Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0001418 (adenocarcinoma)
 68,496 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To investigate a possible relationship between the exposure to tobacco smoke and the presence of ras point mutations, we examined lung adenocarcinoma samples from 27 smokers and from 27 nonsmokers. Activating point mutations in K-ras (also known as KRAS2) and N-ras (also known as NRAS) were determined by using the polymerase chain reaction and oligonucleotide hybridization to detect the mutated sequences. Mutations were more often found in adenocarcinomas obtained from smokers (eight of 27) than in adenocarcinomas obtained from nonsmokers (two of 27) (P = .044, Fisher's exact test). All mutations were present in K-ras codon 12. None of the other parameters examined differed significantly between the ras-positive and ras-negative groups. We conclude that exposure to carcinogenic agents in tobacco smoke is an important factor in the induction of point mutations in K-ras in human lung adenocarcinomas, but that K-ras mutations may also infrequently occur in tumors of non-smokers.
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PMID:Relationship between K-ras oncogene activation and smoking in adenocarcinoma of the human lung. 207 10

Twenty-four Harderian glands from 16 transgenic mice carrying a v-Ha-ras gene under the control of the mouse mammary tumor virus promoter were examined histologically upon death of the animals. Eight glands were histologically normal and eleven were hyperplastic. Four additional glands showed predominantly hyperplasia, but also contained foci of dysplasia and in situ carcinoma. One gland contained an adenocarcinoma. The range of pathology observed in the Harderian glands of these transgenic mice was similar to that which arises spontaneously, although hyperplasia, and not adenoma, occurred in these mice as the benign tumor.
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PMID:Harderian gland pathology in transgenic mice carrying the MMTV/v-Ha-ras gene. 215 84

Increased expression of mouse mammary tumour virus (MMTV) is associated with hyperplastic alveolar growth and subsequent development of mammary cancers in the mouse. The expression of this virus is repressed when mammary tumour cells undergo sarcomatous transformation. We have demonstrated that a spontaneous progression of mouse mammary adenocarcinoma cells into highly malignant cells with the transformed phenotype is accompanied by an increased expression of transforming growth factors alpha and beta (TGF alpha and TGF beta), as well as a decreased expression of MMTV. Mouse mammary adenocarcinoma cells transformed with activated ras oncogene also expressed high levels of the transforming growth factors and a low level of MMTV. Thus a reverse correlation exists between the increased expression of the transforming growth factors and a low level of expression of MMTV. Mouse mammary cells that express high levels of MMTV when treated with exogenous TGF alpha and TGF beta 1 showed a down regulation of MMTV expression in response to TGF beta 1 but not to TGF alpha. These results demonstrate that the repression of MMTV expression in mouse mammary tumour progression may be due in part to an increased expression of TGF beta.
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PMID:Transforming growth factor-beta represses transcription of the mouse mammary tumour virus DNA in cultured mouse mammary cells. 215 76

We have examined the distribution of ras p21 oncoprotein expression in cytologic specimens from 73 primary bronchial carcinomas using an immunocytochemical analysis. The cytologic preparations studied represent the two major groups of histological types of lung cancer: Small Cell Lung Carcinoma (SCLC) and Non-Small Cell Lung Carcinoma (NSCLC) (squamous cell carcinoma and adenocarcinoma). The differential expression of ras p21 oncoprotein correlated with histological classification and was found in 30% of 23 small cell lesions, 61% of 28 squamous cell lung carcinomas and 32% of 22 adenocarcinomas. The ras p21 oncoprotein was commonly expressed in NSCLC cases (48%) as compared to SCLC cases (30%).
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PMID:Immunocytochemical study of RAS oncoprotein in cytologic specimens of primary lung tumours. 216 47

Ras gene is one of the oncogenes most commonly detected in human cancers and consists of three families (H-ras, K-ras, N-ras) that are converted to active oncogenes by point mutations occurring in codon 12, 13, or 61. The authors analyzed mutations of these codons in 12 extrahepatic bile duct carcinomas, nine gallbladder carcinomas, and 20 pancreatic tumors (18 pancreatic adenocarcinomas and two islet cell tumors) by a method to directly sequence nucleotides, using polymerase chain reaction and a direct sequencing method. Point mutations at K-ras codon 12 were found in all of 18 pancreatic adenocarcinomas and in one bile duct carcinoma, but there were no mutations in the remaining 11 bile duct carcinomas, in all of 9 gallbladder carcinomas, or in two islet cell tumors. A very high incidence of ras gene mutations may be used clinically for the diagnosis of debatable cases of pancreatic adenocarcinoma.
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PMID:Analysis of ras gene mutations in biliary and pancreatic tumors by polymerase chain reaction and direct sequencing. 216 48

