex multistage nature of carcinogenesis and most colorectal cancers are thought to develop from adenomas. In this paper we have reviewed in vitro models developed in our laboratory for the study of human colorectal carcinogenesis. For these studies epithelial cell lines have been isolated from hereditary and sporadic colorectal adenomas representing different stages in tumour progression. Karyotypic analysis has shown specific abnormalities of chromosomes 1, 7, 14, 17, 18 and 22 to occur in these premalignant adenoma cell lines. The majority of cell cultures derived from small adenomas (less than 1 cm in diameter) senesced whereas the larger adenomas (greater than 2 cm in diameter) were more likely to give rise to immortal cell lines indicating that the acquisition of in vitro immortality occurs at a relatively late stage of colorectal carcinogenesis. Abnormalities of chromosome I have been implicated in tumour progression and in the in vitro immortalization of colorectal adenomas. Furthermore, several stages have been described in the transformation of an adenoma cell line PC/AA to a tumorigenic phenotype. Sodium butyrate and the potent carcinogen N-methyl-N-nitro-nitrosoguanidine (MNNG) were used in this transformation. Sodium butyrate is proposed to act as a possible promoter of colorectal carcinogenesis, and MNNG to cause the further genetic changes required for the conversion of the premalignant cells to a carcinoma. Markers to study the progression of an adenoma cell line to a tumorigenic phenotype in vitro include in vitro immortalization, aneuploidy, clonogenicity, resistance to the inhibitory effects of sodium butyrate, anchorage independent growth, ras gene activation, production of active proteinases and tumorigenicity in athymic nude mice. A role for a constitutively produced tumour promoter in colorectal carcinogenesis is discussed together with the possibility that different events are involved in the development of sporadic versus hereditary tumours due to the importance of the microenvironment in hereditary cancer. Our in vitro progression provides the first experimental evidence for the adenoma to carcinoma sequence and the cytogenetic evidence suggests that it is relevant to in vivo carcinogenesis.
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PMID:Colorectal carcinogenesis: sequential steps in the in vitro immortalization and transformation of human colonic epithelial cells (review). 224 Oct 98

Toxicology and carcinogenesis studies of pentaerythritol tetranitrate (PETN), an organic nitrate used in explosives and as a therapeutic agent for angina pectoris, were conducted by administering diets containing PETN,NF (National Formulary Grade, a 1:4 mixture of PETN and lactose) to both sexes of F344 rats and B6C3F1 mice in 14-day, 13-week and 2-year studies. PETN was found to be essentially non-toxic in 14-day and 13-week studies at dietary concentrations as high as 10,000 ppm; the weight gain of female rats was lower than that of controls at 5000 and 10,000 ppm in the 13-week study. In the 13-week studies, one in ten high-dose female rats had an adenoma of the Zymbal gland and one in ten high-dose female mice had a hepatocellular adenoma. Dietary concentrations chosen for the 2-year studies were 5000 and 10,000 ppm for male rats and male and female mice, and 1240 and 2500 ppm for female rats. In the 2-year studies, there were no adverse effects on survival or body weight gains in either sex of rats or mice. No neoplastic or non-neoplastic lesions were considered to be related clearly to PETN administration. Neoplasms of the Zymbal gland occurred at low incidences in PETN-exposed groups of both sexes of rats in the 2-year study.
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PMID:No evidence of toxicity or carcinogenicity of pentaerythritol tetranitrate given in the diet to F344 rats and B6C3F1 mice for up to two years. 225 87

Chronic inflammatory bowel disease (CIBD) and colorectal adenoma are considered as precancerous conditions and lesions of large bowel carcinoma, respectively. They, therefore, may be used to study the behavior of such different factors as tumor-associated antigens and nuclear DNA content abnormalities in colorectal carcinogenesis. Tissue concentrations of carcinoembryonic antigen (CEA) were significantly higher in those precancerous lesions (CIBD: 61 +/- 11.2 ng/mg, adenoma: 70 +/- 6 ng/mg; mean +/- standard error of the mean) than in normal colonic mucosa (36 +/- 4.7 ng/mg). Colorectal carcinoma had still higher tissue levels (437 +/- 108.2 ng/mg). No correlation between tissue CEA and tumor differentiation could be found, but there was a significant difference between aneuploid (747 +/- 354 ng/mg) and diploid (139 +/- 43 ng/mg) tumors. Using flow cytometry DNA aneuploidy was present in 31.6%, 10.5%, and 51.6% of CIBD, colorectal adenoma, and carcinoma, respectively. These data suggest that the occurrence of aneuploidy is not strongly dependent on a malignant transformation, but it may also be present in premalignant colorectal lesions without cellular dysplasia.
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PMID:Tissue carcinoembryonic antigen and DNA aneuploidy in precancerous and cancerous colorectal lesions. 231 59

