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)

Polyamine concentrations were evaluated in normal human prostatic tissue as well as hyperplastic prostate. Normal tissues had high concentrations of putrescine and spermine with intermediate spermidine concentrations, whereas there was a dramatic increase in the spermine concentration in patients with hypertrophy of the prostate. Although not highly significant, spermidine concentrations were elevated slightly in benign hyperplasia, whereas the putrescine content was decreased compared to normal tissue. Polyamine concentrations were measured also in human kidney tumors and corresponding healthy kidney tissue. The concentration of spermidine in renal carcinomas was significantly elevated when compared to histologically normal areas of the same kidney. The spermine concentration of the tumor was generally lower but not highly significant (p less than 0.01). These data suggest that polyamines are accumulated above normal levels in pathological conditions such as benign hyperplasia of the prostate and renal carcinoma. In both cases, spermidine turnover rate may be influenced by carcinogenesis.
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PMID:Altered polyamine profiles in prostatic hyperplasia and in kidney tumors. 7 57

Carcinogenicity of phenacetin was tested using Sprague-Dawley rats. Two groups of animals containing 50 males and 50 females per group were fed respectively with 2.5% and 1.25% phenacetin diet for 18 months and fed thereafter with basal diet for 6 months. Control animals containing 65 males and 65 females were fed with basal diet for 24 months. Animals surviving more than 24 months were regarded as effective animals and killed. Rats that died of tumor development within 24 months were also regarded effective animals. Every organ from the killed and dead animals was fixed in 10% formaldehyde solution and examined histopathologically. Effective number of rats was 27 males and 27 females in 2.5% phenacetin feeding group, and 22 males and 25 females in 1.25% phenacetin feeding group. In control group, 19 males and 25 females were effective. Neoplasms including spontaneous tumors were detected in 26 out of 27 males (96.3%) and 21 out of 27 females (77.8%) of 2.5% phenacetin feeding group, and in 20 out of 22 males (90.9%) and 19 out of 25 females (76.0%) of 1.25% phenacetin feeding group. In control group, 1 out of 19 males (5.3%) and 6 out of 25 females (24.0%) showed spontaneous tumor development. Histopathologically, carcinomas of the nasal cavity, such as adenocarcinoma, squamous cell carcinoma, and transitional cell carcinoma, and the urinary passage, as renal cell carcinoma of the kidney pelvis, and transitional cell carcinoma of the urinary bladder, were most conspicuous, suggesting the target organs of phenacetin carcinogenesis. Males showed higher tumor incidence compared to females. The higher the concentration of phenacetin given, higher incidence of tumors was observed.
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PMID:Tumors of Sprague-Dawley rats induced by long-term feeding of phenacetin. 44 75

Endocrine modulation of DMN carcinogenesis was studied in NZR/Gd rats preconditioned by starving 48 hr and then injected i.p. once with 20 mg DMN/kg. Intact rats developed kidney tumors (44% TBA), most of tubular epithelial type resembling human tumors rather than mesenchymal. Thyroidectomy (Tx) 45 days before DMN significantly enhanced DMN carcinogenesis, renal carcinoma incidence increasing to 69%. Renal carcinomas showed more signs of malignancy in Tx rats. Other neoplastic responses useful for further studies including tumors in nasal epithelium (13%), liver (18%, increased to 59% in Tx rats), and lung (40%): these tumors were rare or not previously reported in single-dose experiments in other rat strains. A sex difference in lung tumor incidence (male 70%, female 16%) was statistically significant and thyroidectomy reduced the sex-differential (to 54% and 39% respectively). The increased incidence of kidney and liver tumors could be due to altered metabolism of DMN in tissues of Tx rats.
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PMID:Enhancement of hepatic and renal tumorigenesis with thyroidectomized NZR/Gd rats treated with dimethylnitrosamine. 99 15

