Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:O76050 (neu)
 3,969 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Overexpression of proto-oncogenes (c-onc) may be involved in the initiation and progression of human neoplasia. We investigated the mRNA expression of the proto-oncogenes c-myc, c-fos, c-neu (erb B-2) and Ha-ras in 12 cutaneous melanocytic lesions (four dermal naevi, seven melanomas; one cutaneous metastatis of melanoma) and in normal skin (five cases) by Northern blot analysis; mRNA expression levels were quantified by densitometry of the specific bands. The expression of c-myc mRNA was higher in naevi than in melanomas, whereas c-fos mRNA expression was significantly higher in melanomas than in naevi. No significant differences were detected in the c-neu and Ha-ras mRNA levels in naevi and melanomas. The expression of c-neu mRNA was higher in normal skin than in the melanocytic lesions examined. Our results suggest that enhanced c-myc and c-fos expression may play an important role in the growth of melanocytic naevi and melanomas. The overexpression of c-fos may be involved in the progression of a particular subset of melanoma. Activation of Ha-ras and the c-neu gene, as determined by mRNA overexpression, does not seem to play a significant role in the progression of cutaneous pigmented lesions. Expression of c-neu may have an important function in the proliferation and/or differentiation of normal cells of the epidermis.
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PMID:Proto-oncogene expression in dermal naevi and melanomas. 168 68

Oncogene analyses of four human myeloma cell lines provided no indication of gene amplification or rearrangement using DNA probes for the met, raf, abl, mos, erb B, Her-2-neu, fos, myb-7, fms, L-myc, sis, and myb-1 genes. However, a consistent elevation of up to 23-fold in the level of c-myc mRNA was observed in all of the cell lines studied. No restriction fragment length polymorphism (in exons one, two, or three) or c-myc gene amplification has as yet been demonstrated to account for the c-myc mRNA elevation. The c-myc mRNA has a half-life of 25 min which is comparable to that observed in other systems. The elevation in c-myc mRNA is further evidence for the role of the c-myc proto-oncogene in the pathogenesis of myeloma.
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PMID:Elevated c-myc messenger RNA in multiple myeloma cell lines. 198 Feb 37

The expression of 6 different oncoproteins and 2 tumour suppressor gene products in the plasma cells of 63 bone marrow samples was used to determine a profile of the oncogenic phenotype of patients with multiple myeloma. Dual label flow cytometry after periodatelysine paraformaldehyde fixation was used to detect cell surface phenotype and intracellular protein expression simultaneously. The normal range for both the incidence and intensity of expression was determined for each protein by analysing plasma cells (high CD38 intensity) in 22 normal bone marrow samples. The percentage of myeloma patients with a greater than normal incidence of plasma cells expressing these proteins was 53% for c-myc, 28% for Rb, 28% for bcl-2, 27% for c-fos, 24% for p53 wild, 22% for p53 mutant, 13% for c-neu and 13% for pan-ras. When a panel of 8 antibodies was used, 82% of the samples (n = 28) had an increased incidence of expression by at least one oncoprotein or tumour suppressor gene product. The 5 patients with a normal incidence of expression of all 8 proteins were in plateau stage and 4 had not received chemotherapy for more than 12 months. The number of patients with an increased incidence of expression by 2 or more oncoproteins was significantly greater (X2 = 9.0; p < 0.005) in progressive disease (55%) than in stable disease (14%) but there was no specific phenotype pattern associated with progressive disease. All 6 oncoproteins and both tumour suppressor gene products had a greater incidence and intensity of expression in progressive than in stable disease. The expression of c-myc oncoprotein correlated with c-myc mRNA expression in the same samples (n = 10) but c-myc did not correlate with either the plasma cell labelling index (r = -0.15) nor serum thymidine kinase (r = 0.10). Our results suggest that there is a heterogeneous, non-systematic but almost universal presence of activated oncogenes and tumour suppressor genes in the plasma cells of patients with multiple myeloma and that disease progression is associated with the accumulation of a variety of secondary genetic changes which confer increased malignant behaviour.
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PMID:The oncoprotein phenotype of plasma cells from patients with multiple myeloma. 769 21

2-Amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP), a mutagen found in cooked meat, has been shown to induce mammary gland tumors in rats. Our laboratory recently observed that a high fat diet enhances the incidence and severity of PhIP-induced mammary gland cancer in rats. In the current study, reverse transcription followed by polymerase chain reaction amplification was used to determine whether EGFR, TGF-alpha, neu and c-myc are differentially expressed in PhIP-induced mammary gland tumors classified histologically as benign or malignant and to evaluate whether dietary fat intake influences the expression of these genes. Of 23 total PhIP-induced mammary tumors examined, 43%, 57% and 74% had increased expression of EGFR, TGF-alpha and neu mRNA respectively. Increased expression of these genes appeared to be consistently present in tumors displaying papillomatosis. In contrast, to the other three genes, c-myc mRNA levels were infrequently elevated. The percentage of dietary fat did not appear to influence the expression of EGFR, TGF-alpha or neu in either tumors or mammary gland from control rats. However, the levels of c-myc mRNA were 1.8- and 2.9-fold higher in the control mammary gland and benign PhIP-induced tumors respectively in rats fed the high-fat diet than in rats fed the low-fat diet, suggesting a slight effect of dietary fat (P < 0.08) on c-myc expression. These results suggest that increased expression of EGFR, TGF-alpha and especially neu is associated with PhIP-induced mammary gland cancer in rats.
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PMID:Analysis of EGFR, TGF-alpha, neu and c-myc in 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine-induced mammary tumors using RT-PCR. 860 90

Genetic alterations of the c-myc, c-neu and int-2 oncogenes have been reported in human breast cancer. In order to determine if these oncogenes are activated at different stages of breast cancer progression, we are using an in vitro system in which human breast epithelial cells (MCF-10F) have been transformed with benzo(a)pyrene(BP) or dimethylbenz(a)anthracene (DMBA). DMBA-treated cells gave rise to clones D3 and D3-1, BP-treated cells gave rise to clones BP1 and BP1-E. BP1-E cell line, derived from BP1 cell line, was tumorigenic in SCID mice. Southern blot analysis detected gene amplification and rearrangement of the int-2 oncogene in BP1 and BP1-E cells, but no changes were detected in D3 and D3-1 cells. Amplification of c-neu gene was only observed in BP1 and BP1-E cell lines. Neither amplification nor rearrangement was detected for the c-myc gene. At the transcriptional level, Northern blot analysis showed that int-2 mRNA was increased 1.5, 1.8, 1.3 and 2.0-fold in the BP1, BP1-E, D3 and D3-1 cell lines respectively. c-neu mRNA was increased 8.0-fold in BP1 and BP-1E cells and c-myc mRNA was increased 1.5-fold in D3 cells, but no changes were detected in the other cell lines. The data indicate that BP treatment induces changes both at the genomic and transcriptional level. However, none of the differences explain the tumorigenic properties of the BP1-E cell line. DMBA treatment induces changes that are only reflected at transcriptional level for the two oncogenes studied. Whereas none of these oncogenes can be considered the driving force in the expression of the tumorigenic phenotype, the interaction among them or with other oncogenes in the expression of the transformation phenotype cannot be ruled out.
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PMID:Activation of C-myc, C-Neu and int-2 oncogenes in the transformation of the human breast epithelial-cell line mcf-10f treated with chemical carcinogens in-vitro. 2155 25