Soluble nickel(II) ion, given to male F344/NCr rats as a single i.p. injection of nickel(II) acetate tetrahydrate at a dose of 90 mumols/kg body weight at 5 weeks of age, proved an effective initiator of renal cortical epithelial tumors. The tumors were revealed by subsequent dosing with the known renal tumor promoter, sodium barbital (5,5-diethylbarbituric acid, sodium salt) dissolved in drinking water at a concentration of 500 p.p.m. Only one rat given the nickel injection without subsequent promotion developed a single renal cortical adenoma, while multiple tumors were common in nickel(II) initiated/sodium barbital promoted rats. Renal cortical adenocarcinomas, some of them metastatic to lung, liver, and spleen, occurred only in initiated/promoted rats. No excess incidence of nickel-initiated tumors was found in any other tissues in which sodium barbital is known to promote carcinogenesis, such as liver or thyroid. A single i.p. injection of the Ni(II) salt, 95 mumols/kg, appeared to be associated with an increased concentration of 8-hydroxy-2'-deoxyguanosine in DNA extracted from kidneys of rats 16-48 h after injection.
Carcinogenesis 1990 Apr
PMID:Initiation by nickel acetate and promotion by sodium barbital of renal cortical epithelial tumors in male F344 rats. 232 3

The effect of epidermal growth factor (EGF) on rat stomach carcinogenesis induced by N-methyl-N'-nitro-N-nitro-soguanidine (MNNG) was studied. Male Wistar rats given MNNG for 30 weeks in drinking water (80 micrograms/ml) were treated with s.c. injections of human EGF (10 micrograms/kg, once daily) at various stages of the carcinogenesis. Four (30.8%) out of 13 rats treated with EGF immediately after cessation of the MNNG treatment had stomach tumors including one adenocarcinoma, one adenoma and two carcinoids. No stomach tumor was found in rats treated with MNNG alone or in those treated with MNNG and EGF for different periods such as synchronously for 10 weeks, for 30 weeks or throughout the experiment. These findings suggest a possible enhancing effect of EGF on stomach carcinogenesis in rats.
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PMID:Effect of epidermal growth factor on rat stomach carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine. 236 Apr 55

The purpose of this study was to establish an in vitro model for tumor progression in colorectal carcinogenesis, by transforming the premalignant human colonic PC/AA adenoma cell line to the malignant phenotype. A rare clonogenic variant AA/C1 [colony-forming efficiency (CFE) on plastic of 1.05%] was isolated from the diploid PC/AA adenoma cell line (C. Paraskeva, S. Finerty, and S. Powell, Int. J. Cancer, 41: 908-912, 1988). AA/C1 was aneuploid and when treated with 1 mM sodium butyrate for 14 days gave rise to the AA/C1/SB cell line which had an increased CFE on plastic (6.13%) although the cells remained anchorage dependent and nontumorigenic. After exposure of these AA/C1/SB cells to the carcinogen N-methyl-N'-nitro-N'-nitrosoguanidine an anchorage-independent cell line was isolated (AA/C1/SB10). On continuous in vitro passage, the CFE in agarose of AA/C1/SB10 has increased to 17.3% and the cells have become tumorigenic producing adenocarcinomas in athymic nude mice. AA/C1, AA/C1/SB, and AA/C1/SB10 cell lines have common chromosomal abnormalities including a pericentric inversion of chromosome 1 with deletion of part of the short arm and monosomy for chromosome 18. This in vitro progression provides the first reported experimental evidence for the adenoma to carcinoma sequence in the human colon, and the cytogenetic evidence suggests that it is relevant to in vivo carcinogenesis.
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PMID:Neoplastic transformation of a human colonic epithelial cell line: in vitro evidence for the adenoma to carcinoma sequence. 236 46


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