We analyzed the alteration of int-2, c-erbB-2 and EGFR genes in 32 cases of transitional cell carcinoma of the urinary tract, 15 cases of renal cell carcinoma and 14 cases of prostatic carcinoma by Southern blot hybridization method. Three- to 12 fold amplification of int-2 gene was observed in 4 (12.5%) of 32 transitional cell carcinomas. Of these 4 cases 3 were G3 tumor with muscle invasion and the remaining was G1, pTa tumor with subsequent recurrence of multiple tumors. The other 2 cases (6.3%) with invasive transitional cell carcinoma showed amplification of c-erbB-2 gene. Neither amplification nor gross rearrangement of EGFR gene was detected in transitional cell carcinoma. On the other hand, renal cell carcinomas and prostatic carcinomas had neither amplification nor gross rearrangement of these 3 genes. These results suggest that the int-2 gene located in chromosome locus 11q13 and the c-erbB-2 gene have a specific role in carcinogenesis and in progression of transitional cell carcinoma through their gene amplifications.
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PMID:[int-2 and c-erbB-2 gene amplification in urological cancers]. 136 54

The distribution of O6-methylguanine-DNA methyltransferase (MGMT) activity in extracts of tumors from 74 patients was measured. The results demonstrated that there was considerable variation of MGMT activity in different human tumor tissues as well as in different individuals. The mean values (X +/- SD, pmol/mg of protein) in breast cancer, stomach cancer, small cell lung cancer, non-small cell lung cancer, renal cell carcinoma, esophageal carcinoma, brain tumors, colon carcinoma and malignant melanoma were 1.071 +/- 0.374 (9), 0.515 +/- 0.107 (5), 0.509 +/- 0.251 (5), 0.461 +/- 0.227 (24), 0.329 +/- 0.246 (5), 0.273 +/- 0.376 (5), 0.244 +/- 0.175 (14), 0.242 +/- 0.308 (5) and 0.201 +/- 0.161 (2) respectively. It was notable that six samples (1/24 non-small cell lung cancer, 3/5 esophageal carcinoma, 1/14 brain tumors and 1/5 colon carcinoma) did not have any detectable level of MGMT activity. Activity of glutamine pyruvic transaminase (GPT) was also measured in the same extracts used for the assay of MGMT activity. The activity of GPT in these samples with undetectable level of MGMT activity was similar to those with significant MGMT activity. These results further strengthen the assumption that a certain fraction of human tumors are Mer-.
Carcinogenesis 1992 Sep
PMID:O6-methylguanine-DNA methyltransferase activity in human tumors. 139 31

A rodent model of hereditary cancer in which a single gene mutation predisposes rats to bilateral multicentric renal cell carcinoma (RCC) is described. This rat hereditary cancer syndrome shares certain similarities with von Hippel-Lindau disease (VHLD). In addition to the early development of renal epithelial tumors with morphologic similarity to human RCC, rats which bear the RCC gene are predisposed to the development of secondary primary cancers later in life. Splenic vascular proliferative lesions, including hemangiosarcoma, were seen in 23% of 14-month-old rats of both sexes that had renal tumors. At fourteen months of age, 62% of female rats with renal cell tumors had sarcomas of the lower reproductive tract of probable smooth muscle origin. Non-carrier siblings of affected animals did not have renal, reproductive, or splenic neoplasia. The finding of a specific constellation of familial neoplasms, including multicentric bilateral renal cell carcinoma, in this autosomal dominant disorder of rats suggests that this syndrome is analogous to human VHLD. In addition to its usefulness for studies of the biochemical and molecular mechanisms of renal carcinogenesis, this animal model will provide a unique tool to investigate how cancer susceptibility genes interact with environmental risk factors such as chemical carcinogens.
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PMID:Hereditary renal cell carcinoma in the Eker rat: a rodent familial cancer syndrome. 143 48

