Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P04626 (erbB-2)
 5,251 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We recently proposed a quantitative PCR procedure for the absolute measurement of c-erbB-2 oncogene amplification, based on the simultaneous polymerase chain reaction (PCR) amplification of the target gene and of a competitor DNA molecule acting as internal standard. To increase the number of assayable oncogenes and the accuracy of the quantitative comparison of gene amplification degree within the same tumor, we have now constructed a single synthetic competitor for int-2, c-myc, N-myc epidermal growth factor receptor, and c-erbB-2 genes, and for the reference gene beta-globin. This competitor was constructed by a two-step recombinant PCR procedure and inserted as a 297-bp sequence in a plasmid. The order of primer insertion was designed to obtain competitors of comparable sizes to those of the respective genomic targets, but still easily recognizable from the latter ones by gel electrophoresis. The clone competitor was tested to evaluate the linearity range for each assay. The present application of quantitative PCR based on a multiple competitor represents the first approach for the achievement of a single reagent for the evaluation of a panel of genes potentially amplified in human tumors.
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PMID:Gene amplification for c-erbB-2, c-myc, epidermal growth factor receptor, int-2, and N-myc measured by quantitative PCR with a multiple competitor template. 776

Competitive polymerase chain reaction (PCR) systems were developed for rapid and quantitative estimation of HER-2 (c-erbB-2) and INT-2 oncogene amplification in paraffin-embedded ovarian cancer tissue samples. The beta-globin gene was used as reference and DNA from paraffin-embedded placenta tissue as single copy control. Reliability of the PCR method could be demonstrated by comparing dot blot data with PCR data of identical tumour samples. The PCR method was used to determine HER-2 and INT-2 copy numbers in 196 ovarian cancer samples. HER-2 and INT-2 were found to be amplified in 40 and 19%, respectively. In 8% HER-2 copy numbers were greater than five, but no high INT-2 copies were noted. Kaplan-Meier estimates did not reveal significant association with overall survival. Indirect correlation between HER-2 and INT-2 amplification was observed. The present PCR system is a valuable method for prospective and retrospective studies.
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PMID:HER-2 and INT-2 amplification estimated by quantitative PCR in paraffin-embedded ovarian cancer tissue samples. 810 39

Increases in the average gene copy number (AGCN) of the erbB oncogenes, especially the erbB-2 gene, have been found in a variety of human cancers. Such information is useful with respect to prognosis of the disease. Poor reproducibility and DNA damage complicate quantitative polymerase chain reaction (PCR)-based methods. Therefore, we describe a quantitative PCR method for the estimation of AGCN in the oncogenes erbB-1 (egfr), erbB-2, and erbB-3. The method comprises a competitive and differential PCR in a one-tube reaction (competitive-differential PCR, or cdPCR). Genomic sequences of the oncogene and the human beta-globin (HBB) reference gene and two competitors for the oncogene and reference gene were amplified with two primer pairs simultaneously. The competitors were chosen to be amplified with the same efficiency as the genomic sequences. Using this method, we confirmed egfr and erbB-2 amplification in cancer cell lines and tumor tissue, and we also detected erbB-3 amplifications. Furthermore, gene dosage decreases were detectable, e.g., an erbB-2 hemizygosity in MCF-7 cells. Thus, cdPCR facilitates the detection of both increases and decreases in AGCN with high reproducibility, sensitivity, and accuracy. This method is therefore suitable for clinical studies on erbB oncogene dosage deviations.
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PMID:Competitive-differential polymerase chain reaction for gene dosage estimation of erbB-1 (egfr), erbB-2, and erbB-3 oncogenes. 915 Apr 31

We describe a PCR-based assay for determining c-erbB-2 oncogene amplification in breast cancer in which we use the TaqMan system. Two fluorogenic probes anneal to the target between primers for c-erbB-2 and beta-globin genes and contain both a reporter dye (6-carboxy-fluorescein) and a quencher dye (6-carboxy-tetramethyl-rhodamine). During the extension phase of the PCR cycle, the 5'-->3' exonuclease activity of Taq polymerase cleaves the hybridized fluorogenic probe, resulting in an increase of fluorescence emission of the reporter dye that is quantitative for the amount of PCR product and, under appropriate conditions, for the amount of template. Assay performance showed adequate precision and a lower detection limit and good correlation with the results obtained in the same samples by a competitive PCR assay (n = 25, r = 0.94, P < 0.01). This homogeneous assay is time-saving, avoids usually cumbersome postamplification procedures (that can be additional sources of inaccuracy and contamination), and seems suitable for determination of c-erbB-2 oncogene amplification in tumor specimens.
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PMID:Quantitative polymerase chain reaction-based homogeneous assay with fluorogenic probes to measure c-erbB-2 oncogene amplification. 916 27

Amplification and overexpression of the HER-2/neu (c-erbB-2) oncogene have been observed in many cancers and are associated with a poor prognosis particularly in breast cancer. The human epidermal growth factor (HER)-2 receptor has recently been implicated in Ewing's sarcoma tumor cell line growth and chemosensitivity. The present study evaluates the amplification of HER-2/neu gene in paraffin sections from 42 cases of Ewing's sarcoma by a real-time quantitative polymerase reaction method using LightCycler system (Roche diagnostics, GmbH Mannheim, Germany). The relative copy number of HER-2/neu versus beta-globin was calculated at the crossing point. The mean calculated copy number in these cases of Ewing's sarcoma and normal controls was 26.43 and 26.93, respectively. The p value was 0.215 (p<0.05). Our results demonstrated an absence of HER-2/neu oncogene amplification in Ewing's sarcomas, and we suggest that HER-2/neu is not a biologically or therapeutically important pathway in Ewing's sarcoma.
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PMID:Absence of amplification of HER-2/neu (c-erbB-2) gene in Ewing's sarcoma: a real-time polymerase chain reaction method. 1564 3