Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027627 (metastases)
 103,950 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have examined the level of the c-myc transcript in 6 esophageal, 16 gastric, 19 colorectal and 1 anal cancer tissue samples; these included four lymph nodes and six hepatic metastases obtained surgically. The esophageal cancer tissues were without an increase of the c-myc transcript, some of the gastric cancer samples showed a two to three fold increase and most of the colorectal and the one anal cancer samples showed a two to ten fold increase when compared with a normal mucosal layer. Therefore, the level of the c-myc transcript in human gastrointestinal malignancies shows organ dependency. Local, lymphatic, and hepatic metastases showed little difference in the level of c-myc mRNA from that of the primary tumor.
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PMID:Expression of the c-myc gene in human gastrointestinal malignancies. 361 99

The effects of expression of human c-myc and both mutated (T24) and normal forms of human Ha-ras-1 were studied in an aneuploid rat fibroblast line (208F). Mutated T24 Ha-ras was also studied in a near-diploid cell derived from early passage Chinese hamster lung fibroblasts (CHL). In contrast to the parental fibroblasts, cells expressing any of the human oncogenes engendered rapidly growing tumours in immune-suppressed animals. Blood- and lymph-borne metastases were observed from both ras- and myc-expressing cells. In general ras-expressing cells were more aggressive than those expressing myc. In the 208F background, expression of c-myc was associated with an incidence of mitosis similar to that in tumours expressing T24 Ha-ras, but incidence of single cell death by apoptosis was higher. Quantitatively, expression of human oncogene mRNA was constant during growth in vivo, and similar to that sometimes observed in human neoplasms. Of 9 endogenous proto-oncogenes, 7 showed no change in expression from the parental fibroblasts, but c-abl and c-fos were strongly expressed in all cells expressing human ras or myc. Thus these tumorigenic cells, although transfected with single human oncogenes, all expressed oncogenes with both nuclear- and membrane-associated products.
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PMID:Rodent fibroblast tumours expressing human myc and ras genes: growth, metastasis and endogenous oncogene expression. 366 73

A set of mouse nonoclonal antibodies against the c-myc oncogene product, a 62,000 dalton nuclear binding protein involved in cell cycle control, has been constructed by immunisation with synthetic peptide fragments. One such antibody, CT14, was radiolabelled with 131I and administered to 20 patients with different malignant diseases. Good tumour localisation was observed in 12 out of 14 patients with primary bronchial carcinoma but not in patients with pulmonary metastases from primary tumours elsewhere. Successfully localised tumours were all 3 cm or more in diameter. Monoclonal antibodies against oncogene products may provide novel selective tools for the diagnosis and therapy of cancer.
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PMID:Localisation of lung cancer by a radiolabelled monoclonal antibody against the c-myc oncogene product. 380 Dec 73

The c-myc oncogene was characterized and its expression analyzed in 32 mammary adenocarcinomas and in 2 benign breast tumors from 34 untreated patients. Southern blot hybridization experiments have demonstrated the amplification of the oncogene (3 to 30 fold) in 3 carcinomas. The analysis of total RNA by Northern blot revealed the presence of a 2.4 kb c-myc RNA band. In 7 out of 10 carcinomas from patients with 3 or more than 3 lymph node metastases the level of c-myc expression evaluated by dot blot analysis was 4 to 14 fold greater than that of normal human tissues. In only 5 out of 22 carcinomas from patients without lymph node metastases or less than 3 invaded nodes the level of c-myc expression was also higher (4 to 10 fold). The level of c-myc expression was not significantly enhanced in the 2 benign tumors. It is suggested that the c-myc gene activation could be associated to a higher degree of malignancy of mammary carcinomas.
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PMID:[Analysis of the expression of the oncogene c-myc in human breast adenocarcinoma]. 393 9

Amplified c-myc oncogene was found in the DNAs of 2 of 11 human stomach cancers transplanted into nude mice; the amplification was 8- to 10-fold in one tumor and 13- to 15-fold in the other. Both tumors in which the c-myc oncogene was amplified were poorly differentiated adenocarcinomas, but there was no clear-cut correlation between the histological types or growth rates of the tumors and amplification of the c-myc oncogene. No amplification of the c-myc gene was detected in DNAs from 4 cultured stomach cancer cell lines, 19 primary stomach cancers or 11 metastases to lymph nodes from human stomach cancers.
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PMID:Amplification of the c-myc oncogene in human stomach cancers. 650 Feb 30