Estrogen-induced renal adenocarcinoma usually can be readily detected in castrated hamsters after 9 to 12 months of DES treatment. In the present study, we examined the morphological characteristics of the renal cortices of castrated hamsters that had received 3 months of DES treatment in order to describe early histological evidence of carcinogenesis induction. Twelve Syrian Golden hamsters, 8 to 9 weeks of age, were first castrated and then subjected to either subpannicular implantation of a 20 mg DES pellet (experiment group), or sham operation (controls). Morphological and 2-D morphometric evaluations were conducted sequentially on kidney histological sections. Numbers (N's) or area fractions (AF's) of renal components in the juxta-medullary junction of each kidney section were processed for morphometric evaluation. The DES treatment caused a 15% increase in kidney weight, but not body weight. Dysplastic foci associated with hyperplastic tubules were present in 67% of the left kidneys or 17% of the right kidneys of hamsters in the test group, but were absent in kidneys of controls. DES treatment decreased glomeruli N by 33% and increased the vasculature AF by 169% per examination field. DES also increased AF's of glomeruli, proximal tubules, distal tubules, and vasculature by 17, 81, 53 and 346% per nephron, respectively. Our results showed that, after the first three months of DES-treatment, hamster kidneys developed dysplastic foci and their masses were greater than controls. Increased renal components in the juxta-medullary junction region included glomeruli, tubules, and vasculature. The dysplastic foci may be sites of subsequent malignancies, whereas the increased renal mass might be a result of functional adaptation/expression to exogenous estrogen which might contribute to the carcinogenic process.
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PMID:Morphometric analysis of renal cortex changes induced by diethylstilbestrol (DES) in Syrian hamsters. 147 31

Mutations in codon 12, 13 or 61 of one of the three ras genes, Ha-ras, Ki-ras, and N-ras, convert these genes into active oncogenes. To determine the role mutated ras genes play in the carcinogenesis of renal cell carcinoma, we analysed tumour DNA and unaffected renal tissue derived from 55 patients. The polymerase chain reaction technique was used to amplify DNA fragments containing Ki-, Ha-, and N-ras codons 12, 13, and 61. The amplified fragments were then probed on slot-blots with labeled mutation-specific oligomers. A single Ki-ras mutation (codon 12, gly- greater than val) was detected in a patient with a pT2N2M1 tumour. We concluded that ras oncogene mutations do not play an important role in the initiation of renal cell carcinoma.
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PMID:Mutations in the ras protooncogenes are rare events in renal cell cancer. 159 Oct 47

Several recent studies based on restriction fragment length polymorphism analysis have supported the concept that the accumulation of multiple genetic alterations converts a normal cell to a malignant cell. Activation of oncogenes and/or inactivation of tumor suppressor genes have been observed during tumor progression in colorectal cancer, lung cancer, and breast cancer. To investigate the possibility that multiple genes are altered during the progression of renal cell carcinoma, we have used restriction fragment length polymorphism markers throughout the genome to test for loss of heterozygosity in 38 renal cell carcinomas. Nearly 64% of the tumors had lost heterozygosity on the short arm of chromosome 3. We also observed loss of heterozygosity averaging about 30% at informative loci on six other chromosomal arms (chromosomes 5q, 6q, 10q, 11q, 17p, and 19p). These results lead us to suspect the existence of several tumor suppressor genes associated with carcinogenesis of renal cell carcinoma.
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PMID:Allelotype of renal cell carcinoma. 167 Sep 99

Renal adenocarcinoma was induced in CBA/H/T6J mice by a single intraperitoneal injection of 250 mg/kg of streptozotocin (STZ). Light and electron microscopic examination revealed that the carcinoma was a granular cell type-adenocarcinoma with abundant microvilli, basal lamina and intermediate junction indicating an epithelial cell origin. In histopathological analysis of the process of this carcinogenesis, all of the kidneys examined had a dilatation of proximal tubules in the second month and thereafter. In the fifth month, one of eight kidneys developed an adenoma. The adenoma was found in all the kidneys after the ninth month. An adenocarcinoma developed in one of the 14 kidneys in the twelfth month and in all others in the fifteenth month. In vivo labeling of bromodeoxyuridine on the cells in various stages demonstrated an increase of the labeling index which paralleled with progression of the carcinogenesis process. This finding in in vivo analysis of cell proliferation also supports the idea that serial changes of the kidney which are histopathologically proven correspond to the carcinogenesis process. The original carcinoma (STZ-RCC) has serially been passed in vivo at the present. Intrasplenic injection of STZ-RCC yielded multiple macroscopic foci of metastasis in the liver. This indicates that STZ-RCC has a malignant potential. Thus, STZ-induced mouse renal adenocarcinoma can be applied to the model system to investigate carcinogenesis and biological behaviors of renal cell carcinoma.
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PMID:[Histopathological analysis of chemical carcinogenesis process by streptozotocin in the mouse kidney]. 183 79


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