Adenocarcinomas of the proximal and distal stomach have significant clinical and biological differences. A study was undertaken to determine if a difference in the incidence of mutated ras oncogenes exists between proximal (gastroesophageal junction or cardia) and distal (body or antrum) gastric tumors, and to assess the overall incidence in gastric cancers from non-Asian patients. Deoxyribonucleic acid from 28 primary gastric adenocarcinomas were analyzed for point mutations in codons 12, 13, and 61 of the Ha-ras, Ki-ras, and N-ras protooncogenes using polymerase-catalyzed chain reaction methodology. Twelve tumors were located at the gastroesophageal junction or cardia, and 16 in the body or antrum. Mutated ras genes were detected in 2 of 28 tumors for an overall incidence of 7%. The mutations occurred in codon 61 of the N-ras gene in a proximal gastric cancer and in codon 12 of the Ki-ras gene in a distal gastric cancer. These data indicate that mutations in ras genes are an uncommon event in primary gastric cancers and that there is no meaningful difference in the incidence of ras mutations in proximal and distal stomach cancers.
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PMID:Infrequent point mutations of ras oncogenes in gastric cancers. 217 35

Tumor necrosis factor (TNF-alpha) is a cytokine produced by macrophages and monocytes, and has been shown to have cytolytic, cytostatic or growth-stimulatory activity on transformed cells. However, the mechanism of these growth modulating activities of TNF-alpha is unknown. By studying the response of different oncogene-transformed NIH3T3 cells to TNF-alpha, we showed that the oncogene v-abl confers resistance to the cytostatic and cytolytic activities on TNF-alpha compared to the parental NIH3T3 cells. Most interestingly, v-abl expression also resulted in a growth-enhancing response to TNF-alpha at up to the highest dose of 6,400 units/ml. These altered properties were not due to the transformation event itself, since EJ-ras oncogene transformed NIH3T3 cells were more susceptible to TNF-alpha than the parental cells. Moreover, EMT-6, a mouse adenocarcinoma cell line, which responded similarly to NIH3T3 cells, did not show growth-enhancement at high TNF-alpha dosages. Though resistant to the direct cytotoxic activity of TNF-alpha, the v-abl transformed cell line was effectively killed by macrophages, as were the other cell lines. This suggests tumor cell killing by macrophages must involve mechanisms in addition to the secretion of TNF-alpha.
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PMID:V-abl confers resistance and growth advantage to TNF-alpha in NIH3T3 cells. 218 46

Activation of c-Ki-ras by point mutation within exon 1 was studied in 33 specimens of dysplastic gastrointestinal lesions or of cancers presumed to arise from dysplasia. Samples were obtained from patients with underlying ulcerative colitis or Barrett's esophagus, two diseases associated with dysplasia and increased rates of colonic or esophageal adenocarcinoma, respectively. Genomic DNA was amplified using primers bounding this exon in the polymerase chain reaction. Polymerase chain reaction products were analyzed by direct dideoxy sequencing. Three point mutations in codon 13 of c-Ki-ras were found, all in colonic specimens (two high-grade dysplasias and one adenocarcinoma arising in ulcerative colitis). No point mutations were observed in the second exon of c-Ki-ras or in and around codons 12, 13, and 61 of c-N-ras and C-Ha-ras in a partial sampling of the specimens. These data indicate that ras family protooncogene activation is an uncommon event at this level of malignant progression in these disease states. Carcinogenesis in ulcerative colitis and Barrett's esophagus may proceed via different pathways than in sporadic colon cancer, perhaps involving loss or inactivation of suppressor genes.
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PMID:Activation of c-Ki-ras in human gastrointestinal dysplasias determined by direct sequencing of polymerase chain reaction products. 218 99

The correlation between clinicopathologic findings and point mutation in codon 12 of c-Ki-ras gene was examined in primary lung adenocarcinomas using polymerase chain reaction and oligonucleotide hybridization techniques. The mutation was detected in ten of 67 cases (15%). Microscopically, mutation-positive cases revealed a tendency to be well differentiated (P less than 0.01). Especially, the incidence of the mutation-positive cases was significantly higher in goblet cell type (three of four) than in other types (five of 56) (P less than 0.001). None of 21 cases of pure Clara cell type showed the mutation (P less than 0.05). The mutation was detected frequently in tumors with no lymph node metastasis (P less than 0.05), with larger tumor size (P = 0.01), and T2 cases (P less than 0.01). Cigarette smoking was not always a contributing factor for mutation. This study revealed that the point mutation of c-Ki-ras codon 12 in lung adenocarcinoma has been associated with the cytologic subtype.
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PMID:Association of point mutation in c-Ki-ras oncogene in lung adenocarcinoma with particular reference to cytologic subtypes. 219 10

The objective of this study was to determine whether activation of c-Ki-ras occurs in carcinogen-induced rat pancreatic tumors. DNAs from 27 samples, which included adenomas, carcinomas in situ, and adenocarcinomas arising in azaserine-treated rats and corn oil-gavaged rats along with a nafenopin-induced rat pancreatic adenocarcinoma were examined for mutation of c-Ki-ras at codons 12, 13, and 61 by using the polymerase chain reaction. Our results indicate that activation of c-Ki-ras is not a common event during pancreatic carcinogenesis in the rat.
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PMID:Activation of c-Ki-ras not detectable in adenomas or adenocarcinomas arising in rat pancreas. 219 2


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