The ras family of cellular oncogenes is one of the most frequently detected families of transformation-inducing genes in human solid tumors. The capacity of breast cancers to grow and metastasize have been related to enhanced expression of normal p21ras rather than the mutant form. Transformation in tumours that lack the mutant p21ras has been suggested to result from transcriptional deregulation of ras. cis-Acting sequence elements that participate in the regulation of gene expression in normal tissues and that could serve as potential targets for the deregulation of expression in tumors have been localized in several genes including c-myc and N-ras. Using a mouse mammary metastasis model system of closely related tumor subpopulations that vary in metastatic potential and with defined deficiencies, we show that c-Ha-ras plays a prominent role as a metastasis-modulating gene in this system. We have identified a highly conserved cis-acting sequence element in the first intron of the mouse and rat, and in the first exon of Ha- and Ki-ras genes of human, mouse and rat. This regulatory sequence confers strong transcription enhancer activity that is differentially modulated by steroid hormones in metastatic and nonmetastatic subpopulations. Our results indicate that perturbations in the regulatory activities of cis-acting sequences such as the one we have identified may play an important role in governing oncogenic potency of Ha-ras through transcriptional control mechanisms.
Invasion Metastasis
PMID:Correlation of differences in modulation of ras expression with metastatic competence of mouse mammary tumor subpopulations. 765 20

A three-step immunoperoxidase staining technique was used in order to estimate the immunohistochemical expression of K-ras, c-fos, c-myc and c-erbB-2 oncoproteins, in paraffin sections of 20 patients, with histologically proven adenocarcinoma of the pancreas. The two oncogenes that were found to be associated with pancreatic adenocarcinoma were K-ras and c-erbB-2. in 15 patients (75%) and four patients (20%), respectively. Positive immunostaining was intense, cytoplasmic and was noted in a great percentage of cancer cells. The same model of expression was observed in the examined cases of metastatic tissue from liver and lymph node metastases. The expression of myc and fos oncogenes was nuclear, weak and was observed in a small number of patients.
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PMID:Oncogenes in cancer of the pancreas. 778 91

The purpose of this study was to identify possible alterations in proto-oncogenes (c-fos, c-jun, c-erbB1, c-erbB2 and c-myc) at the protein level in primary lung carcinomas and simultaneous metastatic lymph nodes of 21 patients. The analysis showed that proteins of c-jun and c-myc were expressed in a significantly higher frequency in metastases than in primary lung tumors. Gross differences were not found between primary tumors and metastatic tumors with regard to the expression of c-erbB1, c-erbB2 and c-fos. The finding of cases with a higher expression of c-jun and c-myc in lymph nodes suggests that metastatic capability may be higher in certain cell populations.
Clin Exp Metastasis 1994 Jul
PMID:Analysis of c-fos, c-jun, c-erbB1, c-erbB2 and c-myc in primary lung carcinomas and their lymph node metastases. 791 70

Amplifications of neu and c-myc were evaluated in 218 and 145 breast cancers (BC), respectively. Oncogene amplifications were determined for the most part by Southern blot. An association between the proportion of nodes affected and the intensity of neu amplification in estadiol receptor negative (ER-) BC was found (P = 0.028), which was confirmed by the multi-factor analysis of variance (P = 0.05). A significantly greater incidence in neu amplifications among BC with metastases was also found (P = 0.031). A strong association (P = 0.01) between the neu and myc amplification was observed. There is a strong association between myc amplification and ER- BC (P < 0.01). It is concluded that (1) the combination ER- with neu amplification might define a new group of more aggressive BC, as is suggested by their associated nodal involvement; (2) the linkage of myc amplifications with ER- BC and high grade of neu amplification might reflect a trait of tumor aggressivity.
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PMID:Estradiol receptors in combination with neu or myc oncogene amplifications might define new subtypes of breast cancer. 798 41

For the integration of new cell biological prognostic factors in daily clinical practice, we need to know not only their prognostic power with respect to prediction of relapse free and overall survival, but also their possible relation to response to endocrine therapy or chemotherapy in order to select adequate treatment for each patient. A large number of cell biological parameters are currently available to predict the prognosis of patients with breast cancer, but it is still difficult to predict the response to treatment accurately. A valuable prognostic factor can be a worthless predictive factor for endocrine therapy or chemotherapy, and vice versa. High tumour levels of ER, PGR, AR and PS2 protein predict a relatively good response to endocrine therapy, whereas EGFR positivity, HER2/neu positivity, aneuploidy, high proliferation indices and possibly high u-PA levels indicate a good chance of a poor response to endocrine therapy in metastatic breast cancer. With respect to chemotherapy, a high proliferation rate and HER2/neu amplification predict a good response to therapy in metastatic disease, whereas MDR gene expression and possibly c-myc amplification are related to a worse response. In conclusion, the newer cell biological parameters can be used to select high and low risk patients and type of systemic treatment and can be used as targets for new treatment modalities.
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PMID:Prognostic factors and response to therapy in breast cancer. 801 96


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